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Cardiovascular Reactivity and Development of Preclinical and Clinical Disease States
Abstract
The objective of this review is to evaluate the evidence for the hypothesis that cardiovascular reactivity can predict the development of preclinical (elevated blood pressure, ventricular remodeling, carotid atherosclerosis) and/or clinical cardiovascular disease states.
A review of the literature was conducted examining prospective studies.
Three large epidemiological studies with long-term follow-up periods (20 years or more) have found blood pressure responses to the cold pressor task to be predictive of subsequent essential hypertension in initially normotensive samples. Studies showing less consistent results have tended to use shorter-term follow-up periods. A larger body of literature demonstrates consistent associations between stress-related cardiovascular reactivity and blood pressure elevations in youth over the course of 1 to 6 years; such relationships have not been consistently shown among adult samples. Moderately consistent evidence points to a positive relationship between reactivity and other measures of subclinical disease (increased left ventricular mass and carotid atherosclerosis) among the few prospective studies that have examined these issues to date. A number of additional factors, however, such as baseline levels of disease risk and exposure to psychosocial stress, seem to moderate these relationships. Health status at baseline also seems to moderate the association between reactivity and clinical coronary heart disease in recent reports: two of three existing studies in initially healthy samples show no evidence of a relationship between reactivity and clinical outcomes, whereas three of four studies in samples with preexisting coronary heart disease or essential hypertension show a positive relationship between reactivity and subsequent disease states.
There is reasonable evidence to suggest that cardiovascular reactivity can predict the development of some preclinical states (eg, increased left ventricular mass and blood pressure) states and perhaps even new clinical events in some patients with essential hypertension or coronary heart disease. However, much more information is needed concerning moderating and potentially confounding variables before the robustness of the positive relationships can become clinically useful.
... Variance in compensatory effort may potentially account for discrepancies and varying effect sizes in the noise-performance literature, but especially effort-related responses in the cardiovascular system are of high relevance for occupational health. Individuals may pay psychophysiological costs for compensatory effort since cardiovascular reactivity has been identified as a key variable in the development of essential hypertension and cardiovascular disease (Baumann et al., 1973;Blascovich & Katkin, 1993;Krantz & Manuck, 1984;Light et al., 1992;Menkes et al., 1989;Steptoe & Ross, 1981;Treiber et al., 2003). ...
... Consistent with previous findings on irrelevant noise effects on physiological activation (e.g., Evans & Johnson, 2000;Frankenhaeuser & Johansson, 1976;Lundberg & Frankenhaeuser, 1978;Tafalla & Evans, 1997), participants in the present assigned task characteristics conditions showed stronger responses of cardiac PEP during task performance-our most sensitive measure of effort intensity (Kelsey, 2012;Richter et al., 2008;Wright, 1996)-when they were exposed to irrelevant noise than those who worked in silence. This compensatory effort allows individuals to cope with the distracting properties of noise on cognitive task performance, but may be linked to health risks: Cardiovascular reactivity has been identified as a key variable in the development of essential hypertension and cardiovascular disease (Baumann et al., 1973;Blascovich & Katkin, 1993;Krantz & Manuck, 1984;Light et al., 1992;Menkes et al., 1989;Steptoe & Ross, 1981;Treiber et al., 2003). When environmental factors (such as irrelevant noise) ask for compensatory effort and cannot be prevented, it is thus crucial to identify conditions that allow the maintenance of moderate cardiovascular activity. ...
... These implications are of high relevance, because sources of irrelevant noise at workplaces are numerous, and noise exposure has been associated with compensatory effort when executing cognitive tasks. This compensatory effort might be associated with psychophysiological costs since cardiovascular reactivity has been identified as a key variable in the development of essential hypertension and cardiovascular disease (Baumann et al., 1973;Blascovich & Katkin, 1993;Krantz & Manuck, 1984;Light et al., 1992;Menkes et al., 1989;Steptoe & Ross, 1981;Treiber et al., 2003). ...
Since personal choice fosters commitment and shields action execution against potentially conflicting influences, two laboratory experiments with university students (N = 228) tested whether engaging in action by personal choice versus external assignment of task characteristics moderates the effect of irrelevant acoustic noise on cardiovascular responses reflecting effort. Participants who could personally choose the stimulus color of moderately difficult cognitive tasks were expected to be shielded against the irrelevant noise. By contrast, when the stimulus color was externally assigned, we predicted receptivity for the irrelevant noise to be high. As expected, in both experiments, participants in the assigned color condition showed stronger cardiac pre‐ejection period reactivity during task performance when exposed to noise than when working in silence. On the contrary, participants who could choose the stimulus color were shielded against the noise effect on effort. These findings conceptually replicate and extend research on the action shielding effect by personal choice and hold practical implications for occupational health.
... Вне зависимости от природы стрессора происходит нарастание коагуляции с подавлением фибринолитической, антикоагулянтной систем [15]. Подобно этому стресс-системы, препятствующие снижению уровня гликемии и развитию гипогликемии, приводят к изменению функциональной активности различных систем организма, в том числе эндокринной, иммун-ной [8,9] и сердечно-сосудистой систем [10,11,12,13,14]. ...
... В исследование включено 74 пациента с СД1 (43 мужчины и 31 женщина). На момент включения средний возраст участников составил 30 лет [24][25][26][27][28][29][30][31][32][33][34][35][36][37] при стаже заболевания 14 лет [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22]. Общая характеристика включенных в исследование представлена в таблице 1. ...
BACKGROUND : Usually, a hypoglycemic episode occurs due to inadequacy of the administered insulin dose in accordance with the current physiological situation. Activated systems aimed at increasing blood glucose levels serve as precursors of hypoglycemia and markers of the severity of hyperinsulinemia. Therefore, determining their components can serve as a more subtle and sensitive approach to assessing the physiological appropriateness of different insulin therapy options.
AIM : To investigate the markers (biochemical, clinical, and morphological) and the degree of activation of the stress system preceding the development of hypoglycemic episodes in patients with type 1 diabetes (T1D) undergoing insulin therapy.
MATERIALS AND METHODS: A cross-sectional observational clinical study was conducted involving 74 patients with type 1 diabetes (T1D). All patients underwent examination, which included assessment of the history of hypoglycemic episodes, quality of life using the SF-36 questionnaire, levels of adrenocorticotropic hormone (ACTH), insulin-like growth factor-1 (IGF-1), cortisol, C-reactive protein (CRP), coagulation profile, and 24-hour urinary cortisol excretion. Evaluation of patients’ sleep characteristics was performed based on the results of completed questionnaires: Sleep Questionnaire and Epworth Sleepiness Scale. Patients underwent overnight polysomnography (PSG) with interpretation according to the AASM 2012 standards.
RESULTS: Patients with a higher frequency of hypoglycemic episodes showed a decrease in IGF-1 levels at all stages (140 [123:162]; 98 [93:121], p=0.005), worse quality of life scores across all domains of the SF-36 questionnaire (95 [88:100]; 84 [77:92], p=0.001). As the frequency of hypoglycemic episodes increased, polysomnography data revealed an increase in the number of awakenings lasting more than 3 minutes (2 [1:3]; 3 [2:4]; p=0.03), increased time spent in bed (493.1 [463.95:513.4]; 536.2 [511.6:551]; p=0.03), increased sleep duration (437.5 [430.05:468]; 489 [471.5:519], p=0.006), and in creased total sleep time (382.5 [321.75:422]; 439 [409.5:486], p=0.008).
CONCLUSION : An increase in the frequency of hypoglycemic episodes should be accompanied by activation of the stress response system; however, repeated episodes of hypoglycemia lead to depletion of the stress response system, as evidenced by a decrease in the level of IGF-1 in patients with frequent hypoglycemic episodes. Hypoglycemic episodes occurring not only during night time but also at other times disrupt the sleep structure by increasing the frequency of nocturnal awaken ings.
... A potential correlate of emotion word use with particular relevance is cardiovascular reactivity, which is commonly indexed by differences in heart rate or blood pressure between rest and trial periods (Centers for Disease Control and Prevention, 2020). A long line of research has shown that elevated cardiovascular reactivity to stress and challenge is a risk factor for the development of cardiovascular disease, one of the leading causes of death worldwide (e.g., Krantz & Manuck, 1984;Smith et al., 2013;Treiber et al., 2003). Another long line of research has implicated social relationships in physical health and longevity (e.g., Holt-Lunstad et al., 2010). ...
... Heightened cardiovascular reactivity can be a risk factor for the development of cardiovascular health symptoms (Krantz & Manuck, 1984;Smith et al., 2013;Treiber et al., 2003). Future studies could extend our work to look at longer-term health correlates of emotion word use, such as the development of cardiovascular disease (Haase et al., 2016) to further evaluate the potential of emotion word use as risk markers. ...
Putting feelings into words is often thought to be beneficial. Few studies, however, have examined associations between natural emotion word use and cardiovascular reactivity. This laboratory-based study examined emotion word use (i.e., from computerized text analysis) and cardiovascular reactivity (i.e., interbeat interval changes from baseline) across two interaction contexts (i.e., conflict and positive conversations) in 49 mixed-sex married couples (age: M = 43.11, SD = 9.20) from diverse socioeconomic backgrounds. We focused on both frequency (i.e., relative proportion of emotion words) and diversity (i.e., relative proportion of unique emotion words) of emotion words. Data were collected between 2015 and 2017 and analyzed treating both partners and conversations as repeated measures, resulting in 196 observations overall (four per dyad). Findings showed that (1) when spouses used more negative emotion words (especially anger), they showed higher cardiovascular reactivity. This finding was robust when controlling for covariates; generalized across gender, interaction contexts, and socioeconomic status. Moreover, (2) when spouses used a more diverse negative emotion vocabulary, they showed higher cardiovascular reactivity, but this was not robust when controlling for negative emotion word frequency. Associations between (3) positive emotion word use and cardiovascular reactivity were not statistically significant. Verbalizing negative emotions thus seems to go along with higher cardiovascular reactivity, at least in the short term. Replication is needed across other relationship types, genders, and sexual orientations. These findings highlight emotion word use as an indicator of cardiovascular reactivity, which has implications for the identification of potential health risks that emerge during marital interactions.
... A potential correlate of emotion word use with particular relevance is cardiovascular reactivity, which is commonly indexed by differences in heart rate or blood pressure between rest and trial periods (Centers for Disease Control and Prevention, 2020). A long line of research has shown that elevated cardiovascular reactivity to stress and challenge is a risk factor for the development of cardiovascular disease, one of the leading causes of death worldwide (e.g., Krantz & Manuck, 1984;Smith et al., 2013;Treiber et al., 2003). Another long line of research has implicated social relationships in physical health and longevity (e.g., Holt-Lunstad et al., 2010). ...
... Heightened cardiovascular reactivity can be a risk factor for the development of cardiovascular health symptoms (Krantz & Manuck, 1984;Smith et al., 2013;Treiber et al., 2003). Future studies could extend our work to look at longer-term health correlates of emotion word use, such as the development of cardiovascular disease (Haase et al., 2016) to further evaluate the potential of emotion word use as risk markers. ...
Putting feelings into words is often thought to be beneficial. Few studies, however, have examined associations between natural emotion word use and cardiovascular reactivity. This laboratory-based study examined emotion word use (i.e., from computerized text analysis) and cardiovascular reactivity (i.e., interbeat interval changes from baseline) across two interaction contexts (i.e., conflict and positive conversations) in 49 mixed-sex married couples (age: M = 43.11, SD = 9.20) from diverse socioeconomic backgrounds. We focused on both frequency (i.e., relative proportion of emotion words) and diversity (i.e., relative proportion of unique emotion words) of emotion words. Data were collected between 2015 and 2017 and analyzed treating both partners and conversations as repeated measures, resulting in 196 observations overall (four per dyad). Findings showed that (a) when spouses used more negative emotion words (especially anger), they showed higher cardiovascular reactivity. This finding was robust when controlling for covariates; generalized across gender, interaction contexts, and socioeconomic status. Moreover, (b) when spouses used a more diverse negative emotion vocabulary, they showed higher cardiovascular reactivity, but this was not robust when controlling for negative emotion word frequency. Associations between (c) positive emotion word use and cardiovascular reactivity were not statistically significant. Verbalizing negative emotions thus seems to go along with higher cardiovascular reactivity, at least in the short term. Replication is needed across other relationship types, genders, and sexual orientations. These findings highlight emotion word use as an indicator of cardiovascular reactivity, which has implications for the identification of potential health risks that emerge during marital interactions.
... We focused on ABP as it is a unique and often superior predictor of cardiovascular disease and mortality in comparison to lab-based and clinic BP [26]. Moreover, moment-to-moment elevations in ABP are also predictive of cardiovascular disease over time [27]. We implemented 20-min time periods based on field and laboratory research demonstrating that mood [28] and BP [29] effects can last for at least this time period. ...
... Overall, the present findings likely have clinical implications given the strong link between ABP and health risk [26,27]. Our analyses highlight the need to better understand the impact of negative interpersonal interactions on both mood and ABP and to examine in-the-moment coping mechanisms. ...
Background:
Negative interpersonal interactions are associated with acute increases in ambulatory blood pressure (ABP). Yet, the mechanisms underlying this relationship are unclear.
Purpose:
This study tested whether negative interpersonal interactions predict higher ABP both in the moment and during subsequent observations, and whether increases in negative mood mediate these relations. These associations were tested among Black and Hispanic urban adults who may be at higher risk for negative interpersonal interactions as a function of discrimination. Race/ethnicity and lifetime discrimination were tested as moderators.
Methods:
Using a 24-hr ecological momentary assessment (EMA) design, 565 Black and Hispanic participants (aged 23-65, M = 39.06, SD = 9.35; 51.68% men) had their ABP assessed every 20 min during daytime accompanied by an assessment of negative interpersonal interactions and mood. This produced 12,171 paired assessments of ABP and self-reports of participants' interpersonal interactions, including how much the interaction made them feel left out, harassed, and treated unfairly, as well as how angry, nervous, and sad they felt.
Results:
Multilevel models revealed that more intense negative interpersonal interactions predicted higher momentary ABP. Mediation analyses revealed that increased negative mood explained the relationship between negative interpersonal interactions and ABP in concurrent and lagged analyses. Discrimination was associated with more negative interpersonal interactions, but neither race/ethnicity nor lifetime discrimination moderated findings.
Conclusions:
Results provide a clearer understanding of the psychobiological mechanisms through which interpersonal interactions influence cardiovascular health and may contribute to health disparities. Implications include the potential for just-in-time interventions to provide mood restoring resources after negative interactions.
... Previous work has shown that both BP and muscle sympathetic nerve activity (MSNA) increase with time during a CPT in both younger and older adults 12 . In studies with long-term follow-up periods (>20 years), it was seen that BP responses to CPT predict the development of hypertension in those normotensive initially 13 . In contrast, a study done with a 40-month follow-up period concluded the BP responses during the CPT were not predictive of future increased resting systolic BP but that responses during a mental arithmetic task were positively correlated with higher follow-up BP 10 . ...
