Ambar Kulshreshtha1, Yan Zheng2, Arshed A Quyyumi3, Emir Veledar1, John Votaw4, Irina Uphoff4, Douglas J Bremner5, Jack Goldberg6, Viola Vaccarino1. 1. Department of Epidemiology, Emory University School of Public Health, Atlanta, GA ; Division of Cardiology, Emory University School of Medicine, Atlanta, GA. 2. Department of Epidemiology, Emory University School of Public Health, Atlanta, GA. 3. Division of Cardiology, Emory University School of Medicine, Atlanta, GA. 4. Department of Radiology, Emory University School of Medicine, Atlanta, GA. 5. Department of Psychiatry, Emory University School of Medicine, Atlanta, GA. 6. Vietnam Era Twin Registry, Seattle, WA ; University of Washington School of Public Health, Seattle, WA.
Abstract
OBJECTIVE: Silent myocardial ischemia is common in asymptomatic subjects without a prior history of coronary artery disease (CAD) and is associated with increased morbidity and mortality. Our objective was to determine whether endothelial dysfunction is associated with silent myocardial ischemia and whether the association is independent of genetic and familial factors. MATERIAL AND METHODS: We examined 416 male monozygotic and dizygotic twins aged 47 to 63 years, free of symptomatic CAD. Subclinical ischemia was diagnosed by [13N] ammonia positron emission tomography at rest and after adenosine stress. Endothelial function was measured by flow-mediated dilation (FMD) of the brachial artery. Generalized estimating equations were used for analysis. RESULTS: Fixed perfusion defects were found in 24 (6%) twins and reversible perfusion defects in 90 (22%) twins, indicating subclinical ischemia. There was an inverse correlation between FMD and the reversible perfusion defect score (r = - 0.14, p=0.01) but not the fixed defect score (r= -0.017, p=0.73). From the lowest to the highest quartile of FMD, the prevalence of reversible defects decreased 28% to 14%, p=0.008. In multivariable analysis, reversible defects were significantly associated with each quartile of decreasing FMD (OR =1.3; 95% 1.1, 2.5). In 54 twin pairs discordant for endothelial dysfunction (FMD ≤ 7% dilation from baseline), twins with endothelial dysfunction had 9% higher likelihood of having perfusion defects than their co-twins without endothelial dysfunction (p=0.041). CONCLUSIONS: Endothelial dysfunction is independently associated with silent ischemia and this association is not confounded by genetic or other shared familial factors.
OBJECTIVE:Silent myocardial ischemia is common in asymptomatic subjects without a prior history of coronary artery disease (CAD) and is associated with increased morbidity and mortality. Our objective was to determine whether endothelial dysfunction is associated with silent myocardial ischemia and whether the association is independent of genetic and familial factors. MATERIAL AND METHODS: We examined 416 male monozygotic and dizygotic twins aged 47 to 63 years, free of symptomatic CAD. Subclinical ischemia was diagnosed by [13N] ammonia positron emission tomography at rest and after adenosinestress. Endothelial function was measured by flow-mediated dilation (FMD) of the brachial artery. Generalized estimating equations were used for analysis. RESULTS: Fixed perfusion defects were found in 24 (6%) twins and reversible perfusion defects in 90 (22%) twins, indicating subclinical ischemia. There was an inverse correlation between FMD and the reversible perfusion defect score (r = - 0.14, p=0.01) but not the fixed defect score (r= -0.017, p=0.73). From the lowest to the highest quartile of FMD, the prevalence of reversible defects decreased 28% to 14%, p=0.008. In multivariable analysis, reversible defects were significantly associated with each quartile of decreasing FMD (OR =1.3; 95% 1.1, 2.5). In 54 twin pairs discordant for endothelial dysfunction (FMD ≤ 7% dilation from baseline), twins with endothelial dysfunction had 9% higher likelihood of having perfusion defects than their co-twins without endothelial dysfunction (p=0.041). CONCLUSIONS: Endothelial dysfunction is independently associated with silent ischemia and this association is not confounded by genetic or other shared familial factors.
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