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Low-Dose Aspirin for Prevention of Cardiovascular Risk in Bereavement: Results from a Feasibility Study

Letter to the Editor
this visit. In this task, participants were asked to recall a situation
where they felt alone and abandoned.
The overall sample had a mean age of 58.59 (SD = 13.94), was
54.55% female, and 90.91% were White (vs. non-White). Bereaved
versus nonbereaved and aspirin versus placebo groups did not dif-
fer at p < 0.05 on any of these characteristics. Change scores were
used to reduce the number of variables in the analyses. Cohen’s d
is reported as a measure of effect size.
Bereaved participants reported more depressive symptoms
than nonbereaved participants at baseline: CES-D score 23.80
(SD = 10.29) versus 8.42 (SD = 9.18) (F = 10.09, p < 0.001, d = 1.46).
All 5 bereaved participants receiving aspirin reported fewer de-
pressive symptoms at the second visit, compared to only 1 (of 5)
bereaved participants receiving placebo. A dichotomous variable
(decrease vs. no decrease in depressive symptoms) showed a sig-
nificant difference (χ
2 = 6.67, p < 0.01, d = 3.54).
When including all participants, the separation recall task
elicited an increase in systolic blood pressure: 129.21 mm Hg
(SD = 13.64) to 137.60 mm Hg (SD = 13.16) ( t = 3.59, p < 0.01,
d = 0.63) and diastolic blood pressure: 78.36 mm Hg (SD = 11.46)
to 83.07 mm Hg (SD = 10.88) ( t = 4.58, p < 0.001, d = 0.42). There
was also an increase in anxiety measured with the State-Trait
Anxiety Inventory: 33.05 (SD = 7.75) to 39.85 (SD = 9.78) ( t =
4.47, p < 0.001, d = 0.78). Heart rate increased from 74.12 beats
per minute (bpm) (SD = 10.12) to 75.79 bpm (SD = 8.14) ( t = 2.17,
p < 0.05, d = 0.18) and decreased after the separation recall task:
from 74.12 bpm (SD = 10.12) to 69.62 bpm (SD = 7.97) ( t = 6.64,
p < 0.001, d = 0.50).
Participants receiving aspirin recovered faster from the separa-
tion recall than participants receiving placebo ( Fig.1 ). Heart rate
decreased significantly more in the aspirin group: 5.97 bpm (SD =
2.95) versus 2.32 bpm (SD = 1.50) ( F = 10.38, p < 0.005, d = 1.64).
Using post hoc analysis, we had 71% power to detect this effect.
HRV increased significantly in the aspirin group: log RSA 4.15
(SD = 1.96) to 4.57 (SD = 1.80) ( t = 2.31, p < 0.05, d = 0.22). The
change score of HRV was significantly higher in the aspirin group:
log RSA placebo group –0.17 (SD = 0.38) versus aspirin group
+0.42 (SD = 0.62) ( F = 5.69, p < 0.03, d = 1.18).
To summarize, our results show an attenuated physiological
reactivity to a grief-related stress task and a beneficial effect on
depressive symptoms in the aspirin group. Higher cardiovascular
reactivity to emotional stressors in bereavement could amplify in-
creased cardiovascular risk. Aspirin may have a potential preven-
tive benefit targeting increased cardiovascular risk in bereave-
ment. The effect of aspirin on depressive symptoms is consistent
with previous studies linking depressive symptoms with inflam-
[8] . Further research is needed to investigate this potential
The use of aspirin in secondary prevention of cardiovascular
disease is well established. In primary prevention, aspirin is de-
In the 24 h following the death of a significant person, the in-
cidence of acute myocardial infarction increases 21.1-fold
[1] . Be-
reavement acutely increases mortality and cardiovascular risk in
the surviving spouse for a limited time
[2] . Aside from expectable
psychological distress, acute bereavement is associated with an el-
evation of heart rate and blood pressure, a decrease in heart rate
variability (HRV), and inflammatory and prothrombotic changes
[2, 3] . Acute bereavement as a cardiovascular risk factor is ame-
nable to preventive approaches, because it is predictable and tem-
porary. Despite clear evidence for this risk, no studies to date have
attempted primary prevention.
Low-dose aspirin could be a suitable prevention strategy in
acute bereavement. It targets the main cardiovascular risk factors
during bereavement, is inexpensive, is widely available, does not
require a prescription, and is feasible in other short-term interven-
tions. Low-dose aspirin is widely used for its antiplatelet effect, has
anti-inflammatory properties, and positively influences depressed
[4] , HRV [5] , and blood pressure [6] .