Normotensive individuals with an exaggerated blood pressure response (EBPR) during exercise are at a higher risk of developing hypertension later in life. We assessed vascular and neural differences in those with an EBPR and without. Fifty-five participants (22±4 years, 28 female) completed two maximal exercise tests (Bruce protocol) with brachial artery blood pressure (BP) measured at rest and every 90-seconds throughout the exercise. A third visit assessed carotid-femoral pulse wave velocity, superficial femoral artery flow-mediated dilation (FMD), continuous BP (finger photoplethysmography), and muscle sympathetic nerve activity (MSNA) via fibular nerve microneurography. Continuous BP (n=55) and MSNA (n=44) was assessed at rest for assessment of cardiac and sympathetic baroreflex sensitivity (BRS), and during static handgrip (SHG), post-exercise circulatory occlusion (PECO), and rhythmic handgrip (RHG) exercise. Twenty-four (12 female) participants were classified as EBPR based on American Heart Association guidelines. Peak systolic BP was higher in EBPR (218±20 vs. 177±18 mmHg, P<0.01), but no differences were seen in resting systolic BP (107±8 vs. 104±9 mmHg, P=0.15), FMD (6.2±1.5 vs. 6.9±3.2 %, P=0.43), PWV (5.7±0.5 vs. 5.5±1.4 m/s, P=0.44), or MSNA (19.2±4.6 vs. 16.8±5.9 bursts/min, P=0.14). Both cardiac (19.4±12.0 vs. 21.1±9.7 ms/mmHg, P=0.58) and sympathetic (-3.5±1.4 vs. -3.3±1.1 bursts/100hb/mmHg, P=0.64) BRS were also similar. During SHG, systolic BP was similar (133±18 vs. 124±20 mmHg, P=0.26), despite higher MSNA in the EBPR (41.7±13.7 vs. 28.7±8.6 bursts/min, P<0.01). During PECO, both had similar systolic BP (131±16 vs. 123±22 mmHg, P=0.33), but higher total MSNA (1430±786 vs. 1028±393 AU/min, P=0.02). Systolic BP (129±20 vs. 120±15 mmHg, P=0.14) and MSNA (26.1±6.1 vs. 25.1±10.4 bursts/min, P=0.91) during RHG were also similar. Individuals with an EBPR display larger MSNA, but not BP, responses to SHG and PECO.
... This is in accordance with study done by Victor RG et al 20 which correlated the increase in muscle sympathetic activity during the cold pressor test with the increase in mean arterial pressure. Increased cardiovascular reactivity to the cold pressor test (CPT), a knownsympathoexcitatory stimulus , predicts the future development of hypertension 21 and may represent a preclinical manifestation of hypertension before elevations in peripheral arterial blood pressure are detected says a study. Investigators also hypothesized that the pressor reaction to a cold stimulus was mediated through a neurogenic reflex arc and that repeated pressor episodes led to fixed hypertension 22 . ...
BACKGROUND: A deaf individual has diminished ability to hear sounds like other people do and also cannot speak if he/she has lost ability to hear before age of three. AIMS AND OBJECTIVES: To study and compare cardiovascular autonomic functions in deaf children and normal children. MATERIALS AND METHODS: We conducted a case control study with a sample size of 120 subjects out of which 60 were children from deaf school as cases and 60 were children with normal hearing as controls. Both the groups had 30 males and 30 females. Cardiovascular autonomic function tests such as Systolic Blood Pressure (SBP) response to immediate standing, Blood Pressure (BP) response to Cold pressor test (CPT), Heart Rate (HR) response to immediate standing expressed as 30:15 ratio, HR response to deep breathing were performed and compared among the two groups. Statistical analysis was done using SPSS software version:22 and results are expressed in percentage and proportions. RESULTS: Deaf children showed decrease in SBP on immediate standing, decrease SBP and increase in Diastolic Blood Pressure (DBP) as response to CPT, increase in HR expressed as 30:15 ratio compared to normal children. Depending on response to CPT, 36 subjects were found to be hyperreactors and 84 subjects were normoreactors. CONCLUSION: From the statistically significant results obtained in our study it is inconclusive to proclaim that deaf children are more stressed because of loss of hearing. Also CPT serves as a good study tool to evaluate the hyperreactors who can potentially develop hypertension and other co morbid conditions in their later adulthood.
... The heart rate variability (HRV), quantified by the fluctuations in R-wave to R-wave intervals (RRI), has constituted a useful non-invasive method to evaluate autonomic activity, particularly parasympathetic tone and sympathy-vagal balance at either rest or any physical activities [2][3][4][5]. As the cardiovascular system responds to stressors, HRV may predict certain diseases [6][7][8]. Plus, it can be useful to monitor high performance during training sessions [9][10][11]. Meanwhile, the literature on autonomic activation has explained that the reduction in HRV, consisting of both higher sympathetic and lower parasympathetic activities, can be considered a frequent marker of abnormal and insufficient autonomic nervous system (ANS) adaptation [2,12,13] and the elevation in blood pressure variability [14], which possibly indicates a low heart capacity to respond to multiple physiological and environmental stimuli [14][15][16][17], which is associated with diverse pathological conditions such as coronary heart disease and mortality [18][19][20], future functional decline [21], chronic heart failure [22], sarcopenia [23], and hypertension [24]. ...
Although the use of biofeedback devices is beyond measure, they are widely applied only for clinical purposes. Therefore, this study evaluated whether biofeedback devices could be applied to estimate heart rate variability (HRV) among healthy populations. 60 individuals (46 ± 5 years; 30 women) performed maximal exercise protocol (MEP). At pre- and post-MEP status, HRV indexes were collected by two devices: 1) the electrocardiogram device (ECG); 2) the biofeedback device (BIO). At pre-exercise status, all HRV parameters had significant correlations, ranging from low (r = 0.241) to high (r = 0.779). At post-exercise status, significant correlations for some of the HRV measures were found as well, ranging from low (i.e., r ≤ 0.29) to moderate (i.e., 0.3 ≤ r ≤ 0.49). According to our knowledge, this study is the first attempt to evaluate HRV by biofeedback devices among healthy individuals, which shows they can also be applied as a swift method to examine HRV among healthy individuals, especially in rest conditions.
... According to theories that date back to 1981, there may be a greater risk of developing hypertension if there are increased cardiovascular reactions to acute psychological stresses (also known as active-coping stressors) [21]. Numerous reviews [22][23][24] and meta-analyses [25][26] have supported the "reactivity hypothesis," which has been the subject of extensive research. Many problems remain unresolved, nevertheless, as the original reactivity hypothesis was restricted to the relationship between the consequences of cardiovascular illness and excessive cardiovascular reactivity. ...
... La investigación demuestra que las experiencias intensas, frecuentes y prolongadas de estrés pueden contribuir al desarrollo o a la progresión de una enfermedad, mediante la activación fisiológica que provocan (Lovallo y Gerin, 2003;Treiber et al 2003), y porque los sistemas simpático y neuroendocrino también interfieren en la regulación del sistema inmune, suprimiendo algunas respuestas y mejorando otras (Robles, Glaser y Kiecolt, 2005). ...
Se revisa en la literatura histórica y actual la relación entre personalidad y salud. El vínculo se establece al considerar la personalidad como un módulo que interactúa en un complejo sistema procesual del cual es producto el proceso de salud-enfermedad. Si la salud es bienestar y capacidad adaptativa, ¿cuáles sistemas psicológicos de la personalidad influyen en ella? Se concluye que se relacionan por diversos mecanismos, aunque la revisión imposibilita formular conclusiones estables. Las competencias emocionales podrían enlazar ambas temáticas. Los modelos podrían favorecer aplicaciones clínicas pertinentes, elegir sujetos indicados para la prevención, impulsar políticas de promoción de salud, etc. Son necesarios modelos de investigación que estudien los mecanismos que las unen. Finalmente, las investigaciones sobre personalidad positiva resultan prometedoras.
... In the context of cardiovascular health, for example, epidemiological evidence demonstrates that greater stressor-evoked BP reactivity predicts vascular pathology 14, 15 and early death 16 , consistent with the interpretation that large BP reactions to acute stressors may eventuate in vascular risk -reflected by arterial changes and dysfunction [17][18][19][20][21][22][23][24] . These pathogenic effects may result from repeated pressor influences that injure the endothelial layer of blood vessels via turbulent (non-laminar) blood flow and shear stress 6,25 . ...
Background
Cardiovascular responses to psychological stressors have been separately associated with preclinical atherosclerosis and hemodynamic brain activity patterns across different studies and cohorts; however, what has not been established is whether cardiovascular stress responses reliably link indicators of stressor-evoked brain activity and preclinical atherosclerosis that have been measured in the same individuals. Accordingly, the present study used cross-validation and predictive modeling to test for the first time whether stressor-evoked systolic blood pressure (SBP) responses statistically mediated the association between concurrently measured brain activity and a vascular marker of preclinical atherosclerosis in the carotid arteries.
Methods
624 midlife adults (aged 28-56 years, 54.97% female) from two different cohorts underwent two information-conflict fMRI tasks, with concurrent SBP measures collected. Carotid artery intima-media thickness (CA-IMT) was measured by ultrasonography. A mediation framework that included harmonization, cross-validation, and penalized principal component regression was then employed, while significant areas in possible direct and indirect effects were identified through bootstrapping. Sensitivity analysis further tested the robustness of findings after accounting for prevailing levels of cardiovascular disease risk and brain imaging data quality control.
Results
Task-averaged patterns of hemodynamic brain responses exhibited a generalizable association with CA-IMT, which was mediated by an area-under-the-curve measure of aggregate SBP reactivity. Importantly, this effect held in sensitivity analyses. Implicated brain areas in this mediation included the ventromedial prefrontal cortex, anterior cingulate cortex, insula and amygdala.
Conclusions
These novel findings support a link between stressor-evoked brain activity and preclinical atherosclerosis accounted for by individual differences in corresponding levels of stressor-evoked cardiovascular reactivity.
... Conversely, the concept of skin-deep resilience suggests that, in order to maintain self-control and persistence (i.e., mental resilience) to succeed, physiological health may be compromised in the context of struggles with stressors, particularly for disadvantaged groups (e.g., lower SES, racial minorized groups, Brody et al., 2013). Putting this concept into context, in order to socialize or maintain social relationships with friends (i.e., achieve social success), Black adults who are in the face of various stressors (e.g., structural racism) may experience exaggerated cardiovascular reactivity (a factor that contributes to heightened risks of developing CVDs; Treiber et al., 2003) when they encounter friends compared to White adults. ...
Objetivo: Los estudios han demostrado que el contacto con amigos mejora la salud emocional, pero se sabe poco sobre si los amigos influyen en la salud cardiovascular. Este estudio investigó (a) si los encuentros con amigos y la calidad de estos encuentros se asocian con la reactividad cardiovascular en la vida cotidiana, y (b) si estas asociaciones varían según la raza. Método: Los participantes procedían del Estudio sobre Estrés y Bienestar en la Vida Cotidiana (conocido en inglés como “Stress and Wellbeing in Everyday Life Study”), que incluyó a adultos Negros (n = 76; de 34 a 76 años de edad) y Blancos (n = 87, de 34 a 91 años de edad) que residían en los Estados Unidos. Los participantes proporcionaron información sobre sus antecedentes y redes sociales en una entrevista inicial, seguida de una Evaluación Ecológica Momentánea de cuatro días en la que informaron encuentros sociales cada 3 horas. Al mismo tiempo, los participantes llevaban un monitor de ECG que recopilaba datos fisiológicos en tiempo real. Para evaluar la reactividad cardiovascular, se analizó la variabilidad de la frecuencia cardíaca (HRV, por sus siglas en inglés). Resultados: Los modelos multinivel revelaron que en momentos en que los individuos se encontraban con amigos (particularmente en encuentros positivos), exhibían una reducción momentánea en la HRV (asociación intrapersonal). Pero aquellos con más encuentros con amigos durante el período de estudio (particularmente en encuentros positivos) tuvieron una HRV más alta que aquellos con menos encuentros con amigos durante el período de estudio (asociación entre personas). Estos vínculos se observaron sólo entre los adultos Negros, pero no entre los adultos Blancos. Conclusiones: Este estudio contribuye al modelo conceptual de integración social y enriquece la literatura sobre disparidades raciales en salud cardiovascular desde una perspectiva social. Los hallazgos resaltan las implicaciones de la interacción con amigos para la reactividad cardiovascular momentánea y sugieren que los amigos pueden ser más destacados para la salud cardiovascular para los adultos Negros.
... Many of these studies have focused on cardiovascular reactivity and recovery [11][12][13][14]. Both high cardiovascular reactivity [15][16][17] and/or delayed recovery [18][19][20] are risk factors for cardiovascular diseases, and changes in emotions reflect changes in cardiovascular activity through the sympathetic nervous system (SNS) [21]. In contrast, faster cardiovascular recovery and lower reactivity indicate protective factors and are associated with activity in the parasympathetic nervous system (PNS) [22,23]. ...
Most of the studies on the effect of trait positive affect (PA) and cardiovascular activity have focused on heart rate (HR) and blood pressure (BP) rather than heart rate variability (HRV). However, trait PA might sustain homeostasis for the autonomic system (ANS) by reducing activity in the sympathetic system (SNS) and increasing the activity in the parasympathetic system (PNS). A common index for the PNS is the vagal tone measured indirectly through HRV. The present study assessed whether trait PA influences cardiovascular response to various stress tasks by monitoring participants’ HRV measured by RMSSD (root mean square of successive differences) along with HR and interbeat interval (IBI). A total of 54 participants performed various cognitive tasks and Trier Social Stress Tasks while their vital signs were monitored, and trait PA was measured with PANAS. The cognitive tasks included both high- and low-stress tasks, including fatigue-inducing 20 min Stroop tasks. The results showed overall higher HRV as measured by RMSSD for participants who have higher levels of trait PA, indicating more PNS activity compared with low-trait-PA individuals, particularly at the end of the task performance during the fatigue induction. High-trait-PA individuals also had a lower HR during the fatigue-inducing task and a higher IBI. The results support previous work by further indicating a more adaptive response and consequently better emotional regulation for high-trait-PA individuals in a complex, prolonged task setting.
... A recent systematic review found that exaggerated and blunted reactivity of both the SAM system and HPA axis were related to physical, mental, and behavioral health outcomes (Turner et al., 2020). For example, exaggerated cardiovascular and endocrine reactivity are related to higher resting and ambulatory BP, increased risk of hypertension (Carroll et al., 2017), earlier onset of hypertension (Carroll, Ginty, et al., 2012), depression (Flett et al., 2016), poor sleep (Treiber et al., 2003), increased risk of sudden coronary death , and shorter leukocyte telomeres (Chida & Steptoe, 2010;Massar et al., 2017). This review also found that blunted cardiovascular and endocrine reactivity in response to acute stress are associated with increased risk factors for cardiovascular disease (Brody et al., 1994;Heponiemi et al., 2007;Matthews et al., 2006), addiction (Phillips et al., 2013), symptoms of depression (Phillips et al., 2013) and anxiety , poor sleep quality , and PTSD symptoms in combat veterans (Steudte-Schmiedgen et al., 2015). ...
