Preventive Cardiology

Low left ventricular ejection fraction (LVEF), a measure of global systolic left ventricular dysfunction, is associated with an increased risk of recurrent coronary events or death in persons with cardiac disease. There are few data on the distribution of resting LVEF and component volumes in healthy young adults or on any association of LVEF with coronary risk factors. LVEF and left ventricular end-diastolic and end-systolic volumes (LVEDV and LVESV, respectively) were measured by two-dimensional echocardiography in 1782 men and women 23 to 35 years old without self-reported heart disease (other than mitral valve prolapse, n = 53) who were participants in the multicenter Coronary Artery Risk Development in Young Adults study. Factors analyzed as potential contributors to LVEF, LVEDV, and LVESV included age, gender, race, blood pressure, alcohol use, current smoking, family history of myocardial infarction, total and high-density lipoprotein cholesterol concentrations, obesity, reported physical activity, and fitness as assessed by treadmill exercise testing. LVEF was lower in men (mean 62.6% SD 5.7%) than in women (mean 63.9%, SD 5.7%) (p < 0.01) but did not differ significantly between black and white subjects. Ninety percent of subjects had an LVEF between 53% and 71%. LVEDV and LVESV were > 25% greater in men than in women. From multivariate analysis, male gender, history of hypertension, and current smoking were each positively and independently associated with an approximately 1% lower LVEF. Body surface area, a family history of premature myocardial infarction, and treadmill workload 150 time were positively related, whereas total skinfold thickness was negatively related to LVEDV and LVESV.(ABSTRACT TRUNCATED AT 250 WORDS)

This study was performed to determine if alcohol intake was associated with reduced coronary risk in a high-risk asymptomatic population, and whether this effect was independent of coronary risk factors and coronary calcium. In 1,196 asymptomatic subjects with coronary risk factors, we assessed alcohol consumption history, performed risk factor measurements, and quantified coronary calcium with electron beam computed tomography. These subjects were then followed for a mean of 41 months, and coronary events (myocardial infarction or coronary death) were noted. Significant inverse predictors of coronary events included alcohol use and serum high-density lipoprotein cholesterol level. Direct predictors of events were history of systemic hypertension, smoking, diabetes mellitus, serum cholesterol, and coronary calcium score. Subjects with coronary calcium were 3.1 times more likely to suffer a coronary event than those without calcium (95% confidence interval [CI] limits 1.3 to 7.2). Subjects who drank alcohol had a relative risk of 0.3 (95% CI limits 0.2 to 0.6) for developing coronary events. After controlling for age, gender, and other risk factors with logistic regression, these differences in relative risk persisted (relative risk 0.58; 95% CI limits 0.41 to 0.82). Alcohol consumption is a significant inverse predictor of coronary events, comparable in magnitude to standard risk factors and to radiographically measured coronary calcium. This effect is independent of coronary risk factors and coronary calcium.

We sought to determine significant relations between atherogenic lipoproteins and the contribution of calcified plaque (CP), mixed plaque (MP), and noncalcified plaque (NCP) to the total plaque (TP) burden in patients without previous coronary artery disease. From 823 adult patients without previously established coronary artery disease (52% receiving statin therapy, 34% asymptomatic) but with visible coronary plaque on coronary computed tomographic angiography, we obtained segmental CP, MP, NCP, and TP counts from contrast-enhanced, electrocardiographic-gated computed tomography. Multivariate linear regression analysis was used to determine the associations of clinical factors and lipoprotein levels to CP, MP, and NCP counts and CP/TP, MP/TP, and NCP/TP count ratios. Age, male gender, diabetes, smoking, and statin therapy were significantly associated with the CP count (p <0.001, p <0.001, p = 0.049, p = 0.016, and p = 0.003, respectively). Low-density lipoprotein (LDL) cholesterol was significantly associated with MP and NCP counts (all p values </=0.002). LDL cholesterol was also the only variable to demonstrate significant concurrent relations with CP/TP, MP/TP, and NCP/TP ratios, including an inverse association with CP/TP (p = 0.008) and a positive association with MP/TP (p = 0.032). Analyses using non-high-density lipoprotein cholesterol in place of LDL cholesterol yielded similar results. In conclusion, among the traditional clinical factors used to estimate cardiovascular event risk, LDL cholesterol is associated with an increased MP and NCP burden and is the sole variable that independently predicted relative predominance of CP, MP, and NCP, suggesting a potentially important role for lipoprotein levels in modulating the type of detectable coronary arterial plaque.