To investigate aspirin as a feasible preventive intervention,
acutely bereaved participants ( n = 10) were recruited on average
within 30 days (SD = 14.67) of the death of their spouse; nonbe-
reaved controls ( n = 12) were also recruited. We assessed hemody-
namic markers (blood pressure, heart rate, HRV) and depressive
symptoms (Center for Epidemiologic Studies Depression Scale;
CES-D) during 2 laboratory visits. The first laboratory visit was
used to assess baseline values. Using simple randomization, all par-
ticipants were then randomized to receive tablets containing either
81 mg of aspirin ( n = 12, 41.67% bereaved), the standard dosage
used for prevention in the USA, or placebo ( n = 10, 50% bereaved)
on the 5 days prior to the second laboratory visit. This visit was
scheduled on average 10.55 days (SD = 7.51) after the first visit. We
also included a separation recall task
[7] to assess reactivity during
Received: May 17, 2017
Accepted after revision: September 24, 2017
Published online: February 21, 2018
© 2017 S. Karger AG, Basel
Psychother Psychosom
DOI: 10.1159/000481862
L o w - D o s e A s p i r i n f o r P r e v e n t i o n o f C a r d i o v a s c u l a r
Risk in Bereavement: Results from a Feasibility
Sebastian Karl a, e , Monica Fallon d , Roman Palitsky a ,
Jessica A. Martinez
b, c , Harald Gündel e , Mary-Frances O'Connor a
Departments of a Psychology and b Nutritional Sciences,
University of Arizona, and
c University of Arizona Cancer Center,
Tucson, AZ , USA; d University of Mannheim Business School,
Mannheim, and
e Department of Psychosomatic Medicine and
Psychotherapy, University Hospital of Ulm, Ulm , Germany
Mary-Frances O’Connor
Department of Psychology, University of Arizona
1503 E. University Boulevard, Room 430
Tucson, AZ 85721 (USA)
E-Mail mfoconnor
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Auburn University Libraries - 2/22/2018 4:26:18 PM
Psychother Psychosom
DOI: 10.1159/000481862
bated because the reduction in cardiovascular risk must outweigh
the risk of bleeding. In people with no history of ischemic heart
disease, risks and benefits cancel each other out approximately
[9] .
Increased cardiovascular risk during acute bereavement might
shift this equilibrium toward benefits, especially if aspirin is only
used for a limited time. The American Heart Association recom-
mends low-dose aspirin for patients with diabetes because they
have increased cardiovascular risk
[10] . This could also apply to
other conditions with increased cardiovascular risk, such as acute
Although intended as a feasibility study, the major limitation
of this study was its small sample size. Although this means that
the estimates of the effects may differ in another sample, we report
Cohen’s d for information on the size of the effects. Confounding
variables were controlled for through the within-subject, random-
ized, double-blind study design.
If aspirin has a protective effect for increased cardiovascular
risk in acute bereavement, it is preferable to commence aspirin
treatment as soon as possible after bereavement and continue it
while the risk is elevated. Although bereavement is a rare event, it
affects nearly everyone, creating significant public health concerns
due to increased morbidity and mortality risk. These results war-
rant a larger investigation to confirm the effects and determine the
safety of aspirin use in this population.
Disclosure Statement
The authors declare no conflict of interest.
Funding Sources
Funding was provided in the form of a scholarship to the first
author by the International Graduate School in Molecular Medi-
cine of Ulm University.
Beats per minute
Pre Mid-task Post
Heart rate
p < 0.01
p < 0.01
p < 0.01
log ms
Pre Post
log RSA
p < 0.01
p < 0.02
p < 0.01
p < 0.05
Fig. 1. Changes of heart rate ( a ) and heart
rate variability (log RSA; b ) from before
(pre) to after (post) the separation recall
task (mid-task). Statistically significant dif-
ferences are marked with a bracket and p
value. RSA, respiratory sinus arrhythmia.
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... Cardiovascular biomarkers have shown consistent changes in bereavement when comparing acute (e.g., <6 weeks) and chronic grief within bereaved individuals, and also between bereaved and nonbereaved groups. The shift is seen in tonic activity, although there are some indications that reactivity measures (i.e., phasic activity) may also differ (29,30). These biomarkers include increased heart rate (resting and 24-hour), heart rate variability, systolic and diastolic blood pressure, von Willebrand factor, and platelet/granulocyte aggregates (31)(32)(33)(34). ...