Many studies have examined physiological responses to acute stress in healthy and clinical populations. Some have documented exaggerated physiological stress reactivity in response to acute stress, while others have reported blunted physiological stress reactivity. Although the literature is conflicted, the relationship between abnormal physiological stress reactivity and negative outcomes is well-established. However, past research has neglected a critical aspect of physiological stress response - respiration - and it is unclear whether differences in respiration rate responses to acute stress are related to health outcomes. This secondary cross-sectional analysis explored differences in outcomes between three subgroups: blunted, moderate, and exaggerated respiration rate reactivity to an acute stress task. In a sample of at least mildly-stressed older adults (n = 55), we found that perceived stress (b = -7.63; p = .004) and depression (b = -9.13; p = .007) were significantly lower in the moderate reactivity group compared to the high reactivity group, and that self-reported mindfulness (b = 10.96; p = .008) was significantly lower in the moderate reactivity group as compared to the low reactivity group. Across outcomes, participants in the moderate range of physiological reactivity showed less negative and more positive psychological attributes and better health outcomes, while the blunted subgroup demonstrated more negative and less positive psychological attributes and worse health outcomes overall, when compared to the exaggerated and moderate groups. This study extends the literature by adding respiration to markers of acute physiological stress reactivity and demonstrating the effects of blunted respiration reactivity on negative psychological attributes and health outcomes.
... High or improved levels of HRV indicate good ANS homeostasis characterizing a healthy individual; in contrast, low or reduced levels of HRV often indicate an imbalance in ANS activity. 1 Such a decrease in HRV can be caused by an increase in sympathetic activity and/or a reduction in parasympathetic activity, 2 and can be a predictor of cardiovascular, metabolic, and other adverse health outcomes. [3][4][5] Therefore, the noninvasive measurement of HRV has become a topic of growing interest in biomedical, clinical and epidemiological research. ...
Purpose: The purpose of this study was to investigate the effects of two different postures (sitting and standing) and three different ambient temperatures (10℃, 20℃, and 30℃) on heart rate variability (HRV) among healthy young adults. Methods: Twelve young adult volunteers (males 6, females 6) were recruited. Following acclimatization to any the room temperature (10℃, 20℃ or 30℃), 5-min measurements of HRV were conducted in sitting and standing postures of the subjects. Results: Compared to the sitting posture, measurements obtained in the standing posture revealed a significant decrease in high-frequency power/HF, root mean square of successive differences between RR intervals, standard deviation of Poincaré plot perpendicular to the line-of-identity or SD1 and SD1/standard deviation of Poincaré plot along the line-of-identity or SD2, and a significant increase in low-frequency power/LF and LF/HF under all experimental conditions (p<0.05 to 0.005). Majority of HRV parameters showed significant differences while the values obtained under 10℃ were compared with 20℃ and 30℃ conditions, respectively (p<0.05 to 0.001). Conclusions: Our findings suggest the predominance of sympathetic tone in the standing compared with sitting posture. Furthermore, colder conditions caused a predominance of the parasympathetic activity in both sitting and standing postures, and such effects of ambient temperature on the sympathovagal balance were stronger in the latter posture.
... Stress vulnerability refers to the established predisposition of some individuals to have an elevated psychophysiological response to stressful stimuli. Stress vulnerability has many immediate effects, such as decreased wellbeing and increased risks of incidents, as well as long-term deleterious consequences (e.g., development of mental and cardiovascular disorders) [1][2][3][4] . Determining factors, such as personality traits, that may affect stress vulnerability is necessary to reduce these risks and promote individualized stress management training. ...
The present study aimed at investigating the influence of personality on both anticipatory stress vulnerability and the effectiveness of coping strategies in an occupational stressful context. Following assessment of individual personality traits (Big Five Inventory), 147 volunteers were exposed to the anticipation of a stressful event. Anxiety and cardiac reactivity were assessed as markers of vulnerability to anticipatory stress. Participants were then randomly assigned to three groups and subjected to a 5-min intervention: relaxation breathing, relaxation breathing combined with cardiac biofeedback, and control. The effectiveness of coping interventions was determined through the cardiac coherence score achieved during the intervention. Higher neuroticism was associated with higher anticipatory stress vulnerability, whereas higher conscientiousness and extraversion were related to lower anticipatory stress vulnerability. Relaxation breathing and biofeedback coping interventions contributed to improve the cardiac coherence in all participants, albeit with greater effectiveness in individuals presenting higher score of openness to experience. The present findings demonstrated that personality traits are related to both anticipatory stress vulnerability and effectiveness of coping interventions. These results bring new insights into practical guidelines for stress prevention by considering personality traits. Specific practical applications for health professionals, who are likely to manage stressful situations daily, are discussed.
... The magnitude of the individual stress response considered to be relatively stable (Manuck, 1994;Matthews et al., 2001), contributes to the development of cardiovascular disease (CVD; Obrist, 1981). Evidence suggests that exaggerated stress responses signify a vulnerability to CVDs; including atherosclerosis (Kamarck et al., 1997;Treiber et al., 2003) and increased left ventricular mass (Allen et al., 1997). One systematic review found exaggerated reactivity was associated with a greater risk and earlier onset of hypertension (Turner et al., 2020). ...
Objectives
Blunted cardiovascular reactivity is associated with a distinct behavioural profile of greater exposure to early life adversity, coupled with higher levels of behavioural disengagement and symptoms of depression. The present study sought to extend on this work by investigating if behavioural clusters with distinct patterns of reactivity were related to health and behavioural outcomes at baseline and at a 4‐year follow‐up.
Methods
Hierarchical cluster analyses were conducted using longitudinal data drawn from the Midlife Development in the United States (MIDUS 2) Biomarker Project and the MIDUS 3 follow‐up 4 years later. During MIDUS, 2 participants (N = 513) underwent a standardized stress testing protocol and had their blood pressure and heart rate monitored throughout. In addition, hierarchical cluster analyses were conducted on responses from measures of early life adversity, behavioural disengagement and depression. Binary logistic regressions were conducted to determine whether cluster membership was related to health and behavioural outcomes which were taken at both time points.
Results
Three behavioural clusters emerged with statistically different blood pressure reactivity patterns. The cluster characterized by greater exposure to early life adversity, higher levels of behavioural disengagement and depressive symptoms, had relatively lower blood pressure reactivity patterns compared with both the exaggerated reactivity cluster and the cluster similar to the sample mean. In fully adjusted models, this cluster was associated with hypertension (p = .050) and depressed affect (p = .033), while Cluster 1 characteristic of an exaggerated blood pressure reactivity profile was associated with depressed affect (p < .001). Cluster membership did not significantly predict future health status.
Conclusion
This study extends research on behavioural clusters characteristic of reactivity profiles to demonstrate how they relate to health and behavioural outcomes during MIDUS 2.
... As women demonstrate a greater adrenocortical response to social rejection compared to men, this sex difference may continue into early adulthood (Stroud et al., 2002). Among children and adolescents, greater SBP and DBP reactivity are associated with elevated resting SBP and DBP, increasing individuals' risk for preclinical and clinical CVD states (Treiber et al., 2003). Although there is strong support for the association between ELS and heightened cardiovascular responding, there is also increasing attention to the phenomenon of blunted cardiovascular reactivity among individuals with a history of early adversity (al'Absi et al., 2021). ...
Detrimental effects of early life stress on cardiovascular health are evident in adolescence. Cardiovascular reactivity and recovery in response to interpersonal stress may be a mechanism. This study aimed to evaluate if adolescent girls with higher early life stress demonstrated greater cardiovascular reactivity and slower recovery to peer rejection. A sample of 92 adolescent girls (age: M = 13.24) self-reported early life stressors. Systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) were continuously measured before, during, and after a laboratory peer rejection paradigm. Counter to hypotheses, adolescent girls with higher early life stress had lower, not higher, HR during the recovery period. Early life stress was not associated with SBP or DBP recovery. Additionally, early life stress was not associated with SBP, DBP, or HR reactivity. Future research is needed to assess if blunted cardiovascular reactivity to interpersonal rejection during adolescence is a mechanism linking early life stress and later cardiovascular disease risk in women.
... At the same time, there is substantial variability in how individuals respond to stress (Rab & Admon, 2021;Sapolsky, 2015;Zänkert et al., 2019), with exaggerated or prolonged stress responses associated with adverse health outcomes. Individuals with excessive responses to and impaired recovery from acute stress are at elevated risk for atherosclerosis, hypertension, myocardial infarction, and cardiovascular disease mortality (Chida & Steptoe, 2010;Panaite et al., 2015;Treiber et al., 2003). Furthermore, stress contributes to dementia risk (Justice, 2018;Lyons & Bartolomucci, 2020;Yuede et al., 2018), which may in part be mediated by noradrenergic modulation of β-amyloid and tau production and clearance (Mather, 2021). ...
Acute stress activates the brain’s locus coeruleus (LC)-noradrenaline system. Recent studies indicate that a magnetic resonance imaging (MRI)-based measure of LC structure is associated with better cognitive outcomes in later life. Yet despite the LC’s documented role in promoting physiological arousal during acute stress, no studies have examined whether MRI-assessed LC structure is related to arousal responses to acute stress. In this study, 102 younger and 51 older adults completed an acute stress induction task while we assessed multiple measures of physiological arousal (heart rate, breathing rate, systolic and diastolic blood pressure, sympathetic tone, and heart rate variability, HRV). We used turbo spin echo MRI scans to quantify LC MRI contrast as a measure of LC structure. We applied univariate and multivariate approaches to assess how LC MRI contrast was associated with arousal at rest and during acute stress reactivity and recovery. In older participants, having higher caudal LC MRI contrast was associated with greater stress-related increases in systolic blood pressure and decreases in HRV, as well as lower HRV during recovery from acute stress. These results suggest that having higher caudal LC MRI contrast in older adulthood is associated with more pronounced physiological responses to acute stress. Further work is needed to confirm these patterns in larger samples of older adults.
... Cardiovascular stress reactivity, innervated by the autonomic nervous system, is one of the pathways leading to cardiovascular disease. Dysregulated cardiovascular stress responses marked by either exaggerated or blunted cardiovascular stress reactivity is associated with increased risks of eventual onset and/or progression of cardiovascular disease (Carroll et al., 2017;Hughes et al., 2018;Phillips et al., 2013;Treiber et al., 2003). Personality disorders are generally accompanied by physiological dysfunction involving autonomic nervous system dysfunction (McCloskey et al., 2005;Siever & Weinstein, 2009), which might be reflected in dysregulated cardiovascular responses to stress. ...
This study aimed to investigate whether and how avoidant personality disorder symptoms are related to cardiovascular reactivity to stress tasks with different levels of cognitive demands. The revised Chinese edition of the avoidant personality disorder subscale of Personality Diagnosed Questionnaire-4+ (PDQ-4+) was administered to 222 undergraduate students randomly assigned to psychological stress tasks (i.e., mental arithmetic tasks) with low, moderate, or high cognitive demands (manipulated by task difficulty), during which their physiological data were continuously collected. Results showed that avoidant personality disorder symptoms and cognitive demands of tasks interactively predicted systolic blood pressure (SBP) and diastolic blood pressure (DBP) reactivity. In specific, avoidant personality disorder symptoms were not associated with SBP reactivity under the low- and moderate-demand conditions and DBP reactivity under the low-demand condition but were associated with blunted SBP reactivity under the high-demand condition and blunted DBP reactivity under the moderate- and high-demand conditions. These findings indicate that the association between avoidant personality disorder symptoms and cardiovascular reactivity to psychological stress is contingent on the cognitive demands of tasks, which have potential implications for physical health.
... Stress vulnerability refers to the established predisposition of some individuals to have an elevated psychophysiological response to stressful stimuli. Stress vulnerability has many immediate effects, such as decreased wellbeing and increased risks of incidents, as well as long-term deleterious consequences (e.g., development of mental and cardiovascular disorders) [1][2][3][4] . Determining factors, such as personality traits, that may affect stress vulnerability is necessary to reduce these risks and promote individualized stress management training. ...
Objective: The present study aimed at investigating the influence of personality on both anticipatory stress vulnerability and effectiveness of coping strategies in a real-life context. Methods: Following assessment of individual personality traits (Big Five Inventory), 147 volunteers were exposed to the anticipation of a stressful event. Anxiety and cardiac reactivity were assessed as markers of vulnerability to anticipatory stress. Then, participants were randomly assigned to three groups and subjected to a 5-min intervention: relaxing breathing, relaxing breathing combined with cardiac biofeedback, and control. The effectiveness of coping interventions was determined through the cardiac coherence score achieved during the intervention. Results. Higher neuroticism was associated with higher anticipatory stress vulnerability, whereas lower conscientiousness and extraversion were related to lower anticipatory stress vulnerability. Relaxing breathing and biofeedback coping interventions contributed to improve the cardiac coherence in all participants, albeit with greater effectiveness in individuals presenting higher score of openness to experience. Conclusions. The present findings demonstrated that personality traits are related to both anticipatory stress vulnerability and effectiveness of coping interventions. These results bring new insights into practical guidelines for stress prevention by considering personality traits. Specific practical applications for health professionals, who are likely to manage stressful situations daily are discussed.
... reactivity hypothesis' proposes that exaggerated cardiovascular responses to stress throughout life may ultimately lead to sustained hypertension through vascular remodelling and altered autoregulation and there is now a reasonable body of prospective data to support this hypothesis(201). The association between birthweight and resting blood pressure is generally stronger in older individuals and increased cardiovascular youth may be a marker of ±ose low birthweight individuals more likely to go on to develop hypertension.Stressed blood pressure has been related to birthweight in one previous study. ...
p>The first study compared three tests of central HPAA function in a group of low birthweight men aged 60-69 years from Hertfordshire, UK. There were no differences in the free cortisol response to awakening or ACTH and cortisol responses during a 100μg corticotrophin-releasing hormone (CRH) test, but low birthweight men had significantly smaller pituitary-adrenal responses during a dexamethasone-suppressed CRH test. While these findings do not explain the HPAA abnormalities associated with low birthweight in previous studies, they provide further evidence of dysregulation of the HPAA in men who were small at birth.
In further analysis of the data, blood pressure, glucose tolerance and plasma lipid concentrations were not related to these measures of central HPAA activity, despite significant positive correlations with morning cortisol concentrations. These data suggest that other mechanisms, for example altered glucocorticoid metabolism, are responsible for elevating circulating cortisol concentrations in men with cardiovascular risk factors.
The second study explored cortisol and blood pressure responses to a series of psychological stress tests in a group of young men and women from Adelaide, Australia. Cortisol responses were not related to size at birth in either sex, but in women there was a significant inverse relationship between birthweight and blood pressure reactivity. This study provides the first human evidence that haemodynamic responses to psychological stress may be programmed antenatally, suggesting a potential mechanism linking reduced fetal growth with raised blood pressure and cardiovascular disease in later life.
