Our objectives were to study anger as a trigger of acute myocardial infarction (MI) and to explore potential effect modification by usual behavioral patterns related to hostility.
This study was a case-crossover study within the Stockholm Heart Epidemiology Program. Exposure in the period immediately preceding MI was compared with exposure during a control period for each case. From April 1993 to December 1994, 699 patients admitted to coronary care units in Stockholm County were interviewed.
During a period of 1 hour after an episode of anger, with an intensity of at least "very angry," the relative risk of MI was 9.0 (95% CI, 4.4-18.2). In patients with premonitory symptoms, the time of disease initiation may be misclassified. When restricting the analyses to those without such symptoms, the trigger risk was 15.7 (95% CI, 7.6-32.4). The possibility of examining effect modification was limited by a lack of statistical power (eight exposed cases). Results of the analyses suggested, however, an increased trigger effect among subjects reporting nonhostile usual behavior patterns, nonovert strategies of coping with aggressive situations (not protesting when being treated unfairly), and nonuse of beta-blockers.
The hypothesis that anger may trigger MI is further supported, with an increased risk lasting for approximately 1 hour after an outburst of anger. It is suggested that the trigger risk may be modified by personal behavior patterns.
"Anger has been related to hyperactivity of the cardiovascular response and autonomic activation that likely increases morbidity and mortality among patients with coronary artery disease (CAD) . Anger triggers acute myocardial infarction onset  , and the relative risk of myocardial infarction was found to be 9.0 after 1 h of an anger episode . The anger recall task is a stress task with high ecological validity and is used widely to explore the cardiovascular responses in patients with CAD   and in healthy controls    . "
[Show abstract][Hide abstract] ABSTRACT: Background and purpose:
One psychopathological mechanism that links anger to coronary artery disease (CAD) is cardiac autonomic imbalance. Blood volume amplitude (BVA) and pulse transit time (PTT) are related to peripheral arterial elasticity and cardiac conduction, which are used as indirect markers for autonomic activation. The purposes of this study were to examine the relationships between BVA and PTT, and the reactivity of BVA and PTT during the anger recall task in patients with CAD.
Methods and subjects:
A total of 112 patients with CAD and 93 healthy controls were recruited; BVA and PTT were collected during baseline, the neutral episode, the anger episode, and after recovery.
There were significant positive correlations between BVA and PTT in all participants. BVA reactivity during the anger episode was greater in patients with CAD than in healthy controls, and there were also lower BVA recovery values after the neutral and anger episodes. However, there was no significant difference in BVA reactivity between the two groups in the neutral episode. PTT recovered to baseline levels after the neutral and anger episodes in healthy controls, but not in the patients with CAD.
BVA and PTT were associated with peripheral vascular elasticity and cardiac conduction that were regulated by the cardiac autonomic system. Peripheral vasoconstriction and changes in travel time between left ventricular and peripheral vasculature during the anger episode, and impaired recovery to baseline levels may relate to the psychopathological mechanisms of CAD.
Journal of Cardiology 05/2014; 65(1). DOI:10.1016/j.jjcc.2014.03.012 · 2.78 Impact Factor
"A reduced risk of AMI associated with consumption of cardiovascular medications could be viewed in the light of their beneficial mechanisms against triggering circumstances through the abolition of vasoconstrictive, hemodynamic, and prothrombotic internal triggering mechanisms (C ˇ ulic´, 2007; C ˇ ulicét al., 2005). The possibility of a protective effect particularly for b-blockers against emotional triggering of AMI has been suggested by both observational (C ˇ ulicét al., 2000, 2005) and case-crossover studies (Mittleman et al., 1995; Möller et al., 1999). In the present report, such an effect was observed in autumn, whereas a similar trend was observed for calcium antagonists in spring. "
[Show abstract][Hide abstract] ABSTRACT: Most recently, the possible impact of transitions to and from daylight saving time (DST) on the increased incidence of acute myocardial infarction (AMI) has been suggested. The goal of this report was to analyze independent influence of DST transitions on the incidence of AMI with simultaneous control for the confounding presence of situational triggers such as physical exertion, emotional stress, heavy meals, and sexual intercourse, as well as for other clinical factors. Detailed information was obtained from 2412 patients and included baseline characteristics, working status, exact time of AMI, possible external triggers, cardiovascular risk factors, and prehospital medication. AMI incidence on days after the DST was compared with incidence during control periods and patient characteristics, cardiovascular medication, and circumstances of AMI were evaluated to identify potential risk modifiers. Relative risks of AMI and differences in patient characteristics were expressed through incidence ratios and odds ratios, respectively, with 95% confidence intervals (CIs). Multivariate analysis was performed by using a stepwise multiple regression to assess the independent predictive significance of the characteristics of patients for the AMI occurring in the posttransitional period. The incidence ratio for AMI for the first four workdays after the spring DST transition was 1.29 (95% CI: 1.09-1.49) and the excess was particularly prominent on Monday. In autumn, the incidence ratio for AMI for this 4-d period was 1.44 (95% CI: 1.19-1.69), with peaks on Tuesday and Thursday. The independent predictors for AMI during this period in spring were male sex (p = 0.03) and nonengagement in physical activity (p = 0.02) and there was a trend for the lower risk of incident among those taking calcium antagonists (p = 0.07). In autumn, the predictors were female sex (p = 0.04), current employment (p = 0.006), not taking β-blocker (p = 0.03), and nonengagement in physical activity (p = 0.02). The present report supports the possibility that DST transitions represent additional chronobiological feature of AMI, and that risk of an onset varies according to sex, employment status, and the taking of cardiovascular medication. (Author correspondence: firstname.lastname@example.org).
Chronobiology International 05/2013; 30(5). DOI:10.3109/07420528.2013.775144 · 3.34 Impact Factor
"Sudden, unexpected events with a high emotional content  , such as, earthquakes    , terrorist attacks    , sports matches  , sexual activities  , or episodes of anger   can lead to malignant ventricular arrhythmias and hence to sudden cardiac death (SCD), mainly in patients with structural heart disease. The body reacts to these stressful circumstances by increasing sympathetic nervous activity and reducing vagal control of heart rate and blood pressure , such imbalance known to be a trigger for malignant ventricular arrhythmias   . "
[Show abstract][Hide abstract] ABSTRACT: Emotionally charged events are associated with an increased risk of sudden cardiac death (SCD). In this study we assessed RR and QT variability index (QTVI) at baseline during anger recall test (AR). We calculated QTVI from a 5-min ECG recording and from a 10-beats segment around the presumed maximum sympathetic activation in thirty post-myocardial infarction patients under β-blocker therapy and 10 controls underwent. In all groups, the low-frequency component of RR and SBP increased during AR. In all recordings, the QTVI calculated on a 5-min ECG recording and the QTVI(10 beats) were higher in patients than in controls (P < 0.05). The QTVI during AR remained unchanged from baseline within each group. Conversely, during AR, the QTVI(10 beats) in controls diminished significantly (P < 0.05) from baseline whereas in patients remained unchanged. The inability to buffer an acute stress-induced increase in sympathetic activity could explain why events charged with acute stress are associated with an increased risk of ventricular arrhythmias in this setting of patients and support the role of cognitive behavior stress management strategies.
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