... Finally, as researchers with interest in translational applications, clinical trials should examine how intervention during acute and chronic grief could improve health. In acute grief, we have published a very small feasibility trial of low-dose aspirin as a potential primary prevention strategy (29). As a risk factor, bereavement is often predictable and the increased risk is temporary. ...
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Objective: Using an integrative view of psychology, neuroscience, immunology and psychophysiology, the present review of literature curates the findings that have had an impact on the field of bereavement research, and shaped its development. Methods: Beginning with Lindemann's systematic descriptions of medical and psychological responses to the death of a loved one, specific studies that investigate medical outcomes following loss, their psychological predictors, and biopsychosocial mechanisms are discussed. This selective review culminates in recommendations for the field for future research, including greater integration of these disparate fields of inquiry. Results: Morbidity and mortality following the death of a loved one has long been a topic of research. Early researchers characterized somatic and psychological symptoms and studied immune cell changes in bereaved samples. More recent research has repeatedly demonstrated increased rates of morbidity and mortality in bereaved samples, as compared to married controls, in large epidemiological studies. Recent developments also include the development of criteria for prolonged grief disorder (also termed complicated grief). Newer methods, including neuroimaging, have observed that the greatest impact of the death of a loved one is in those who have the most severe psychological grief reactions. Mechanisms tying bereavement to medical outcomes are scarce, but differences in rumination, in inflammation and in cortisol dysregulation between those who adapt well and those who do not, have been offered with some evidence. Conclusions: Recommendations to propel the field forward include longitudinal studies to understand differences between acute reactions and later adaptation, comparing samples with grief disorders from those with more typical responses, and integrating responses in brain, mind and body.
... This result is similar to that of Buckley et al. [40], who also found a positive association between bereavement and SBP in Australia. Studies have shown that people who have lost a loved one exhibit maladaptive neuroendocrine and immune patterns and poorer health behaviours than prior to the loss, which exposes them to mental and physical health risks [41][42][43]. The implications are vast in a country like South Africa which is already burdened with high mortality due to causes such as human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) and tuberculosis (TB), and injury and homicide, and NCDs such as cardiovascular diseases and diabetes [22]. ...
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The relationship between negative events, neighbourhood characteristics, and systolic blood pressure in developing countries is not well-documented, particularly using longitudinal data. To explore this relationship, we analysed panel data from the first three waves of the South African National Income Dynamics Study using a correlated random effects model adjusted for confounding risk factors. Our sample comprised of 15,631 respondents in 2008, 14,443 respondents in 2010/2011, and 14,418 respondents in 2012, all aged above 15 years. The prevalence of at least one negative household event across the three waves was approximately 30%. In any of the three waves, the adjusted prevalence of hypertension was 23.84%. This share was 21.75% in 2008 (95% CI 18.06–25.44), 23.16% in 2010/11 (95% CI 19.18–27.14), and 18.39% in 2012 (95% CI 16.03–20.75). In our adjusted correlated random effects model, we found that systolic blood pressure was significantly higher among respondents from households that reported death of a household member (0.85 mmHg; p = 0.02) and a reduction in grant income and remittances (2.14 mm Hg; p = 0.01). We also found no significant association between systolic blood pressure and neighbourhood income level. In a country with social and economic challenges, our results indicate that grief and negative financial events are adversely associated with blood pressure, which may explain in part the significant burden of hypertension in low- and middle-income countries.
Bereavement due to loss of a partner is one of the most stressful life events, often leading to adverse physiological responses. Spousal loss has been associated with an increased morbidity and mortality, particularly from cardiovascular disease. Use of aspirin and/or beta adrenergic blockers have previously been suggested to play a role in cardiovascular risk associated with early bereavement. However, the available literature regarding this topic is limited. In this review article, we explore the potential beneficial role of aspirin and beta blockers in early bereavement. Our systematic review suggests that most studies have found aspirin and beta blockers to be beneficial in preventing adverse cardiovascular outcomes associated with early bereavement. Further randomized controlled long-term studies are warranted with adequate sample size to clearly establish the role of these medications on cardiovascular disease in late bereavement.