In summary, this research does not support the idea that the HPAA is upregulated centrally in low birthweight individuals, but adds to the evidence that the activity of the axis may be influenced by factors affecting fetal growth. The work presented in this thesis has added complexity to the role of the HPAA in the fetal origins of adult disease, and confirms that this is likely to remain an exciting area of research in years to come.</p
... More generally, researchers have found that physiological reactivity to stress in the lab is predictive of how the body responds to stress over time. For example, Treiber et al. (2003) found that in large epidemiological studies following individuals over long periods of time (20 years or more), blood pressure responses of initially normotensive individuals to stress-inducing manipulations were predictive of subsequent incidence of essential hypertension. In this way, repeated exposure to discrimination may work to prime the body to be more physically reactive in stressful or potentially stressful social situations (see also Guyll, Matthews, & Bromberger, 2001). ...
Interpersonal discrimination contributes to health inequalities for disadvantaged groups across numerous stigmatized identities. This effect has been found using cross-sectional, prospective, and experimental designs. Interpersonal discrimination has been associated with poor health across a wide range of mental health outcomes, including greater rates of depression, psychological distress, anxiety, and negative well-being, and also physical health outcomes such as hypertension, diabetes, respiratory problems, self-reported ill health, low birth weight, and cardiovascular disease. This chapter examines the relationship between interpersonal discrimination and health. It first reviews the literature, focusing on current best measurement practices, and then provides support for the theoretical model of the pathways by which interpersonal discrimination impacts health outcomes. The chapter then presents an updated meta-analysis that further supports the model and expands on types of discrimination and outcomes. It concludes with a discussion of directions for future research.
... Research has also linked increased resting sympathetic activity to increased behavioral problems in preschoolers (Esposito et al., 2016), though studies have also found the opposite relation , or no relation (Nelson et al., 2021). Sympathetic reactivity has been associated with health and psychosocial functioning, with elevated reactivity predicting cardiovascular risk (Treiber et al., 2003) and reduced reactivity predicting increased substance use (Brenner and Beauchaine, 2011), poorer emotion regulation abilities (Stifter et al., 2011), and increased aggression (Posthumus et al., 2009) in children. It should be noted that, like PNS reactivity, sympathetic reactivity must be interpreted in the context of task demands. ...
Parental socialization may influence the development of children’s autonomic nervous system (ANS), a key stress-response system. However, to date no quantitative synthesis of the literature linking parenting and child ANS physiology has been conducted. To address this gap, we conducted a pre-registered meta-analysis. A systematic review of the literature identified 103 studies (n = 13,044 participants) with available effect sizes describing the association between parenting and either parasympathetic nervous system (PNS) or sympathetic nervous system (SNS) activity in children. The overall analysis revealed non-significant associations between parenting and child ANS physiology on average. However, moderation analyses revealed a positive association between more positive parenting and higher resting PNS activity that was stronger when a study was experimental rather than correlational, and when the sample included children with a clinical condition. In conclusion, well-controlled experimental studies show that positive parenting is associated with the development of higher resting PNS activity, an effect that may be stronger among children who are at elevated developmental risk.
... Research has also linked increased resting sympathetic activity to increased behavioral problems in preschoolers (Esposito et al., 2016), though studies have also found the opposite relation , or no relation (Nelson et al., 2021). Sympathetic reactivity has been associated with health and psychosocial functioning, with elevated reactivity predicting cardiovascular risk (Treiber et al., 2003) and reduced reactivity predicting increased substance use (Brenner and Beauchaine, 2011), poorer emotion regulation abilities (Stifter et al., 2011), and increased aggression (Posthumus et al., 2009) in children. It should be noted that, like PNS reactivity, sympathetic reactivity must be interpreted in the context of task demands. ...
Parental socialization may influence the development of children’s autonomic nervous system (ANS), a key stress-response system. However, to date no quantitative synthesis of the literature linking parenting and child ANS physiology has been conducted. To address this gap, we conducted a pre-registered meta-analysis. A systematic review of the literature identified 103 studies (n = 13,044 participants) with available effect sizes describing the association between parenting and either parasympathetic nervous system (PNS) or sympathetic nervous system (SNS) activity in children. The overall analysis revealed non-significant associations between parenting and child ANS physiology on average. However, moderation analyses revealed a positive association between more positive parenting and higher resting PNS activity that was stronger when a study was experimental rather than correlational, and when the sample included children with a clinical condition. In conclusion, well-controlled experimental studies show that positive parenting is associated with the development of higher resting PNS activity, an effect that may be stronger among children who are at elevated developmental risk.
... Следует напомнить, что более высокая реактивность ССС на стрессорное воздействие надежно предсказывает возникновение АГ, доклинических и клинических проявлений ССЗ [45,46]. Существуют противоречивые данные о взаимосвязях враждебности/гнева с реактивностью ССС. ...
The review presents the main aspects of the relationship between psychoemotional factors, hostility, anger and cardiovascular diseases. The first chapter describes the main historical stages in the study of this problem, starting from the Middle Ages and ending with fundamental research of the 19-20 centuries. In the second part, the authors demonstrated that hostility/anger are a risk factor for the CVD development and affect the prognosis and course of CVD (hypertension, ischemic heart disease, various cardiac arrhythmias, etc.). In the third chapter, there were studies that found that high rates of hostility/ anger reduced the effectiveness of cardiovascular therapy. In the fourth part, there are the main correlation mechanisms of negative emotions, hostility/anger and the cardiovascular system, carried out through the relationships with the activation of the hypothalamic-pituitary-adrenal, autonomic nervous system, platelet activation, with the changes in the risk factors characteristics etc. In the final chapter, the authors suggested prospects for further study of the problem, probably associated with the assessment of behavioral interventions, pharmacological or complex effects on the severity of hostility/anger to reduce CVD mortality in individuals with high rates of hostility / anger.
... Otherwise, literature about biological mediators in the relationship between marital status and health has been broad (Robles & Carroll, 2011). Among all the possible alternatives, allostatic processes have captured the attention of most researchers, which include cardiovascular reactivity (Linden, Gerin, & Davidson, 2003;Trieber et al., 2003), neuroendocrine (Robles & Kiecolt-Glaser, 2003) and immune pathways (Kiecolt-Glaser, Fisher, Ogrocki et al., 1987;Kiecolt-Glaser, Kennedy, Malkoff et al., 1988). ...
This research report scrutinizes the relationship that is said to exist between marital status and individuals' health status-both physical and psychological aspects of wellness to be included-, as literature on this topic has identified that unmarried individuals usually have worse health conditions than their married equivalents, but this could have been altered due to the increasing changes in partnership. To better understand it, this paper briefly describes the current state of research on the topic, reviewing the existing literature and illustrating some relevant changes in the marital and household tendencies of the last decades, while presenting the causal mechanisms that could be underneath the studied relationship, such as marital quality. Then, the correlation between marital status and health has been statistically studied using an individual-level population dataset, in an attempt to bolster those findings from previous reports and studies. This statistical validation-or not-allows to draw suitable conclusions, whether confirming or discrediting the hypothesis made.
... The cardiovascular stress reactivity hypothesis postulates that exaggerated cardiovascular reactions to acute psychological stress are associated with elevated risk for preclinical and clinical endpoints of cardiovascular disease (for reviews see, Chida & Steptoe, 2010;Gerin et al., 2000;Krantz & Manuck, 1984;Lovallo, 2005;Taylor et al., 2003;Treiber et al., 2003;Turner et al., 2020). Indeed, there is robust cross-sectional and prospective research demonstrating an association between exaggerated cardiovascular stress reactivity and the development of high blood pressure (BP) and hypertension (e.g., Carroll et al., 2011Carroll et al., , 2012Chida & Steptoe, 2010). ...
Cardiovascular reactions to acute psychological stress have been associated with cognitive function. However, previous work has assessed cardiovascular reactions and cognitive function in the laboratory at the same time. The present study examined the association between cardiovascular reactions to acute psychological stress in the laboratory and academic performance in final year high school students. Heart rate, blood pressure, stroke volume, and cardiac output reactions to an acute psychological stress task were measured in 131 participants during their final year of high school. Performance on high school A‐levels were obtained the following year. Higher heart rate and cardiac output reactivity were associated with better A‐level performance. These associations were still statistically significant after adjusting for a wide range of potentially confounding variables. The present results are consistent with a body of literature suggesting that higher heart rate reactions to acute psychological stress are associated with better cognitive performance across a variety of domains.
INTRODUCTION
Caregiver–care recipient (CR) interactions are central to caregiving, yet little is known about dementia caregivers’ daily experiences with CRs. This study examines within‐day effects of time interacting with CRs and interaction quality on caregivers’ heart rate (HR) and whether friend interactions buffer these effects.
METHODS
Dementia caregivers (N = 221) completed baseline interviews and 5‐day ecological momentary assessments (EMAs), reporting time and interaction quality with CRs and friend interactions every 3 hours while wearing heart monitors.
RESULTS
Within‐day analyses revealed time with CRs was associated with increased HR, primarily due to negative interactions. Friend interactions buffered the adverse effects of time interacting with CR and negative CR interactions on elevated HR. Moreover, positive CR interactions were linked to lower HR when paired with friend interactions.
DISCUSSION
Findings provide insights into interventions that reduce negative exchanges within the caregiver–CR dyad and friend‐based programs, which could enhance cardiovascular health among dementia caregivers.
Highlights
More time interacting with the care recipient (CR) was associated with an elevated heart rate (HR).
Negative daily experiences with CRs are more salient in contributing to caregivers’ cardiovascular strain.
Friend interactions can temporarily buffer the adverse effects mentioned above.
Positive CR interactions linked to lower HR when paired with friend interactions.
Socializing with friends can be beneficial, even if some interactions are negative.
Background
Cardiovascular responses to psychological stressors have been separately associated with preclinical atherosclerosis and hemodynamic brain activity patterns across different studies and cohorts; however, what has not been established is whether cardiovascular stress responses reliably link indicators of stressor‐evoked brain activity and preclinical atherosclerosis that have been measured in the same individuals. Accordingly, the present study used cross‐validation and predictive modeling to test for the first time whether stressor‐evoked systolic blood pressure responses statistically mediated the association between concurrently measured brain activity and a vascular marker of preclinical atherosclerosis in the carotid arteries.
Methods and Results
Six hundred twenty‐four midlife adults (aged 28–56 years, 54.97% women) from 2 different cohorts underwent 2 information‐conflict functional magnetic resonance imaging tasks, with concurrent systolic blood pressure measures collected. Carotid artery intima‐media thickness was measured by ultrasonography. A mediation framework that included harmonization, cross‐validation, and penalized principal component regression was then used. Brain areas where functional magnetic resonance imaging activity exhibited reliable direct and indirect effects were identified through bootstrapping. Sensitivity analysis further tested the robustness of findings after accounting for prevailing levels of cardiovascular disease risk and brain imaging data quality. Task‐averaged patterns of functional magnetic resonance imaging activity across distributed brain areas exhibited a generalizable association with carotid artery intima‐media thickness, which was reliably mediated by an area under the curve measure of aggregate systolic blood pressure reactivity. Importantly, this effect held in sensitivity analyses. Implicated brain areas in this mediation included the ventromedial prefrontal cortex, anterior cingulate cortex, insula, and amygdala.
Conclusions
These novel findings support a link between stressor‐evoked brain activity and preclinical atherosclerosis, which is accounted for by individual differences in corresponding levels of stressor‐evoked cardiovascular reactivity.
Peer victimization and bullying behaviors are prevalent during adolescence and have been linked to depression. This study examined whether peer rejection reactivity, defined as physiological responses to peer exclusion, moderated the associations of victimization and bullying behaviors with depressive symptoms 12 months later in a sample of female youths (N = 79, Mage = 13.37 ± 2.31). Participants underwent the Yale Interpersonal Stressor-Child, during which systolic and diastolic blood pressure and heart rate were continuously measured. Parent and youth reports of the youth’s depressive symptoms were utilized. Our results demonstrate that peer rejection reactivity moderates the relationship between victimization and subsequent depressive symptoms but does not moderate the relationship between bullying behaviors and subsequent depressive symptoms. Higher victimization was associated with increased youth-reported depressive symptoms among girls with high reactivity but decreased depressive symptoms among girls with low reactivity. Future research can explore whether reducing emotional and physiological reactivity to peer rejection, as well as increasing interpersonal effectiveness in peer relationships, can reduce depressive symptoms in adolescent girls experiencing victimization.
Social and demographic changes in the recent decades have led to an increase in the prevalence of social isolation and loneliness in modern society. Social isolation and loneliness are common but underrated factors that determine health, especially cardiovascular health. In addition, the results of various studies have shown that the negative impact of loneliness and social isolation leads to dysfunction of other systems. Social isolation and loneliness are accompanied by the development of oxidative stress in brain structures. This stress activates neurons in the prefrontal cortex and limbic areas, which is accompanied by prolonged increased production of glucocorticoid hormones, eventually leading to resistance to glucocorticoids. At the same time, the sympathetic nervous system is also activated, which, against the backdrop of resistance to glucocorticoids, causes a persistent increase in blood pressure and the development of a pro-inflammatory state. As a result, lonely people experience increased peripheral vascular resistance and increased blood pressure. In addition, the atherosclerotic changes in the arteries develop faster. Although the molecular mechanisms responsible for increased cardiovascular risk in lonely and socially isolated people are not well studied, these changes have been proven to contribute to an increased risk of developing cardiovascular disease. Current measures to fight against loneliness and social isolation have the potential to reduce their negative impact on health. However, given their limited use, their effectiveness for society as a whole is insufficient. In order to better understand the mechanisms of the negative impact of loneliness and social isolation on cardiovascular health, more in-depth research and the development of more effective interventions are needed.
Non-Hispanic Black (BL) individuals have the highest prevalence of hypertension and cardiovascular disease (CVD) compared to all other racial/ethnic groups. Previous work focused on racial disparities in sympathetic control and blood pressure (BP) regulation between young BL and White (WH) adults, have mainly included men. Herein, we hypothesized that BL women would exhibit augmented resting sympathetic vascular transduction and greater sympathetic and BP reactivity to cold pressor test (CPT) compared to WH women. Twenty-eight young healthy women (BL:n=14, 224 years; WH:n=14, 224 years) participated. Beat-to-beat BP (Finometer), common femoral artery blood flow (duplex Doppler ultrasound), and muscle sympathetic nerve activity (MSNA; microneurography) were continuously recorded. In a subset (BL n=10, WH n=11), MSNA and BP were recorded at rest and during a two-minute CPT. Resting sympathetic vascular transduction was quantified as changes in leg vascular conductance (LVC) and mean arterial pressure (MAP) following spontaneous bursts of MSNA using signal-averaging. Sympathetic and BP reactivity was quantified as changes in MSNA and MAP during the last minute of CPT. There were no differences in nadir LVC following resting MSNA bursts between BL (-8.74±3.45%) and WH women (-7.48±3.52%; P=0.431). Likewise, peak increases in MAP following MSNA bursts were not different between groups (BL:+2.80+1.4mmHg; vs. WH: +3.02±1.2mmHg; P=0.623). During CPT, increases in MSNA and MAP were also not different between BL and WH women, with similar transduction estimates between groups (ΔMAP/ΔMSNA; P=0.182). These findings indicate that young, healthy BL women do not exhibit exaggerated sympathetic transduction or augmented sympathetic and BP reactivity during CPT.
