Background Most data linking chronic stress with cardiovascular disease (CVD) risk factors and outcomes have focused on single‐domain stress measurements. We evaluated the association between a novel composite measure of chronic perceived stress and CVD risk factors and outcomes in a diverse population. Methods and Results Individual chronic stress subcomponents (generalized stress, psychosocial, financial, and neighborhood stress) were standardized and integrated to create a novel composite stress score (CSS). Participants from the DHS (Dallas Heart Study) phase 2 (2007–2009) visit without prevalent CVD who completed chronic stress questionnaires were included (n=2685). Associations between CSS and demographics, cardiac risk factors, and health behaviors were assessed in multivariable analyses. Cox proportional hazards models adjusting for traditional risk factors were used to determine associations of the CSS with adjudicated atherosclerotic CVD and global CVD (atherosclerotic CVD, heart failure, and atrial fibrillation) outcomes. CSS was higher among participants who were younger, women, and Black or Hispanic individuals, with lower income and educational attainment (P<0.0001 for each). In multivariable regression models adjusting for age, sex, race and ethnicity, income and education, higher CSS associated with hypertension, smoking, higher body mass index, hemoglobin A1C, high‐sensitivity C‐reactive protein, and sedentary time (P<0.01 for each). Over a median follow‐up of 12.4 years, higher CSS associated with atherosclerotic CVD (adjusted hazard ratio [HR]. 1.22 per SD [95% CI, 1.01–1.47]) and global CVD (adjusted HR, 1.20 [95% CI, 1.03–1.40]). No interactions were seen between CSS, demographic factors, and outcomes. Conclusions Composite measures of chronic stress are higher in vulnerable populations and may help identify individuals at risk for CVD who may benefit from enhanced prevention strategies.

Graphical Abstract Graphical Abstract

The editorial content of Cardiology Rounds is determined solely by the Cardiovascular Division of Brigham and Women’s Hospital. This publication is made possible by an educational grant. of the heart and recognized by a characteristic pattern of hemodynamic, renal, neural, and hormonal responses. 7 And, in 1988, Professor Jay Cohn suggested that HF should be defined as “a syndrome in which cardiac dysfunction is associated with reduced exercise tolerance, a high incidence of ventricular arrhythmias, and shortened life expectancy. 8” The Task Force of the European Society of Cardiology defined HF “as a condition when symptoms of HF, objective evidence of cardiac dysfunction, and response to treatment directed towards HF exist. 9” The definitions above were proposed to recognize systolic HF, since diastolic HF was only appreciated rather recently. The contemporary clinical definition of systolic HF is “a clinical syndrome associated with congestive symptoms and/or symptoms of low cardiac output due to impaired ventricular pump function (reduced EF).”

2 whereas genetic syndromes of high HDL-C are often associated with decreased risk of CHD. These observations led to the recommendation for the inclusion of HDL-C in routine screening of all adults 3 and as an independent risk factor in the assessment of

Cardiovascular disease (CVD) accounts for over 40% of all deaths in women in the United States and is the leading killer of women in most developed countries. For many years, nearly all studies of coronary artery disease (CAD) excluded women. This was likely due to age bias, rather than gender bias, as men present with CVD at a younger age. The problem of CVD in women has therefore been masked by the protective effect from cardiac death in young premenopausal women. This issue of Cardiology Rounds reviews the role of gender in CAD with specific emphasis on the current understanding of the role that ovarian function and hormone replacement therapy (HRT) plays in atherosclerosis.

1