To conduct a systematic review and meta-analysis on the relevance of low social support for the development and course of coronary heart disease (CHD). Three electronic databases were searched (MEDLINE, PsycINFO/PSYNDEX, and Web of Science 2007/03). More than 1700 papers were screened in a first step. We included prospective studies assessing the impact of social support in either an initially healthy study population (etiologic studies) or in a study population with preexisting CHD (prognostic studies). Myocardial infarction in etiologic studies; cardiovascular mortality and all-cause mortality in prognostic studies. Effects were reported as relative risk (RR) or hazard ratio (HR). There is some evidence for an impact of low functional social support on the prevalence of CHD in etiologic studies (RR, range, 1.00–2.23). In contrast, there is no evidence of an impact of low structural social support on the prevalence of myocardial infarction in healthy populations (RR, range, 1.01–1.2). In prognostic studies, results consistently show that low functional support negatively affects cardiac and all-cause mortality (pooled RR, range, 1.59–1.71). These results were also confirmed in analyses adjusted for other risk factors for disease progression (pooled HR, 1.59). It remains unclear whether low structural social support increases mortality in patients with CHD (pooled RR, between 1.56; pooled HR, 1.12, NS). Because the perception of social support seems important for CHD prognosis, monitoring of functional social support is indicated in patients with CHD, and interventions to increase the perception of positive social resources are warranted.

A hypercoagulable state before overt thrombosis resulting from an imbalance between the coagulation and fibrinolysis systems is related to cardiovascular disease progression and acute coronary syndromes. Psychological stressors and depressive and anxiety disorders also are associated with coronary artery disease. This review explores whether changes in blood coagulation, anticoagulant, and fibrinolytic activity may constitute psychobiological pathways that link psychological factors with coronary syndromes. Literature on coagulation, anticoagulation, and fibrinolysis measures in conjunction with psychological factors (mental stress, psychosocial strain, and psychiatric disorders) was identified by MEDLINE search back to 1966 and through checking the bibliographies of these sources. Sixty-eight articles were critically reviewed. In healthy subjects, acute mental stress simultaneously activates coagulation (ie, fibrinogen or von Willebrand factor) and fibrinolysis (ie, tissue-type plasminogen activator) within a physiological range. In patients with atherosclerosis and impaired endothelial anticoagulant function, however, procoagulant responses to acute stressors may outweigh anticoagulant mechanisms and thereby promote a hypercoagulable state. Chronic psychosocial stressors (job strain or low socioeconomic status) are related to a hypercoagulable state reflected by increased procoagulant molecules (ie, fibrinogen or coagulation factor VII) and by reduced fibrinolytic capacity. There is also some evidence that points to hypercoagulability in depression. Different categories of psychological measures to varying extent are associated with characteristic patterns of coagulation and fibrinolysis activity. Associations between psychological factors and several coagulation and fibrinolysis variables related to atherosclerosis provide a plausible biobehavioral link to coronary artery disease.