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      Association of Transient Endothelial Dysfunction Induced by Mental Stress With Major Adverse Cardiovascular Events in Men and Women With Coronary Artery Disease

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          Abstract

          Is mental stress–induced endothelial dysfunction associated with major adverse cardiovascular events? This cohort study of patients with stable coronary artery disease found a graded positive association between transient endothelial dysfunction with mental stress and major adverse cardiovascular events. Impairment in endothelium-dependent relaxation induced by mental stress confers an increased hazard for adverse events and could be an important risk biomarker for patients with stable coronary artery disease. This cohort study assesses the association of mental stress–induced impairment in endothelium-dependent relaxation with adverse cardiovascular outcomes among individuals with stable coronary artery disease. Acute mental stress can result in transient endothelial dysfunction, but the prognostic relevance of this phenomenon is unknown. To determine the association between mental stress–induced impairment in endothelium-dependent relaxation as assessed by brachial artery flow-mediated vasodilation and adverse cardiovascular outcomes among individuals with stable coronary artery disease. This cohort study was conducted at a university-affiliated hospital network between June 2011 and August 2014. A cohort of individuals with stable coronary artery disease were included. Data analysis took place from November 2018 to May 2019. Study participants were subjected to a laboratory mental stress task (public speaking). Flow-mediated vasodilation was measured before and 30 minutes after a public-speaking mental stress task. We examined the association of the rest (prestress), poststress, and δ flow-mediated vasodilation (poststress minus prestress levels) with an adjudicated composite end point of adverse events, including cardiovascular death, myocardial infarction, unstable angina leading to revascularization, and heart failure hospitalization, after adjusting for sociodemographic factors, medical history, and depression. A total of 569 patients were included (mean [SD] age, 62.6 [9.3] years; 420 men [73.8%]). Flow-mediated vasodilation decreased from a mean (SD) of 4.8% (3.7%) before mental stress to 3.9% (3.6%) after mental stress (a 23% reduction; P  < .001), and 360 participants (63.3%) developed transient endothelial dysfunction (a decrease in flow-mediated vasodilation). During a median (interquartile range) follow-up period of 3.0 (2.9-3.1) years, 74 patients experienced a major adverse cardiovascular event. The presence of transient endothelial dysfunction with mental stress was associated with a 78% increase (subdistribution hazard ratio [sHR], 1.78 [95% CI, 1.15-2.76]) in the incidence of major adverse cardiovascular event. Both the δ flow-mediated vasodilation (sHR, 1.15 [95% CI, 1.03-1.27] for each 1% decline) and poststress flow-mediated vasodilation (sHR, 1.14 [95% CI, 1.04-1.24] for each 1% decline) were associated with major adverse cardiovascular event. Risk discrimination statistics demonstrated a significant model improvement after addition of either poststress flow-mediated vasodilation (change in the area under the curve, 0.05 [95% CI, 0.01-0.09]) or prestress plus δ flow-mediated vasodilation (change in the area under the curve, 0.04 [95% CI, 0.00-0.08]) compared with conventional risk factors. In this study, transient endothelial dysfunction with mental stress was associated with adverse cardiovascular outcomes in patients with coronary artery disease. Endothelial responses to stress represent a possible mechanism through which psychological stress may affect outcomes in patients with coronary artery disease.

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          Most cited references22

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          Guidelines for the ultrasound assessment of endothelial-dependent flow-mediated vasodilation of the brachial artery

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            Close relation of endothelial function in the human coronary and peripheral circulations.