Emotion suppression may be linked to poor health outcomes through elevated stress-related physiology. The current meta-analyses investigate the magnitude of the association between suppression and physiological responses to active psychological stress tasks administered in the laboratory. Relevant articles were identified through Medline, PsychINFO, PubMed, and ProQuest. Studies were eligible if they (a) used a sample of healthy, human subjects; (b) assessed physiology during a resting baseline and active psychological stress task; and (c) measured self-report or experimentally manipulated suppression. Twenty-four studies were identified and grouped within two separate random effects meta-analyses based on study methodology, namely, manipulated suppression (k = 12) and/or self-report (k = 14). Experimentally manipulated suppression was associated with greater physiological stress reactivity compared to controls (Hg = 0.20, 95% CI [0.08, 0.33]), primarily driven by cardiac, hemodynamic, and neuroendocrine parameters. Self-report trait suppression was not associated with overall physiological stress reactivity but was associated with greater neuroendocrine reactivity (r = 0.08, 95% CI [0.01, 0.14]). Significant moderator variables were identified (i.e., type/duration of stress task, nature of control instructions, type of physiology, and gender). This review suggests that suppression may exacerbate stress-induced physiological arousal; however, this may differ based upon the chosen methodological assessment of suppression.
This chapter applies the biopsychosocial model to understanding how stress impacts physical and mental health for Arab/MENA Americans, using the Model of Cumulative Racial/Ethnic Trauma for Americans of MENA descent (Awad et al., Am Psychol 74(1):76–87, 2019) as the primary framework. The chapter presents a brief overview of some stress models, including Lazarus and Folkman’s transactional model (Stress, appraisal and coping. Springer, 1984), the minority stress model (Meyer, Psychol Bull 129(5):674–697, 2003), and Hatzenbuehler’s psychological mediation model (Psychol Bullet 135(5):707–730, 2009), and covers the impact of stressors associated with migration, acculturation, discrimination, and identity. More specifically, the authors discuss physical harassment, xenophobia, social exclusion, racial epithets, bullying, and institutional discrimination as noteworthy forms of discrimination faced by Arab/MENA Americans. This chapter also provides a summary of the research literature pertaining to moderators and mediators that help explain the relationships between discrimination and various health outcomes, such as family, religion, acculturation, and ethnic identity, and point to the inherently complicated nature of identity and recognition in the lives of Arab/MENA Americans. The authors conclude with a call for general health reports and large-scale data collection efforts to incorporate Arab/MENA American experiences so that accurate information about this population can become more readily available. The authors also encourage researchers to continue exploring mediators and moderators to ultimately provide guidance for how practitioners may intervene and ultimately reduce the negative impacts of stress on health outcomes.KeywordsArab/MENA AmericansRacial/Ethnic TraumaMigrationAcculturationDiscriminationIdentityFamilyReligion
Objectives:
Daily stress and cardiovascular reactivity may be important mechanisms linking cumulative life event stress with cardiovascular health and may help to explain racial health disparities. However, studies have yet to examine links between exposure to life events stress, daily stress exposure, and cardiovascular reactivity. This study assessed links between trajectories of life event stress exposure, daily stressors, and cardiovascular reactivity among Black and White individuals.
Methods:
Participants are from the Stress and Well-being in Everyday Life Study (SWEL) in which 238 individuals (109 Black 129 White; ages 33 to 93), drawn from the longitudinal Social Relations Study (SRS), reported life event stress in 1992, 2005, 2015, and 2018. Of those individuals, 169 completed an ecological momentary assessment study in which they reported stress exposure every three hours and 164 wore a heart rate monitor for up to five days.
Results:
Latent class growth curve models revealed two longitudinal trajectories of life event stress: moderate-increasing and low-decreasing. Individuals in the moderate-increasing stress trajectory reported greater daily stress exposure and links did not vary by race. Black individuals in the low-decreasing trajectory and White individuals in the moderate-increasing trajectory showed positive associations between daily stress and heart rate (i.e., were reactive to daily stress exposure). The link between daily stress and heart rate was not significant among the Black individuals in the moderate- increasing trajectory and White individuals in the low-decreasing trajectory.
Discussion:
Individuals who experience more life events across the adult life course report greater daily stress exposure which has important implications for daily cardiovascular health. Black individuals with moderate-increasing life event stress show evidence of blunted daily stress reactivity (non significant association between daily stress and heart rate) whereas Black individuals with low-decreasing life event stress show evidence of stress reactivity (positive association between daily stress and heart rate). White individuals showed the opposite pattern (albeit marginally). These findings expand the weathering hypothesis and indicate that chronic life event stress may be associated with blunted stress reactivity among Black individuals.
Social relationships influence physical health, yet questions remain regarding the nature of this association. For instance, when it comes to predicting health-relevant processes in daily life, few studies have examined (a) the relative importance of both positive and negative relational experiences, and (b) variability in relational experiences (in addition to mean levels). To address these gaps, we conducted a daily study ( N = 4,005; ~ 30,000 observations) examining relationships, stress, and physiology in daily life. Heart rate and blood pressure were assessed using an optic sensor and integrated with an app-based study. Results demonstrated that higher mean levels of positive and lower mean levels of negative relational experiences predicted lower stress, better coping, and better physiological functioning in daily life, such as lower systolic blood pressure reactivity. Greater variability in negative (but not positive) relational experiences predicted lower stress, better coping, and lower systolic blood pressure reactivity.
The topic of stress regulation and sports can be viewed from two differing perspectives. From the point of view of sports as a health-promoting activity, the focus is on sports as a means to stress regulation. The central question is the degree to which sports, exercise, and physical activity can help us to cope with daily challenges, so that the negative health effects of these stressors can be avoided or reduced. From the point of view of performance sports, on the other hand, the central focus is stress regulation during sporting activity. In other words, how can athletes cope with high levels of training and psychological pressure, without suffering a drop in physical performance or psychological complaints? From this perspective, important factors are those which allow high-performance and elite athletes to perform at the highest level under pressure. The first section of this chapter presents the theoretical foundations of stress regulation and sports; in the second section, the two perspectives presented here will be discussed in detail.
The study determines the peculiarities of the response of the central and peripheral links of to a cold stimulus in people with different levels of blood pressure (BP). The dynamics of blood pressure, heart rate, rheographic index and cardiorhythmography before and after the cold pressor test were evaluated. A significantly higher increase in systolic and diastolic BP in response to the cold pressor test was found in the persons with a normal high level of initial blood pressure (130/85–139/89 mm Hg) (p < 0.05). During the examination, a higher percentage of those with a hyperreactive blood pressure response was found (25%). In the experiment participants with initial blood pressure > 130/85 mm Hg a significant influence of the sympathetic nervous system on the cardiovascular system central and peripheral links in response to cold stress was observed. The individuals with normal (120/80– 129/84 mm Hg) and normal low (110/70-120/80 mm Hg) blood pressure showed a satisfactory response of the cardiovascular system to cold stress, so they should expect less health risks when working at low ambient temperatures.
Previous research has indicated that gratitude and affect-balance play key stress-buffering roles. However, to date there is limited research on the impact of gratitude and affect balance on cardiovascular recovery from acute psychological stress, and whether affect balance moderates the relationship between gratitude and cardiovascular reactions to acute psychological stress. In this study, 68 adults completed measures of state gratitude, positive and negative affect, and completed a laboratory-based cardiovascular stress-testing protocol. This incorporated a 20-minute acclimatization period, a 10-minute baseline, a 6-minute arithmetic stress task, and an 8-minute recovery period. Mixed-effects growth curve models were fit and the results indicated that state gratitude predicted lower systolic blood pressure responses throughout the stress-testing period. Affect balance was found to moderate the association between state gratitude and diastolic blood pressure responses to stress, amplifying the effects of state gratitude. These findings suggest that state gratitude has a unique stress-buffering effect on both reactions to and recovery from acute psychological stress.
p>Inconclusive previous research has hinted at the significance of social support in cancer-related outcomes. Some recent studies have also attempted to show the role of proangiogenic cytokines as the possible underlying mechanisms in this relationship between social support and cancer progression. This thesis aimed to further investigate these pathways by investigating the association between social support, loneliness and disease markers in colorectal cancer.
This thesis systematically reviewed the longitudinal prospective findings ( N = 27) on the relationship between social support and cancer progression, and found that the evidence from methodologically sound studies ( n = 16) was strong for breast cancer (67%) but not for other types of cancer (0%) and mixed cancers (50%). It also suggested that disease-related variables should be considered when assessing the role of psychosocial factors in cancer-related outcomes.
Study 1 adapted and validated an Implicit Association Test of loneliness (IAT-L). This IAT-L showed low internal consistency, and weak construct and criterion-related validity in this study on 50 healthy volunteers (mean age = 24.1 years). In order to overcome these weaknesses, Study 2 used a modified IAT-L and investigated the relationship between implicit loneliness, social support, and cardiovascular reactivity to stress, to establish its predictive validity in another sample of 23 healthy female volunteers (mean age = 22.1 years). Results yielded satisfactory internal consistency of the modified tool (IAT-L (M)), and implicit loneliness was found to be more strongly correlated with cardiovascular reactivity to stress than the explicit measures of social support and loneliness. Finally, Study 3 used the IAT-L (M) to investigate whether implicit loneliness was related with the in situ levels of four important biological markers (three cytokines and oxytocin) along with explicit measures of social support and loneliness in 51 colorectal cancer patients (mean age = 68.3 years). Results showed that implicit loneliness explained significant variance in vascular endothelial growth factor (VEGF), extending previous findings with an implicit test.</p
Objective:
The present study sought to examine whether anxiety propensity dimensions (general trait anxiety vs. trait social anxiety) interact with stressor types (tasks with social vs. non-social challenges) to determine cardiovascular stress responses.
Methods:
A 2 × 3 mixed-factorial experimental design was employed. The State-Trait Anxiety Inventory, the Social Performance and Social Interaction Anxiety Scales were administered to 233 participants, who engaged in a stress task with either social or non-social challenges during which their cardiovascular data were continuously collected.
Results:
General trait anxiety negatively predicted heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP) reactivity (β = -0.16, p = 0.001; β = -0.17, p = 0.001; β = -0.18, p < 0.001), and positively predicted HR, SBP, DBP recovery (β = 0.16, p = 0.012; β = 0.15, p = 0.014; β = 0.15, p = 0.011), regardless of stress types. Social performance anxiety (β = -0.23, p = 0.002; β = -0.25, p = 0.001; β = -0.24, p = 0.001) and social interaction anxiety (β = -0.22, p < 0.001; β = -0.25, p < 0.001; β = -0.22, p < 0.001) only negatively predicted HR, SBP, DBP reactivity to the stress task with social challenges. No associations were observed between trait social anxiety and cardiovascular recovery from the stress task with social or non-social challenges.
Conclusions:
These findings suggest that different trait anxiety dimensions interact with stressor types in affecting cardiovascular stress responses, which have different health implications.
Hypertension (high blood pressure) is a global health problem associated with increased risk of developing cardiovascular disease and other medical consequences. It has long been suspected that psychological factors are associated with elevated blood pressures and an increased incidence of hypertension. Complementing the genetic and lifestyle factors known to be involved in the etiology of hypertension, evidence supports contributing roles of: (1) negative affect, (2) suppressed hostility, (3) emotional defensiveness, (4) cognitive functioning, and (5) cardiovascular reactivity to stress. Typical intervention approaches for hypertension include an array of anti-hypertensive medications although several psychological treatments for patients seeking help in controlling or preventing hypertension show promise.
Background. The "Report of the Second Task Force on Blood Pressure Control in Children - 1987" developed normative blood pressure (BP) data for children and adolescents. These normative data are used to classify BP levels. Since 1987, additional BP data in children and adolescents, the use of newer classes of drugs, and the role of primary prevention of hypertension have expanded the body of knowledge regarding the classification and treatment of hypertension in the young. Objective. To report new normative BP data in children and adolescents and to provide additional information regarding the diagnosis, treatment, and prevention of hypertension in children. Methods. A working group was appointed by the director of the National Heart, Lung, and Blood Institute as chair of the National High Blood Pressure Education Program (NHBPEP) Coordinating Committee. Data on children from the 1988 through 1991 National Health and Nutrition Examination Survey III and nine additional national data sets were combined to develop normative BP tables. The working group members produced initial draft documents that were reviewed by NHBPEP Coordinating Committee representatives as well as experts in pediatrics, cardiology, and hypertension. This reiterative process occurred for 12 draft documents. The NHBPEP Coordinating Committee discussed the report, and additional comments were received. Differences of opinion were adjudicated by the chair of the working group. The final report was sent to representatives of the 44 organizations on the NHBPEP Coordinating Committee for vote. It was approved unanimously by the NHBPEP Co-ordinating Committee on October 2, 1995. Conclusions. This report provides new normative BP tables for children and adolescents, which now include height percentiles, age, and gender. The fifth Korotkoff sound is now used to define diastolic BP in children and adolescents. New charts have been developed to guide practicing clinicians in antihypertensive drug therapy selection. The primary prevention of hypertension in these age groups is discussed. A statement on public health considerations in the treatment of children and adolescents is provided.
THE PURPOSE of the "Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure" (JNC VI) is to provide guidance for primary care clinicians. The committee recognizes that the responsible clinician's judgment of the individual patient's needs remains paramount. Therefore, this national guideline should serve as a tool to be adapted and implemented in local and individual situations. Using evidence-based medicine and consensus, the report updates contemporary approaches to hypertension control. Among the issues covered are the important need for prevention of high blood pressure by improving lifestyles, the cost of health care, the use of self-measurement of blood pressure, the role of managed care in the treatment of high blood pressure, the introduction of new combination antihypertensive medications and angiotensin II receptor blockers, and strategies for improving adherence to treatment. The JNC VI report places more emphasis than earlier reports on absolute
There is increasing recognition in the medical and scientific communities
of the importance of behavioral and psychosocial factors in the prevention,
development, and treatment of cardiovascular disorders.1
The purpose of this article is to review the evidence and mechanisms for the
effects of acute and chronic stress in individuals with preexisting coronary
artery disease (CAD), and evidence for the efficacy of psychosocial interventions
in patients with CAD.
To examine the combined influence of workplace demands and changes in blood pressure induced by stress on the progression of carotid atherosclerosis.
Population based follow up study of unestablished as well as traditional risk factors for carotid atherosclerosis, ischaemic heart disease, and other outcomes.
