Biobehavioral variables and mortality or cardiac arrest in the Cardiac Arrhythmia Pilot Study (CAPS)

Ahern, David K.; Gorkin, Larry; Anderson, Jeffrey L.; Tierney, Camlin; Hallstrom, Alfred P.; Ewart, Craig K.; Capone, Robert J.; Schron, Eleanor B.; Kornfeld, Donald S.; Herd, J. Alan; Richardson, David W.; Follick, Michael J.

doi:10.1016/0002-9149(90)90736-k

Cited by 426 publications

(176 citation statements)

References 26 publications

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“…21 In the Cardiac Arrhythmia Pilot Study composed of 502 post-AMI patients with significant ventricular arrhythmias, patients who reported a high incidence of depressive symptoms between 6 and 60 days after their AMI exhibited a 20-fold 1-year risk of mortality or cardiac arrest. 22 Prospective studies subsequently showed that the diagnosis of major depression before discharge from hospitalization for an AMI conferred a substantial Ͼ4-fold increased independent risk of subsequent cardiac death. 23 Recent data in almost 900 ACS patients revealed an increased mortality rate associated with depression over 5 years of follow-up.…”

Section: Discussionmentioning

confidence: 99%

Platelet/Endothelial Biomarkers in Depressed Patients Treated With the Selective Serotonin Reuptake Inhibitor Sertraline After Acute Coronary Events

et al. 2003

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Background-Depression after acute coronary syndromes (ACSs) has been identified as an independent risk factor for subsequent cardiac death. Enhanced platelet activation has been hypothesized to represent 1 of the mechanisms underlying this association. Selective serotonin reuptake inhibitors (SSRIs) are known to inhibit platelet activity.Whether treatment of depressed post-ACS patients with SSRIs alters platelet function was not known. Accordingly, we serially assessed the release of established platelet/endothelial biomarkers in patients treated with sertraline vs placebo in the Sertraline AntiDepressant Heart Attack Randomized Trial (SADHART). Methods and Results-Plasma samples (baseline, week 6, and week 16) were collected from patients randomized to sertraline (nϭ28) or placebo (nϭ36). Anticoagulants, aspirin, and ADP-receptor inhibitors were permitted in this study. Platelet factor 4, ␤-thromboglobulin (␤TG), platelet/endothelial cell adhesion molecule-1, P-selectin, thromboxane B 2 , 6-ketoprostaglandin F 1a , vascular cell adhesion molecule-1, and E-selectin were measured by ELISA. Treatment with sertraline was associated with substantially less release of platelet/endothelial biomarkers than was treatment with placebo. These differences attained statistical significance for ␤TG (Pϭ0.03) at weeks 6 and 16 and for P-selectin (Pϭ0.04) at week 16. Repeated-measures ANOVA revealed a significant advantage for sertraline vs placebo for diminishing E-selectin and ␤TG concentrations across the entire treatment period. Conclusions-Treatment

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Section: Discussionmentioning

confidence: 99%

Platelet/Endothelial Biomarkers in Depressed Patients Treated With the Selective Serotonin Reuptake Inhibitor Sertraline After Acute Coronary Events

et al. 2003

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“…Also, depressive symptoms that are not sufficient in magnitude to meet the criteria for major depression occur at least as commonly among cardiac patients. 2,3 Recent epidemiological studies evaluating the relationship between depression and CAD among healthy [3][4][5][6][7][8][9][10][11] and CAD [12][13][14][15][16][17][18][19] populations consistently demonstrate a significant prospective relationship between the occurrence of major depression episodes and the incidence of cardiac events (Table 1). Two additional findings are notable.…”

Section: Depression and Related Syndromesmentioning

confidence: 99%

Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

1999

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Abstract-Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis.Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys.Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. ...

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“…Anxiety, alone or comorbid with depression, has been associated with cardiovascular risk and outcomes, [130][131][132][133] although some studies have shown inconsistent associations between anxiety and mortality risk. [134][135][136][137] Similarly, well-established associations have been documented between elevated levels of hostility/anger and subclinical atherosclerosis, 138 incident myocardial infarction, [139][140][141][142] CVD progression, 143 and CVD and all-cause mortality 140,145 and with selected CVD risk factors, including hypertension, 146 lowdensity lipoprotein, inflammation (C-reactive protein), [147][148][149] and behavioral risk factors. 150 A meta-analytic review found that perceived stress was associated with a 27% increased risk of CVD.…”

Section: Psychological Mechanismsmentioning

confidence: 99%

Social Determinants of Risk and Outcomes for Cardiovascular Disease

Havranek¹,

Mujahid²,

Barr³

et al. 2015

Circulation

1,149

732

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Biobehavioral variables and mortality or cardiac arrest in the Cardiac Arrhythmia Pilot Study (CAPS)

Cited by 426 publications

References 26 publications

Platelet/Endothelial Biomarkers in Depressed Patients Treated With the Selective Serotonin Reuptake Inhibitor Sertraline After Acute Coronary Events

Platelet/Endothelial Biomarkers in Depressed Patients Treated With the Selective Serotonin Reuptake Inhibitor Sertraline After Acute Coronary Events

Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

Social Determinants of Risk and Outcomes for Cardiovascular Disease

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