            The relation between endothelium-dependent vasodilator function in the brachial and coronary arteries was determined in the same subjects. Coronary artery endothelial dysfunction precedes the development of overt atherosclerosis and is important in its pathogenesis. A noninvasive assessment of endothelial function in a peripheral conduit vessel, the brachial artery, was recently described, but the relation between brachial artery function and coronary artery vasodilator function has not been explored. In 50 patients referred to the catheterization laboratory for the evaluation of coronary artery disease (mean age +/- SD 56 +/- 10 years), the coronary vasomotor response to serial intracoronary infusions of the endothelium-dependent agonist acetylcholine (10(-8) to 10(-6) mol/liter), was studied. Endothelium-dependent vasodilation was also assessed in the brachial artery by measuring the change in brachial artery diameter in response to reactive hyperemia. Patients with coronary artery endothelial dysfunction manifested as vasoconstriction in response to acetylcholine had significantly impaired flow-mediated vasodilation in the brachial artery compared with that of patients with normal coronary endothelial function (4.8 +/- 5.5% vs. 10.8 +/- 7.6%, p < 0.01). Patients with coronary artery disease also had an attenuated brachial artery vasodilator response compared with that of patients with angiographically smooth coronary arteries (4.5 +/- 4.6% vs. 9.7 +/- 8.1%, p < 0.02). By multivariate analysis, the strongest predictors of reduced brachial dilator responses to flow were baseline brachial artery diameter (p < 0.001), coronary endothelial dysfunction (p = 0.003), the presence of coronary artery disease (p = 0.007) and cigarette smoking (p = 0.016). The brachial artery vasodilator response to sublingual nitroglycerin was independent of coronary endothelial responses or the presence of coronary artery disease. The positive predictive value of abnormal brachial dilation ( < 3%) in predicting coronary endothelial dysfunction is 95%. This study demonstrated a close relation between coronary artery endothelium-dependent vasomotor responses to acetylcholine and flow-mediated vasodilation in the brachial artery. This noninvasive method may become a useful surrogate in assessing the predisposition to atherosclerosis in patients with cardiac risk factors.
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              Greater cardiovascular responses to laboratory mental stress are associated with poor subsequent cardiovascular risk status: a meta-analysis of prospective evidence.

              An increasing number of studies has tested whether greater cardiovascular responses to acute mental stress predict future cardiovascular disease, but results have been variable. This review aimed quantitatively to evaluate the association between cardiovascular responses to laboratory mental stress and subsequent cardiovascular risk status in prospective cohort studies. We searched general bibliographic databases, PsycINFO, Web of Science, and PubMed, up to December 2009. Two reviewers independently extracted data on study characteristics, quality, and estimates of associations. There were 169 associations (36 articles) of stress reactivity and 30 associations (5 articles) of poststress recovery in relation to future cardiovascular risk status, including elevated blood pressure, hypertension, left ventricular mass, subclinical atherosclerosis, and clinical cardiac events. The overall meta-analyses showed that greater reactivity to and poor recovery from stress were associated longitudinally with poor cardiovascular status (r=0.091 [95% CI: 0.050 to 0.132], P<0.001, and r=0.096 [95% CI: 0.058 to 0.134], P<0.001, respectively). These findings were supported by more conservative analyses of aggregate effects and by subgroup analyses of the methodologically strong associations. Notably, incident hypertension and increased carotid intima-media thickness were more consistently predicted by greater stress reactivity and poor stress recovery, respectively, whereas both factors were associated with higher future systolic and diastolic blood pressures. In conclusion, the current meta-analysis suggests that greater responsivity to acute mental stress has an adverse effect on future cardiovascular risk status, supporting the use of methods of managing stress responsivity in the prevention and treatment of cardiovascular disease.
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                Author and article information

                Journal
                JAMA Cardiology
                JAMA Cardiol
                American Medical Association (AMA)
                2380-6583
                September 11 2019
                Affiliations
                [1 ]Emory Clinical Cardiovascular Research Institute, Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia
                [2 ]Rollins School of Public Health, Department of Epidemiology, Emory University, Atlanta, Georgia
                [3 ]Atlanta VA Medical Center, Decatur, Georgia
                [4 ]Rollins School of Public Health, Department of Biostatistics and Bioinformatics, Emory University, Atlanta, Georgia
                [5 ]Department of Epidemiology, College of Public Health and Health Professions, University of Florida, Gainesville
                [6 ]Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia
                [7 ]Department of Radiology, Emory University School of Medicine, Atlanta, Georgia
                Article
                10.1001/jamacardio.2019.3252
                6739728
                31509180
                75a2618c-d0b6-4fae-b9d6-952cdaa4df72
                © 2019
                History

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