Eastern Finland.
591 men aged 42-60 who were fully employed at baseline and had complete data on the measures of carotid atherosclerosis, job demands, blood pressure reactivity, and covariates.
Change in ultrasonographically assessed intima-media thickness of the right and left common carotid arteries from baseline to 4 year follow up.
Significant interactions between workplace demands and stress induced reactivity were observed for all measures of progression (P < 0.04). Men with large changes in systolic blood pressure (20 mm Hg or greater) in anticipation of a maximal exercise test and with high job demands had 10-40% greater progression of mean (0.138 v 0.123 mm) and maximum (0.320 v 0.261 mm) intima-media thickness and plaque height (0.347 v 0.264) than men who were less reactive and had fewer job demands. Similar results were obtained after excluding men with prevalent ischaemic heart disease at baseline. Findings were strongest among men with at least 20% stenosis or non-stenotic plaque at baseline. In this subgroup reactive men with high job demands had more than 46% greater atherosclerotic progression than the others. Adjustment for atherosclerotic risk factors did not alter the results.
Men who showed stress induced blood pressure reactivity and who reported high job demands experienced the greatest atherosclerotic progression, showing the association between dispositional risk characteristics and contextual determinants of disease and suggesting that behaviourally evoked cardiovascular reactivity may have a role in atherogenesis.
This study assesses the prognostic value of mental stress-induced ischemic left ventricular wall motion abnormalities and hemodynamic responses in patients with stable coronary artery disease (CAD). Seventy-nine patients (76 men and 3 women) with prior positive exercise test results were exposed to mental arithmetic and a simulated public speech stress in 2 prior studies. Ischemic wall motion abnormalities were monitored using echocardiography or radionuclide ventriculography (RNV). During mental stress testing, new or worsened ischemic wall motion abnormalities to mental stress and exercise were ascertained, as were peak changes in blood pressure and heart rate to mental stress. The occurrence of subsequent cardiac events (including cardiac death, nonfatal myocardial infarction, or revascularization procedures) was ascertained. New cardiac events were observed in 28 of 79 patients (35%) after a median follow-up duration of 3.5 years (range 2.7 to 7.3). Survival analysis indicated that 20 of 45 patients with mental stress ischemia (44%) experienced new cardiac events more frequently than those without mental stress ischemia (8 of 34; 23%; p = 0.048). Type of cardiac event did not differ between mental stress-positive and stress-negative patients. After controlling for baseline blood pressure and study group status (echocardiography vs RNV), there was a significantly higher relative risk of subsequent events for patients with high versus low peak stress-induced diastolic blood pressure responses (RR = 2.4, confidence interval 1.1 to 5.2; p = 0.03). These results demonstrate that ischemic and hemodynamic measures obtained from mental stress testing may be useful in assessing prognosis in CAD patients with prior positive exercise test results.
A pattern of left ventricular hypertrophy evident on the electrocardiogram is a harbinger of morbidity and mortality from cardiovascular disease. Echocardiography permits the noninvasive determination of left ventricular mass and the examination of its role as a precursor of morbidity and mortality. We examined the relation of left ventricular mass to the incidence of cardiovascular disease, mortality from cardiovascular disease, and mortality from all causes in 3220 subjects enrolled in the Framingham Heart Study who were 40 years of age or older and free of clinically apparent cardiovascular disease, in whom left ventricular mass was determined echocardiographically. During a four-year follow-up period, there were 208 incident cardiovascular events, 37 deaths from cardiovascular disease, and 124 deaths from all causes. Left ventricular mass, determined echocardiographically, was associated with all outcome events. This relation persisted after we adjusted for age, diastolic blood pressure, pulse pressure, treatment for hypertension, cigarette smoking, diabetes, obesity, the ratio of total cholesterol to high-density lipoprotein cholesterol, and electrocardiographic evidence of left ventricular hypertrophy. In men, the risk factor-adjusted relative risk of cardiovascular disease was 1.49 for each increment of 50 g per meter in left ventricular mass corrected for the subject's height (95 percent confidence interval, 1.20 to 1.85); in women, it was 1.57 (95 percent confidence interval, 1.20 to 2.04). Left ventricular mass (corrected for height) was also associated with the incidence of death from cardiovascular disease (relative risk, 1.73 [95 percent confidence interval, 1.19 to 2.52] in men and 2.12 [95 percent confidence interval, 1.28 to 3.49] in women). Left ventricular mass (corrected for height) was associated with death from all causes (relative risk, 1.49 [95 percent confidence interval, 1.14 to 1.94] in men and 2.01 [95 percent confidence interval, 1.44 to 2.81] in women). We conclude that the estimation of left ventricular mass by echocardiography offers prognostic information beyond that provided by the evaluation of traditional cardiovascular risk factors. An increase in left ventricular mass predicts a higher incidence of clinical events, including death, attributable to cardiovascular disease.
Left ventricular hypertrophy (LVH) is a powerful, independent contributor to cardiovascular complications and all-cause death. Although the basis for adverse risk in LVH is incompletely understood, several pathophysiologic mechanisms are believed to play important roles. Demand ischemia on the basis of increased left ventricular muscle mass, impaired coronary vasodilator reserve, and abnormal coronary autoregulation act in concert to sensitize the hypertrophied ventricle to ischemia and infarction. The abnormal increase in interstitial fibrosis and collagen volume fraction in pathologic LVH may also contribute to life-threatening arrhythmias as well as impaired diastolic function and heart failure. The imposition of supply ischemia from associated epicardial coronary artery disease further worsens the risk for cardiac morbidity and mortality. Risk factor modification in order to prevent LVH is justified; however, additional long-term studies are needed to determine whether regression of established LVH results in improved prognosis.
The Hypertension Detection and Follow-up Program (HDFP) data are reported by diastolic blood pressure (DBP) stratum for four race-sex subgroups. For Stratum I (entry DBP 90–104 mm Hg) in each of the race-sex subgroups (black male, black female, white male, and white female), Stepped Care (SC) participants experienced a reduced mortality as compared to Referred Care (RC). For black males and females in all three entry DBP strata, mortality was lower in the SC than RC. Only in three subgroups did the SC mortality exceed RC: Stratum II (entry DBP 105–114 mm Hg) white females and Stratum III (entry DBP 115+ mm Hg) white males and females. Possible explanations for these deviant findings are discussed. The HDFP was designed to determine the difference in total 5-year mortality between SC and RC; subgroup analyses may be subject to large chance variation and must be interpreted with great caution. The value of vigorous treatment of “mild” hypertension (Stratum I) in males and females, black and white, and the value of treatment for all blood pressure strata in blacks are confirmed by this analysis.
Pathology laboratories in nine cooperating centers collected arteries from 1532 persons 15 through 34 years of age who died of external causes, principally homicides, accidents, and suicides. A central laboratory stained the arteries and evaluated the atherosclerotic lesions. All of the aortas and about half of the right coronary arteries in the youngest age group (15 through 19 years) had lesions. The mean percent intimal surface involved by lesions, in 5-year age groups, increased from 15 through 34 years. Raised lesions increased with age in extent and prevalence in the aorta and the right coronary artery. Black subjects had more extensive fatty streaks than white subjects in all three arterial segments. Young women had more extensive fatty streaks in the abdominal aorta; young men had more in the thoracic aorta. Male subjects had more extensive and a higher prevalence of raised lesions than did female subjects in the right coronary artery. White and black subjects did not differ significantly in the extent of raised lesions. Among the three arterial segments, the right coronary had the least percentage of intimal surface involved with all types of lesions but had the highest proportion of raised lesions among total lesions. These results confirm the origin of atherosclerosis in childhood and show that the prevalence and extent of fatty streaks and fibrous plaques increase rapidly during the 15- through 34-year age span.
To assess the prognostic significance of left ventricular mass and geometry in initially healthy persons with essential hypertension. An observational study of a prospectively identified cohort. University medical center. Two hundred and eighty patients with essential hypertension and no pre-existing cardiac disease were evaluated using echocardiography between 1976 and 1981. Two hundred and fifty-three subjects or their family members (90%) were contacted for a follow-up interview an average of 10.2 years after the initial echocardiogram was obtained; the survival status of 27 patients lost to follow-up was ascertained using National Death Index data. Left ventricular mass exceeded 125 g/m2 in 69 of 253 patients (27%). Cardiovascular events occurred in a higher proportion of patients with than without left ventricular hypertrophy (26% compared with 12%; P = 0.006). Patients with increased ventricular mass were also at higher risk for cardiovascular death (14% compared with 0.5%; P less than 0.001) and all-cause mortality (16% compared with 2%; P = 0.001). Electrocardiographic left ventricular hypertrophy did not predict risk. Patients with normal left ventricular geometry had the fewest adverse outcomes (no cardiac deaths; morbid events in 11%), and those with concentric hypertrophy had the most (death in 21%; morbid events in 31%). In a multivariate analysis, only age and left ventricular mass--but not gender, blood pressure, or serum cholesterol level--independently predicted all three outcome measures. Echocardiographically determined left ventricular mass and geometry stratify risk in patients with essential hypertension independently of and more strongly than blood pressure or other potentially reversible risk factors and may help to stratify the need for intensive treatment.
In a cooperative multicenter study (Pathobiological Determinants of Atherosclerosis in Youth, PDAY) of 1532 young persons 15 through 34 years of age who died of external causes and were autopsied in medical examiners’ laboratories, we quantified atherosclerosis of the aorta and the right coronary artery. We analyzed postmortem blood cells for glycohemoglobin and postmortem serum for lipoprotein cholesterol and thiocyanate (as an indicator for smoking). We measured the thickness of the panniculus adiposus and the body mass index (weight per height squared) as indicators of adiposity. Glycohemoglobin levels exceeding 8% were associated with substantially more extensive fatty streaks and raised lesions in the right coronary artery in persons more than 25 years of age and with more extensive raised lesions in the aorta in persons more than 30 years of age. Both thickness of the panniculus adiposus and body mass index were associated with more extensive fatty streaks and raised lesions in the right coronary artery. The associations of atherosclerotic lesions with glycohemoglobin and adiposity were not explained by a less favorable lipoprotein profile or smoking. The results show that atherosclerosis in young adults is associated with the prediabetic or early diabetic state, as indicated by elevated glycohemoglobin levels, and with obesity.
Twenty-year coronary heart disease (CHD) incidence is analyzed for 279 men, CHD-free at the ages of 47 through 57 years and characterized by three examinations before 20 annual follow-up examinations. Sixty men developed CHD, 42 dying or suffering infarction. Among 20 entry characteristics, three had major predictive power, especially for CHD death or infarction: cold pressor test, a high level of serum cholesterol, and systolic blood pressure. Smoking and relative weight seemed unimportant. Major CHD incidence was proportional to cholesterol to the 3.4 power. Five-variable multiple logistic analysis permitted placement of men into deciles of estimated risk differing more than tenfold in CHD incidence. The combination of only cholesterol and systolic pressure was nearly as good. The multiple logistic coefficients applied to five-year data on 1,287 men among whom 182 CHD developed in 182 yielded satisfactory agreement between observed and predicted distributions of CHD cases in classes of estimated risk.
Objective: To examine the association of echocardiographically determined left ventricular mass with incidence of coronary heart disease in an elderly cohort.
Design: Cohort study with a follow-up period of 4 years.
Setting: Population-based.
Subjects: Elderly original volunteer subjects of the Framingham Heart Study who were free of clinically apparent coronary heart disease. This group included 406 men (mean age, 68 years; range, 60 to 90) and 735 women (mean age, 69 years; range, 59 to 90).
Measurements and Main Results: During 4 years of follow-up, coronary heart disease events occurred in 37 men and 33 women. Baseline echocardiographically determined left ventricular mass was associated with incidence of coronary disease in both sexes (P < 0.01). After adjusting for age, systolic blood pressure, smoking, and the ratio of total/high density lipoprotein cholesterol, the relative risk for a coronary event, per 50 g/m increment in left ventricular mass/height, was 1.67 in men (95% CI, 1.24 to 2.23) and 1.60 in women (95% CI, 1.10 to 2.32).
Conclusions: Echocardiographic assessment of left ventricular mass offers prognostic information beyond that provided by traditional risk factors, which can improve our ability to identify individuals at high risk for coronary heart disease. These findings may have widespread implications regarding the applications of echocardiography in clinical practice.
Objective.
—To evaluate the effect of echocardiographically determined left ventricular hypertrophy (LVH) on survival in comparison with number of stenosed vessels and left ventricular systolic dysfunction.Design.
—Cohort study based on a consecutive sample from a hospital registry, with a mean follow-up of 5 years.Setting.
—An inner-city public hospital in Chicago, Ill.Patients.
—The study included 1089 consecutive black patients who underwent both coronary angiography and M-mode echocardiography as part of a diagnostic evaluation.Results.
—Nonstenosed coronary arteries, single-vessel disease, and multivessel disease were found in 48%, 16%, and 36% of patients, respectively; LVH (left ventricular mass index >131 g/m2 in men and >100 g/m2 in women) was detected in 50% of patients. Hypertrophy without coexistent obstructive coronary disease was associated with a lower survival rate than that observed for single-vessel disease and was similar to multivessel disease. When LVH, number of diseased vessels, and left ventricular dysfunction were subjected to multivariate analysis, hypertrophy conferred a relative risk (RR) of 2.4 (95% confidence interval [CI], 1.7 to 3.2). By comparison, the presence of a single stenosed vessel did not increase the risk of death. Multivessel disease and ejection fraction less than 45% were associated with an RR of 1.6 (95% CI, 1.1 to 2.2) and 2.0 (95% CI, 1.4 to 2.7), respectively. Calculation of the attributable risk fraction demonstrated that for every 100 deaths in this cohort, LVH independently accounted for 37. The corresponding attributable risk fractions were 1%, 22%, and 9% for single-vessel disease, multivessel disease, and ventricular dysfunction, respectively.Conclusions.
—Left ventricular hypertrophy was associated with a greater RR and attributable risk than the traditional measures of coronary disease severity. The high prevalence and powerful risk of LVH make an important contribution to the adverse survival rates among black patients with heart disease and may account for much of the black-white differential.(JAMA. 1995;273:1592-1597)
Resting cardiovascular parameters were predicted from anthropometric data, resting baseline cardiovascular data, and cardiovascular responses to three laboratory stressors completed 1 year earlier. Subjects were 106 male and female children (72 Whites, 34 Blacks) aged 6–7 years at the initial evaluation. During initial testing, blood pressure, heart rate, cardiac output, and total peripheral resistance were assessed at rest and also during a forehead cold pressor task, postural change, and treadmill exercise. The same cardiovascular parameters were then assessed at rest 1 year later. After controlling for significant anthropometric measures and the pertinent previous year's resting data, systolic and diastolic responses to the cold pressor were predictive of respective follow-up resting levels. Postural change heart rate responses were predictive of follow-up resting heart rate after controlling for initial resting levels. Exercise cardiac index reactivity predicted follow-up cardiac index after controlling for earlier resting levels and adiposity. Follow-up total peripheral resistance index was predicted by earlier resting levels.© 1997 Elsevier Science B.V.