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Background: Bereavement is associated with an increased risk of cardiovascular disease; however, no reports exist of interventions to reduce risk. In a randomized, double-blind, placebo-controlled trial of 85 recently bereaved participants, we determined whether β-blocker (metoprolol 25 mg) and aspirin (100 mg) reduce cardiovascular risk markers and anxiety, without adversely affecting bereavement intensity. Methods: Participants were spouses (n = 73) or parents (n = 12) of deceased from 5 hospitals in Sydney, Australia, 55 females, 30 males, aged 66.1 ± 9.4 years. After assessment within 2 weeks of bereavement, subjects were randomized to 6 weeks of daily treatment or placebo, and the effect evaluated using ANCOVA, adjusted for baseline values (primary analysis). Results: Participants on metoprolol and aspirin had lower levels of home systolic pressure (P = .03), 24-hour average heart rate (P < .001) and anxiety (P = .01) platelet response to arachidonic acid (P < .001) and depression symptoms (P = .046) than placebo with no difference in standard deviation of NN intervals index (SDNNi), von Willebrand Factor antigen, platelet-granulocyte aggregates or bereavement intensity. No significant adverse safety impact was observed. Conclusions: In early bereavement, low dose metoprolol and aspirin for 6 weeks reduces physiological and psychological surrogate measures of cardiovascular risk. Although further research is needed, results suggest a potential preventive benefit of this approach during heightened cardiovascular risk associated with early bereavement.
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There is a considerable body of evidence indicating that chronic adverse experience, especially chronic psychosocial stress/trauma, represents a major risk factor for the development of many somatic and affective disorders, including inflammatory bowel disease (IBD) and posttraumatic stress disorder (PTSD). However, the mechanisms underlying the development of chronic stress-associated disorders are still in large part unknown, and current treatment and prevention strategies lack efficacy and reliability. A greater understanding of mechanisms involved in the development and persistence of chronic stress-induced disorders may lead to novel approaches to prevention and treatment of these disorders. In this review, we provide evidence indicating that increases in immune (re-)activity and inflammation, potentially promoted by a reduced exposure to immunoregulatory microorganisms (“Old Friends”) in today’s modern society, may be causal factors in mediating the vulnerability to development and persistence of stress-related pathologies. Moreover, we discuss strategies to increase immunoregulatory processes and attenuate inflammation, as for instance contact with immunoregulatory Old Friends, which appears to be a promising strategy to promote stress resilience and to prevent/treat chronic stress-related disorders.
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We now know that depression is associated with a chronic, low-grade inflammatory response and activation of cell-mediated immunity, as well as activation of the compensatory anti-inflammatory reflex system. It is similarly accompanied by increased oxidative and nitrosative stress (O&NS), which contribute to neuroprogression in the disorder. The obvious question this poses is 'what is the source of this chronic low-grade inflammation?' DISCUSSION: This review explores the role of inflammation and oxidative and nitrosative stress as possible mediators of known environmental risk factors in depression, and discusses potential implications of these findings. A range of factors appear to increase the risk for the development of depression, and seem to be associated with systemic inflammation; these include psychosocial stressors, poor diet, physical inactivity, obesity, smoking, altered gut permeability, atopy, dental cares, sleep and vitamin D deficiency. The identification of known sources of inflammation provides support for inflammation as a mediating pathway to both risk and neuroprogression in depression. Critically, most of these factors are plastic, and potentially amenable to therapeutic and preventative interventions. Most, but not all, of the above mentioned sources of inflammation may play a role in other psychiatric disorders, such as bipolar disorder, schizophrenia, autism and post-traumatic stress disorder.
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The evolution in the understanding of the neurobiology of most prevalent mental disorders such as major depressive disorder (MDD), bipolar disorder or schizophrenia has not gone hand in hand with the synthesis and clinical use of new drugs that would represent a therapeutic revolution such as that brought about by selective serotonin reuptake inhibitors (SSRIs) or atypical antipsychotics. Although scientists are still a long way from understanding its true aetiology, the neurobiological concept of depression has evolved from receptor regulation disorder, to a neurodegenerative disorder with a hippocampal volume decrease with the controversial reduction in neurotrophins such as BDNF, to current hypotheses that consider depression to be an inflammatory and neuroprogressive process. As regards antidepressants, although researchers are still far from knowing their true mechanism of action, they have gone from monoaminergic hypotheses, in which serotonin was the main protagonist, to emphasising the anti-inflammatory action of some of these drugs, or the participation of p11 protein in their mechanism of action. In the same way, according to the inflammatory hypothesis of depression, it has been proposed that some NSAIDS such as aspirin or drugs like simvastatin that have an anti-inflammatory action could be useful in some depressive patients. Despite the fact that there may be some data to support their clinical use, common sense and the evidence advise us to use already tested protocols and wait for the future to undertake new therapeutic strategies.
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The death of a loved one is recognized as one of life's greatest stresses, with reports of increased mortality and morbidity for the surviving spouse or parent, especially in the early months of bereavement. The aim of this paper is to review the evidence to date to identify physiological changes in the early bereaved period, and evaluate the impact of bereavement interventions on such physiological responses, where they exist. Research to date suggests that bereavement is associated with neuroendocrine activation (cortisol response), altered sleep (electroencephalography changes), immune imbalance (reduced T-lymphocyte proliferation), inflammatory cell mobilization (neutrophils), and prothrombotic response (platelet activation and increased vWF-ag) as well as hemodynamic changes (heart rate and blood pressure), especially in the early months following loss. Additional evidence suggests that bereavement interventions have the potential to be of value in instances where sleep disturbance becomes a prolonged feature of complicated grief, but have limited efficacy in maintaining immune function in the normal course of bereavement.
Background Low-dose aspirin is of definite and substantial net benefit for many people who already have occlusive vascular disease. We have assessed the benefits and risks in primary prevention. Methods We undertook meta-analyses of serious vascular events (myocardial infarction, stroke, or vascular death) and major bleeds in six primary prevention trials (95000 individuals at low average risk, 660000 person-years, 3554 serious vascular events) and 16 secondary prevention trials (17000 individuals at high average risk, 43 000 person-years, 3306 serious vascular events) that compared long-term aspirin versus control. We report intention-to-treat analyses of first events during the scheduled treatment period. Findings in the primary prevention trials, aspirin allocation yielded a 12% proportional reduction in serious vascular events (0.51% aspirin vs 0.57% control per year, p=0.0001), due mainly to a reduction of about a fifth in non-fatal myocardial infarction (0.18% vs 0.23% per year, p<0.0001). The net effect on stroke was not significant (0.20% vs 0.21% per year, p=0.4: haernorrhagic stroke 0.04% vs 0.03%, p=0.05; other stroke 0.16% vs 0.18% per year, p=0.08). Vascular mortality did not differ significantly (0.19% vs 0.19% per year, p=0.7). Aspirin allocation increased major gastrointestinal and extracranial bleeds (0.10% vs 0.07% per year, p<0.0001), and the main risk factors for coronary disease were also risk factors for bleeding. In the secondary prevention trials, aspirin allocation yielded a greater absolute reduction in serious vascular events (6.7% vs 8.2% per year, p<0.0001), with a non-significant increase in haernorrhagic stroke but reductions of about a fifth in total stroke (2.08% vs 2.54% per year, p=0.002) and in coronary events (4.3% vs 5.3% per year, p<0.0001). In both primary and secondary prevention trials, the proportional reductions in the aggregate of all serious vascular events seemed similar for men and women. Interpretation In primary prevention without previous disease, aspirin is of uncertain net value as the reduction in occlusive events needs to be weighed against any increase in major bleeds. Further trials are in progress. Funding UK Medical Research Council, British Heart Foundation, Cancer Research UK, and the European Community Biomed Programme.
Acute psychological stress is associated with an abrupt increase in the risk of cardiovascular events. Intense grief in the days after the death of a significant person may trigger the onset of acute myocardial infarction (MI), but this relationship has not been systematically studied. We conducted a case-crossover analysis of 1985 participants from the multicenter Determinants of Myocardial Infarction Onset Study interviewed during index hospitalization for an acute MI between 1989 and 1994. We compared the observed number of deaths in the days preceding MI symptom onset with its expected frequency based on each patient's control information, defined as the occurrence of deaths in the period from 1 to 6 months before infarction. Among the 1985 subjects, 270 (13.6%) experienced the loss of a significant person in the prior 6 months, including 19 within 1 day of their MI. The incidence rate of acute MI onset was elevated 21.1-fold (95% confidence interval, 13.1-34.1) within 24 hours of the death of a significant person and declined steadily on each subsequent day. The absolute risk of MI within 1 week of the death of a significant person is 1 excess MI per 1394 exposed individuals at low (5%) 10-year MI risk and 1 per 320 among individuals at high (20%) 10-year risk. Grief over the death of a significant person was associated with an acutely increased risk of MI in the subsequent days. The impact may be greatest among individuals at high cardiovascular risk.