Objective:
The aim of this study was to examine whether blood pressure reactions to mental stress predicted future blood pressure and hypertension.
Methods:
Blood pressure was recorded at an initial medical screening examination after which blood pressure reactions to a mental stress task were determined. A follow-up screening assessment of blood pressure and antihypertensive medication status was undertaken 10 years later. Data were available for 796 male public servants, between 35 and 55 years of age upon entry to the study.
Results:
Systolic blood pressure reactions to mental stress were positively correlated with follow-up screening systolic blood pressure and to a lesser extent, follow-up diastolic pressure. In multivariate tests, by far the strongest predictors of follow-up blood pressures were initial screening blood pressures. In the case of follow-up systolic blood pressure, systolic reactions to stress emerged as an additional predictor of follow-up systolic blood pressure. With regard to follow-up diastolic blood pressure, reactivity did not enter the analogous equations. The same outcomes emerged when the analyses were adjusted for medication status. When hypertension at 10-year follow-up was the focus, both systolic and diastolic reactions to stress were predictive. However, with correction for age and initial screening blood pressure, these associations were no longer statistically significant.
Conclusions:
The results of this study provide modest support for the hypothesis that heightened blood pressure reactions to mental stress contribute to the development of high blood pressure. At the same time, they question the clinical utility of stress testing as a prognostic device.
We assessed the relation of risk factors for cardiovascular disease to early atherosclerotic lesions in the aorta and coronary arteries in 35 persons (mean age at death, 18 years). Aortic involvement with fatty streaks was greater in blacks than in whites (37 vs. 17 percent, P less than 0.01). However, aortic fatty streaks were strongly related to antemortem levels of both total and low-density lipoprotein cholesterol (r = 0.67, P less than 0.0001 for each association), independently of race, sex, and age, and were inversely correlated with the ratio of high-density lipoprotein cholesterol to low-density plus very-low-density lipoprotein cholesterol (r = -0.35, P = 0.06). Coronary-artery fatty streaks were correlated with very-low-density lipoprotein cholesterol (r = 0.41, P = 0.04). Mean systolic blood-pressure levels also tended to be higher in the four subjects with coronary-artery fibrous plaques than in those without them: 112 mm Hg as compared with 104 (P = 0.09). These results document the importance of risk-factor levels to early anatomical changes in the aorta and coronary arteries. The progression of fatty streaks to fibrous plaques is uncertain, but these data suggest that a rational approach to the prevention of cardiovascular disease should begin early in life.
Objective.
—To evaluate the association of echocardiographically determined left ventricular mass (LVM) with incidence of stroke or transient ischemic attack in an elderly cohort.
Background: We examined the relation between cardiovascular reactivity (the response of the cardiovascular system to psychological stress) and the severity and progression of carotid atherosclerosis.
Methods: Using duplex ultrasonography, we measured the change in the area of all detectable plaques in the extracranial carotid arteries during 2 years. Cardiovascular reactivity was assessed by measuring changes in hemodynamics during a frustrating cognitive task (the Stroop Color Word Interference Task). Established risk factors for atherosclerosis were measured by interviewing patients, a physical examination, and blood assays for 351 subjects with a wide range of types of atherosclerotic disease.
Results: Atherosclerotic plaques were present in the carotid arteries of 273 (78%) subjects. In a forward stepwise multiple regression analysis, it was found that greater age (β = 0.46), a history of hypertension (β = 0.20), use of lipid level-lowering agents (β = 0.18), a longer history of smoking (β = 0.13), a larger cholesterol: high-density lipoprotein ratio (β = 0.13), a smaller change in heart rate during the task (β = -0.12), and a higher resting systolic blood pressure (SBP; β = 0.11) were associated significantly with a greater plaque area (R2 = 0.35). In 136 untreated subjects who were followed up for 2 years, a greater change in SBP during the task (b = 0.28), a higher total cholesterol: high-density lipoprotein ratio (β = 0.23), a shorter resting preejection period (β = -0.19), and a lower body mass index (β = -0.17) were significant predictors of the change in atherosclerosis, after controlling for age and initial plaque area in a stepwise multiple regression analysis (R2 = 0.24).
Conclusions: These results support the hypothesis that hemodynamic responses under conditions of mental stress may influence the progression of atherosclerosis.
Background: A prospective study evaluated the prevalence of 40% to 100% extracranial carotid arterial disease (ECD) by carotid duplex ultrasonograms and its association with coronary artery disease (CAD) and incidence of new coronary events in 949 patients with a mean age of 82 +/- 8 years.
Methods: Technically adequate bilateral carotid duplex ultrasonograms were obtained in 949 unselected patients, mean age 82 +/- 8 years, in a chronic care facility. The prevalence of CAD and incidence of coronary events were determined in patients with and without ECD. Follow-up was 45 +/- 22 months. Data were analyzed by chi-square analyses.
Results: CAD was present in 87 of 150 patients (58%) with ECD and in 314 of 799 patients (39%) without ECD (P < 0.001). Coronary events occurred in 70 of 87 patients (80%) with ECD and CAD (group A), in 188 of 314 patients (60%) with CAD and no ECD (group B), in 28 of 63 patients (44%) with ECD and no CAD (group C), and in 133 of 485 patients (27%) with no ECD and no CAD (group D). Significant P values were P < 0.001 comparing A with B, A with C, A with D, and B with D; P < 0.01 comparing C with D; and P < 0.025 comparing B with C.
Conclusions: Patients with ECD have a higher prevalence of CAD and a higher incidence of coronary events than patients without ECD. Patients with CAD and ECD have a higher incidence of coronary events than patients with CAD and no ECD. Patients with ECD and no CAD have a higher incidence of coronary events than patients with no ECD and no CAD.
(C) Lippincott-Raven Publishers.
After measuring blood pressure and heart rate at rest and during a video game procedure in 477 children enrolled in 3rd grade, 434 (91%) children had these measurements repeated a year later in 4th grade. Black children demonstrated greater blood pressure and heart rate reactivity than White children in both years, and an increase in heart rate reactivity from 3rd to 4th grade. Gender effects were inconsistent. Systolic and diastolic blood pressures during the video game were more highly correlated from year-to-year than were the resting measures. Regression analysis indicated that systolic reactivity was significantly related to subsequent systolic pressure at rest, particularly among Black girls. Diastolic reactivity was associated with subsequent resting diastolic pressure only among White children. Associations between reactivity and future blood pressure were independent of initial resting blood pressure. This study suggests that cardiovascular reactivity to psychological stress may be one important factor in future level of blood pressure and that the increased heart rate reactivity of Black children may be associated with the prevalence of hypertension among Black adults.
The neuroticism scale of the German version of the Eysenck Personality Inventory was found to be negatively associated (r = −0.38) with mean blood pressure increase over a 4-year period in a sample of 75 German adult normotensives. Alcohol consumption was also an independent protective factor, and combining alcohol, neuroticism and baseline blood pressure in a multiple regression equation resulted in a multiple r of 0.60. Neither heart rate nor mean blood pressure responses during mental arithmetic were associated with long-term blood pressure increase. Thus, the present data do not support the reactivity hypothesis which links cardiovascular overreactivity to psychological Stressors with risk for hypertensive development. Results are discussed in terms of stress coping strategies.
Background-Exaggerated cardiovascular reactivity to psychological demands may contribute to the development of left ventricular (LV) hypertrophy. We examined the cross-sectional association between anticipatory blood pressure (BP) responses to bicycle exercise and LV mass in the Kuopio Ischemic Heart Disease Risk Factor Study, a population-based epidemiological sample. Methods and Results-Among 876 men from 4 age cohorts (ages 42, 48, 58, and 64 years), we collected echocardiographic assessments of LV mass along with measures of BP response taken before bicycle ergometry testing. Anticipatory BP responses were positively associated with LV mass, with significant associations only among younger (age <50 years) subjects with elevated resting pressures (3-way interactions for anticipatory BP x age x resting pressure for systolic and diastolic BP, all P<0.05; for younger subjects with elevated systolic BP, P<0.01; and for younger subjects with elevated diastolic BP, P<0.001). Among these subgroups, exaggerated anticipatory BP responses (tup quartile) were associated with an incremental increase in LV mass of 10% or greater, corrected for body surface area. Results remained significant after adjusting for age, education, salt consumption, and resting BP, and the pattern of findings was maintained among men with no previous history of cardiovascular disease. Conclusions-The tendency to show exaggerated presser responses to psychological demands may be a significant independent correlate of LV mass, especially among young men with high resting pressures. This is the first study to examine such associations in a middle-aged population sample.
Precursors of sudden death were sought in men--1838 civil servants in Albany, New York, and 2282 residents of Framingham, Massachusetts--under continuous surveillance for 16 years. In men 45-74 years old there were 234 deaths attributed to coronary heart disease (CHD) of which 109 occurred within one hour of onset of symptoms. More than half of all deaths due to CHD occurred outside the hospital and about 80 per cent of these were sudden. Most were unheralded by prior symptoms of CHD. Persons at high risk of death from CHD, including sudden death, can be identified long before the terminal unexpected catastrophe. The same precursive stigmata exist in persons subject ot coronary attacks whether or not immediately fatal. The risk of sudden death in these two populations was positively correlated with high blood pressure, the electrocardiographic pattern of left ventricular enlargement, obesity, and heavy cigarette usage. Sudden death is a common and possibly incidental expression of lethal coronary heart disease. The potential candidate for sudden death cannot be confidently distinguished from the individual who succumbs more slowly of myocardial infarction. The inescapable conclusion is that the prevention of sudden death requires the prevention of coronary attacks.
During the 5 years of this investigation, resting blood pressure and pressor reactivity were measured in 292 white children and 46 black children in 1987, 1988, 1989, and 1991. In 1987, all children were in the third grade; in 1991, the children were in the seventh grade. Reactivity was assessed with a standardized psychological stressor, a television video game. Children displayed significant stability of absolute blood pressure and heart rate reactivity between grades 3 and 7. At all examinations, black children demonstrated blood pressure reactivity that was significantly greater in magnitude (both absolute level and change from resting measurements) than that of white children. Black children exhibited significantly greater heart rate reactivity only when defined as change from the resting measurements; absolute levels of heart rate reactivity were comparable for blacks and whites. For black children, blood pressure reactivity in 1987 was the strongest predictor of resting blood pressure (both systolic and diastolic) in 1991. Among white children, resting blood pressure was the strongest predictor of future resting blood pressure. Further research is needed to determine if ethnic differences in children's pressor reactivity are associated with ethnic differences in the prevalence of hypertension.
HYPERTENSIVE heart disease can be defined as the response of the heart to the afterload imposed on the left ventricle by the progressively increasing arterial pressure and total peripheral resistance produced by hypertensive vascular disease. Although the response sometimes appears to be out of proportion to the level of the arterial pressure, it is primarily the result of the hemodynamic overload. Hypertension can cause or is related to various cardiac manifestations, among them left ventricular hypertrophy, congestive heart failure, cardiac dysrhythmias, and ischemic heart disease. Although the risk of atherosclerotic coronary heart disease is related to the systolic and diastolic . . .
The possible relationship between mental stress-induced cardiovascular reactivity and clinical prognosis was examined in a pilot study of 13 postinfarction patients. All patients had previously participated in the placebo condition of a secondary intervention trial. On completion of the trial, blood pressure, heart rate, and venous plasma catecholamines were evaluated at rest and in response to a modified Stroop test on two occasions. At follow-up 39 to 64 months later, five patients had suffered a new clinical event (reinfarction and/or stroke). These patients had shown significantly larger systolic and diastolic blood pressure responses to the Stroop test than had patients who remained event-free at follow-up. Catecholamine concentrations also differed between groups during mental stress, but on only one of the two test days. Groups did not differ on baseline measurements, cardiovascular response to exercise testing, fasting serum lipid and glucose concentrations, age, or duration of follow-up.
To assess the long-term predictive importance of high cardiovascular reactivity in relation to subsequent blood pressure, 51 men from a pool of 204 men originally tested at age 18 to 22 years were recruited for blood pressure assessment 10 to 15 years later. Initial testing uniformly involved monitoring of systolic pressure, diastolic pressure, and heart rate during a reaction time task involving threat of shock. In 30 of the 51 men who participated at follow-up, initial testing had also included separate visits to obtain relaxation-only baseline levels of the cardiovascular indices. At follow-up, in addition to clinic-type stethoscopic determinations, blood pressure and heart rate were assessed during work and social and leisure activities via ambulatory monitoring. Men with higher levels of systolic pressure during the task showed higher stethoscopic and ambulatory systolic pressure at follow-up. Likewise, men with higher levels of diastolic pressure during the task showed higher diastolic levels at follow-up. In the 30 men with both good task and baseline data from initial testing, those with high heart rate reactivity (task minus baseline) showed higher systolic, diastolic, and heart rate levels at follow-up than low heart rate reactors, even though their baseline blood pressures had not differed at initial testing. Similarly, men with high systolic reactivity showed higher diastolic pressure at follow-up than low systolic reactors. Multiple regression analyses also demonstrated that systolic, diastolic, and heart rate reactivity improve prediction of follow-up blood pressure when added to models incorporating the standard risk factors, baseline blood pressure, and parental history of hypertension.
Exogenous prostaglandin (PG) administration has been proposed as a vasodilator therapy for heart failure patients. The effects of this therapy on renal function have not been well studied in this disorder. Therefore, we investigated the renal effects of the PGI2 analog iloprost in comparison to PGE2 in 12 conscious dogs before and after induction of a low cardiac output state by rapid right ventricular pacing (250 beats/min for 10 days). In healthy dogs, 5 to 150 ng/kg/min iloprost increased renal plasma flow without affecting glomerular filtration rate and decreased urine flow without affecting natriuresis. PGE2 at the same dosages increased renal plasma flow and urinary sodium excretion without changing the glomerular filtration rate or amount of diuresis. In dogs with low cardiac output and lower basal renal plasma flow, iloprost did not change renal plasma flow, but decreased glomerular filtration rate and filtration fraction. In these animals, PGE2 insignificantly increased renal plasma flow, but significantly augmented urine flow and sodium excretion. We therefore conclude that in an experimental low cardiac output state, PGI2 may cause a deterioration of renal function. In contrast, PGE2 induces natriuresis and diuresis despite an attenuated increase in renal plasma flow. Thus, PGE2 promises to exert a more favorable profile of renal effects in heart failure therapy.