Attachment theory is a conceptual framework for emotional-motivational behaviour and stress regulation in social relationships. However, few experimental studies have investigated attachment-related autonomic stress responses in adults. In a sample of 50 healthy subjects, we investigated autonomic cardiovascular reactions and subjective stress-load to a newly developed, attachment-related short-term stressor (separation recall, SR). The overall magnitude of the cardiovascular response to SR was comparable to the well established mental arithmetic (MA) stress test. However, the SR induced higher levels of sadness and impaired diastolic blood pressure recovery, whereas MA was associated with higher levels of anger and greater heart rate increase. Recovery scores to the attachment-stressor but not the mental arithmetic were related to attachment avoidance as measured by self-report, especially when taking into account the content of the reported episodes of the SR. In sum, our newly developed attachment-related short-term stressor has proven good performance in a first study.
Aspirin has been found to prevent angiotensin II-induced hypertension and to induce nitric oxide (NO) release from vascular endothelium. Low-dose aspirin has also been shown to reduce blood pressure (BP) when administered at bedtime, as opposed to upon awakening, in untreated hypertensive patients and high-risk pregnant women. Accordingly, we investigated the effects on ambulatory BP of aspirin administered at different times of the day in prehypertension. We studied 244 subjects with prehypertension, 43.0 +/- 13.0 years of age, randomly divided in three groups: nonpharmacological hygienic-dietary recommendations; the same recommendations and aspirin (100 mg/day) on awakening; or the same recommendations and aspirin at bedtime. BP was measured for 48 consecutive hours before and after 3 months of intervention. Ambulatory BP was unchanged in subjects randomized to either nonpharmacological intervention or aspirin on awakening. A significant ambulatory BP reduction was, however, observed in the subjects who received aspirin at bedtime (decrease of 6/3 mm Hg in the 24-h mean of systolic (SBP)/diastolic BP (DBP), respectively; P < 0.001), without changes in heart rate (HR) from baseline. BP was homogeneously controlled along the 24 h after bedtime aspirin administration (6/4 mm Hg reduction in activity mean of SBP/DBP; 6/3 mm Hg reduction in sleep-time mean, respectively). This prospective trial documents a significant effect on BP of low dose aspirin only when ingested at bedtime by prehypertensive subjects. The timed administration of low-dose aspirin could thus provide a valuable and cost-effective approach for BP control in subjects at elevated risk of developing hypertension.
Loss of autonomic balance characterized by increased sympathetic activity and decreased vagal activity has been implicated as a major cardiovascular risk factor. Aspirin's cardioprotective abilities involve a multitude of physiologic processes. However, the effects of aspirin on cardiac autonomic activity are unknown. In a double-blind crossover study, 22 subjects randomly received either aspirin or placebo in the amounts of 325 mg with each meal (three times per day) over a 2.5-day period. The total amount of aspirin ingested was 2,275 mg, which resulted in plasma levels of 3.3 mg/dl. At the conclusion of each treatment, subjects were evaluated for autonomic physiology activity using standard autonomic tests. Power spectral analyses of the electrocardiograms were used to delineate autonomic function. A 2×4 repeated measures analysis of variance revealed significant and favorable changes in autonomic activity after the use of aspirin. Specifically, at rest high-frequency (HF) power was significantly higher (mean, 1,090±1,463.5 msec2) compared with the placebo (mean, 692±742 msec2) (p2) after aspirin compared with placebo (mean, 1,100±906 msec2). After the aspirin treatment, a significantly lower LF-to-HF power ratio (mean, 1.7±2 msec2) was noted at rest when compared with the placebo (mean, 2.5±2.7 msec2) (p2) compared with placebo (mean, 213±184 msec2) (p2) (mean, 5.3±8.4 msec2) (p
The American Heart Association (AHA) and the American Diabetes Association (ADA) have each published guidelines for cardiovascular disease prevention: The ADA has issued separate recommendations for each of the cardiovascular risk factors in patients with diabetes, and the AHA has shaped primary and secondary guidelines that extend to patients with diabetes. This statement will attempt to harmonize the recommendations of both organizations where possible but will recognize areas in which AHA and ADA recommendations differ.