The ability to identify the hypertensive patient who is destined to suffer a morbid or fatal complication in the long presymptomatic phase of this condition, when its natural history would be most subject to amelioration, is limited by the weak relation between the level of blood pressure and the occurrence of complications. Recent research indicates that the level of left ventricular (LV) mass--most conveniently measured by echocardiography--reflects the combined effects of a variety of factors involved in the pathophysiology of hypertension, including obesity, exaggerated blood pressure responses to everyday activity, high sodium intake and blood viscosity, and genetic factors predisposing to hypertension. Prospective studies indicate that LV mass is a stronger predictor of subsequent morbid events and death than blood pressure or other conventional risk factors except age. Preliminary findings of close relations between LV mass and arterial disease and between the change in LV mass during antihypertensive treatment and subsequent events contribute to explaining the strong predictive value of LV mass. Further research is needed to clarify the biologic basis of these observations and to determine whether stratification of hypertensive patients based on their level of LV mass can improve the treatment of hypertension.
Using paired isolated perfused rat tail artery segments, it was found that enalaprilat, an ACE inhibitor, augmented 1.6-fold the contractile responses to phenylephrine (PE), an alpha 1-adrenoceptor agonist. Similarly, enalaprilat potentiated 1.9-fold the alpha 1-adrenoceptor antagonist activity of doxazosin in paired rat tail artery segments. In rats treated with deoxycorticosterone acetate (DOCA) 20 mg/kg i.m. twice weekly for 5 weeks, plasma renin activity fell from a control value of 5.73 +/- 0.93 to 0.04 +/- 0.01 ng of AI/ml/h. The inhibition of circulating renin activity in these animals was associated with a loss of the potentiating effects of enalaprilat upon the alpha 1-adrenoceptor antagonist action of doxazosin. The results are interpreted as indicating that angiotensin II (AII) can modulate the functional activity of alpha 1-adrenoceptors in vascular smooth muscle.
Left ventricular hypertrophy (LVH) is a cardiac end-organ response to increased pressure or volume load. For the past 40 years the electrocardiogram (ECG) has been used in the Framingham Heart Study for the detection of LVH. There is an increased risk of developing coronary heart disease following the appearance of LVH on the ECG. ECG LVH also carries a high risk for mortality. The overall risk of mortality in subjects with ECG LVH exceeds that following myocardial infarction. Over the past three decades there has been a significant decline in prevalence of ECG LVH concomitant with increased utilization of antihypertensive drug therapy. The recent introduction of echocardiography into the Framingham Heart Study has resulted in the development of new echocardiographic criteria for LVH. Echocardiographic LVH is more prevalent than ECG LVH. Corresponding prevalence rates for these two methods (per 1,000) are 174 vs. 24, respectively. Ambulatory ECG monitoring documents an association of echocardiographic LVH with increased risk for ventricular arrhythmias. Data from Framingham and elsewhere suggest that echocardiographically defined LVH is an important predictor of risk for cardiovascular disease morbidity and mortality. The extent to which prevention or regression of LVH, in response to antihypertensive drug therapy will alter the substantial risks associated with this condition, awaits additional investigation.
IN the 19th century there were two major hypotheses to explain the pathogenesis of atherosclerosis: the "incrustation" hypothesis and the "lipid" hypothesis. The incrustation hypothesis of von Rokitansky,1 proposed in 1852 and modified by Duguid,2 suggested that intimal thickening resulted from fibrin deposition, with subsequent organization by fibroblasts and secondary lipid accumulation. The lipid hypothesis, proposed by Virchow3 in 1856, suggested that lipid in the arterial wall represented a transduction of blood lipid, which subsequently formed complexes with acid mucopolysaccharides; lipid accumulated in arterial walls because mechanisms of lipid deposition predominated over those of removal. The two hypotheses are now . . .
Atherosclerotic diseases and their thrombotic complications remain the leading causes of mortality and morbidity in Western society. In the United States, cardiovascular disease is responsible for one in every 2.4 (41.4%) deaths and is the leading single cause of mortality. Furthermore, the presence of atherosclerotic disease (defined as thickening of the arterial wall through the accumulation of lipids, macrophages, T-lymphocytes, smooth muscle cells, extracellular matrix, calcium and necrotic debris) is more prevalent, but by itself rarely fatal. The crucial, final common process for the conversion of a nonocclusive, often clinically silent atherosclerotic lesion to a potentially fatal condition is often plaque disruption. The mortality associated with atherosclerotic disease relates to the acute coronary syndromes, including acute myocardial infarction, unstable angina pectoris and sudden cardiac death. Substantial clinical, experimental and postmortem evidence demonstrates the central role that a superimposed acute thrombosis on a disrupted atherosclerotic plaque plays in the onset of acute coronary syndromes. Therefore, therapeutic approaches to date have focused on reducing such thrombotic complications of atherosclerotic plaques (i.e., antiplatelet, anticoagulant and thrombolytic therapies) to reduce the resulting morbidity and mortality. In this review, we will focus on the current theories of atherogenesis and how they impact on our understanding of acute coronary syndromes.
Cardiovascular reactivity in response to the cold pressor test has been associated with an increased risk of coronary heart disease in middle-aged men. We studied 905 white male medical students, median age 22 years, in the Johns Hopkins Precursors Study. Systolic blood pressure, systolic blood pressure change during the cold pressor test, smoking, cholesterol, Quetelet index, and family history of coronary heart disease were measured on enrollment during 1948-1964. Incidence of cardiovascular morbidity and mortality was ascertained by annual questionnaires and death certificates. There was no association between change in systolic blood pressure during the cold pressor test, whether examined as a continuous variable or a 20 mm Hg or more rise, and the risk of subsequent cardiovascular disease or coronary heart disease. These findings did not change after adjustment for cardiovascular disease risk factors. Previously reported associations may have been due to preexisting arteriosclerosis, which increases the rise in systolic blood pressure during the cold pressor test. We conclude that cardiovascular reactivity to the cold pressor test in young adulthood is not a strong predictor of future cardiovascular disease.
To assess the prognostic significance of left ventricular mass and geometry in initially healthy persons with essential hypertension.
An observational study of a prospectively identified cohort.
University medical center.
Two hundred and eighty patients with essential hypertension and no pre-existing cardiac disease were evaluated using echocardiography between 1976 and 1981. Two hundred and fifty-three subjects or their family members (90%) were contacted for a follow-up interview an average of 10.2 years after the initial echocardiogram was obtained; the survival status of 27 patients lost to follow-up was ascertained using National Death Index data.
Left ventricular mass exceeded 125 g/m2 in 69 of 253 patients (27%). Cardiovascular events occurred in a higher proportion of patients with than without left ventricular hypertrophy (26% compared with 12%; P = 0.006). Patients with increased ventricular mass were also at higher risk for cardiovascular death (14% compared with 0.5%; P less than 0.001) and all-cause mortality (16% compared with 2%; P = 0.001). Electrocardiographic left ventricular hypertrophy did not predict risk. Patients with normal left ventricular geometry had the fewest adverse outcomes (no cardiac deaths; morbid events in 11%), and those with concentric hypertrophy had the most (death in 21%; morbid events in 31%). In a multivariate analysis, only age and left ventricular mass--but not gender, blood pressure, or serum cholesterol level--independently predicted all three outcome measures.
Echocardiographically determined left ventricular mass and geometry stratify risk in patients with essential hypertension independently of and more strongly than blood pressure or other potentially reversible risk factors and may help to stratify the need for intensive treatment.
The mass of left ventricular (LV) muscle plays a central role in hypertension. Echocardiographic LV mass has been shown to reflect the level of blood pressure over time, obesity, diet, and other factors, and to serve as the strongest predictor yet discovered, other than advancing age, of cardiac complications of hypertension. Recent research suggests, in addition, that individuals destined to become hypertensive have increased LV mass before hypertension becomes clinically apparent. Several published studies have compared LV mass in groups of normotensive children to young adults considered to be at high or low genetic risk of hypertension based on the presence or absence of hypertension in their parents. In each instance LV mass was higher in the offspring of hypertensive parents and this difference exceeded that expected for small differences in body habitus or arterial pressure. A longitudinal study in children also showed that LV mass predicted subsequent blood pressure level. We recently performed a study of 132 initially normotensive employed adults, 15 (11%) of whom developed borderline hypertension during a 5-year follow-up. The development of hypertension was not predicted by subject age, body habitus, blood pressure, or a variety of biochemical measurements. The only baseline measurement that predicted development of hypertension was that of LV mass (92 +/- 25 v 77 +/- 19 g/m2, P less than .005), and the likelihood of developing hypertension increased progressively from 3% in the lowest quartile of LV mass of 24% in the highest quartile.(ABSTRACT TRUNCATED AT 250 WORDS)
The extent of carotid artery atherosclerosis as measured by B-mode ultrasound has been shown to be strongly and independently correlated with the presence or absence of coronary atherosclerotic disease (CAD), but no studies to date have used carotid B-mode ultrasound to compare the extent of atherosclerotic disease in the two arterial circulations. We used data from a registry of patients undergoing cardiac catheterization and B-mode ultrasound of the carotid arteries to compare the extent of CAD (number of major coronary vessels with 50% or greater stenosis as judged by a consensus interpretation) with the extent of extracranial carotid atherosclerosis. Four hundred thirty-four patients (234 men, 200 women) greater than 40 years of age were stratified by gender and then divided into quartiles on the basis of a B-mode score that was derived by summing arterial wall thickness at nine sites in the left and nine sites in the right carotid arteries. Evaluation of extent of CAD for the four B-mode quartiles showed that men in the lowest B-mode quartile were over six times more likely to have normal coronary arteries than three- to four-vessel CAD, while men in the highest B-mode quartile were over 10 times more likely to have three- to four-vessel CAD than normal coronary arteries. The findings were similar for women but not as dramatic. Gender-specific discriminant function models using traditional risk factors alone or in combination with B-mode score were developed to predict the extent of CAD.(ABSTRACT TRUNCATED AT 250 WORDS)
We investigated the determinants of maximal intima-media thickness of common carotid arteries in a population-based sample of 1224 Eastern Finnish men aged 42, 48, 54 or 60 years. A high-resolution B-mode ultrasonographic examination was performed as part of the Kuopio Ischaemic Heart Disease Risk Factor Study (KIHD). The maximal intima-media thickness (IMT) varied between 0.48 mm and 4.09 mm (mean value +/- SD, 0.94 mm +/- 0.38 mm). Age (standardized partial coefficient, beta = 0.238, P less than 0.0001), ambulatory pulse pressure (beta = 0.130, P less than 0.0001), cigarette-years of smoking (beta = 0.125, P less than 0.0001), serum LDL cholesterol concentration (beta = 0.125, P less than 0.0001), history of ischaemic heart disease (beta = 0.125, P less than 0.0001), pre-exercise systolic blood pressure (beta = 0.070, P = 0.0113) and diabetes (beta = 0.068, P = 0.0072) were most strongly associated with IMT. This study confirms the role of systolic blood pressure, smoking and serum LDL cholesterol levels as major risk factors for increased carotid intima-media thickness.
The frequency of ventricular premature complexes and the degree of impairment of left ventricular ejection fraction are major predictors of cardiac mortality and sudden death in the year after acute myocardial infarction. Recent studies have implicated psychosocial factors, including depression, the interaction of social isolation and life stress, and type A-B behavior pattern, as predictors of cardiac events, controlling for known parameters of disease severity. However, results tend not to be consistent and are sometimes contradictory. The present investigation was designed to test the predictive association between biobehavioral factors and clinical cardiac events. This evaluation occurred in the context of a prospective clinical trial, the Cardiac Arrhythmia Pilot Study (CAPS). Five-hundred two patients were recruited with greater than or equal to 10 ventricular premature complexes/hour or greater than or equal to 5 episodes of nonsustained ventricular tachycardia, recorded 6 to 60 days after a myocardial infarction. Baseline behavioral studies, conducted in approximately 66% of patients, included psychosocial questionnaires of anxiety, depression, social desirability and support, and type A-B behavior pattern. In addition, blood pressure and pulse rate reactivity to a portable videogame was assessed. The primary outcome was scored on the basis of mortality or cardiac arrest. Results indicated that the type B behavior pattern, higher levels of depression and lower pulse rate reactivity to challenge were significant risk factors for death or cardiac arrest, after adjusting statistically for a set of known clinical predictors of disease severity. The implication of these results for future research relating behavioral factors to cardiac endpoints is discussed.
To evaluate the consistency, strength, and independence of the relation of carotid atherosclerosis to coronary atherosclerosis, we quantified coronary artery disease risk factors and extent of carotid atherosclerosis (B-mode score) in 343 coronary artery disease patients and 167 disease-free control patients. In univariable analyses, there was a strong association between coronary status and extent of carotid artery disease in men and women older than and younger than 50 years (p less than 0.001 for men and women greater than 50 years, p less than 0.001 for women less than or equal to 50 years, p = 0.045 for men less than or equal to 50). The relation remained strong after control for age in men and women older than 50 years and in women younger than 50 (p less than 0.001 for men and women greater than 50 years, p = 0.003 for women less than or equal to 50) but did not persist after control for age in men younger than 50. Logistic models that included coronary disease risk factors, with or without B-mode score, as independent variables and presence or absence of coronary disease as the outcome variable indicated that the extent of carotid atherosclerosis was a strong, statistically significant independent variable in models for men and women older than 50 years of age. Next, we examined the usefulness of B-mode score as an aid in screening for coronary artery disease in men and women older than 50 years. Classification rules, both including and excluding B-mode score, were developed based on logistic regression and, for comparison, recursive partitioning (decision trees). The performance of these rules and the bias of their performance statistics were estimated. The improved classification of the study sample when B-mode score was incorporated in the rule was statistically significant only for men (p = 0.015). However, the addition of B-mode score was found to 1) increase the median discrimination score for both sex groups based on the logistic model, and 2) yield better sensitivities and specificities for rules based on recursive partitioning. Thus B-mode score is strongly, consistently, and independently associated with coronary artery disease in patients older than 50 and is at least as useful as well-known risk factors for identifying patients with coronary artery disease.
High blood pressure (BP) defines a prognostically heterogeneous group. Because BP varies according to time, setting and means of observation, it has been postulated that BP reactivity might better predict cardiovascular disease (CVD) than does unidimensional measurements. To assess BP reactivity, the difference between pretreatment nurse (RN) and physician (MD) diastolic BP (DBP)--systematically recorded in that order--or MD-RN DBP, was obtained in 1737 previously untreated patients with sustained, RN BP greater than or equal to 160 and/or 95 mmHg. Patients stratified by tertiles of MD-RN DBP [(I) less than or equal to - 3, (II) -2 to 3 and (III) greater than or equal to 4 mmHg] were similar by sex, race, age, body mass index, cholesterol, electrocardiography, prior CVD, smoking and pretreatment or attained in-treatment BPs. During 14 years of followup, myocardial infarction (MI) incidence per 1000/year were, tertile I (3.2), II (3.7), III (7.6) (relative risk = 2.4, III vs I + II, p less than 0.05), whereas stroke incidence and non-CVD mortality were evenly distributed. By Cox survival analysis, controlling for other entry characteristics only age, sex and DBP reactivity remained predictive (p less than or equal to 0.03) of MI or total CVD. Thus, BP reactivity, probably a centrally-mediated phenomenon, identifies a subgroup of hypertensives with an increased propensity for MI despite successful BP control.