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McEvoy J.W.,Johns Hopkins University | Nasir K.,Johns Hopkins University | Nasir K.,Center for Wellness and Prevention | Defilippis A.P.,Johns Hopkins University | And 14 more authors.
Arteriosclerosis, Thrombosis, and Vascular Biology | Year: 2015

Objective - We sought to assess the impact of smoking status, cumulative pack-years, and time since cessation (the latter in former smokers only) on 3 important domains of cardiovascular disease: inflammation, vascular dynamics and function, and subclinical atherosclerosis. Approach and Results - The Multi-Ethnic Study of Atherosclerosis (MESA) cohort enrolled 6814 adults without prior cardiovascular disease. Smoking variables were determined by self-report and confirmed with urinary cotinine. We examined cross-sectional associations between smoking parameters and (1) inflammatory biomarkers (high-sensitivity C-reactive protein [hsCRP], interleukin-6, and fibrinogen); (2) vascular dynamics and function (brachial flow-mediated dilation and carotid distensibility by ultrasound, as well as aortic distensibility by MRI); and (3) subclinical atherosclerosis (coronary artery calcification, carotid intima-media thickness, and ankle-brachial index). We identified 3218 never smokers, 2607 former smokers, and 971 current smokers. Mean age was 62 years and 47% were male. There was no consistent association between smoking and vascular distensibility or flow-mediated dilation outcomes. However, compared with never smokers, the adjusted association between current smoking and measures of either inflammation or subclinical atherosclerosis was consistently stronger than for former smoking (eg, odds ratio for hsCRP>2 mg/L of 1.7 [95% confidence interval, 1.5-2.1] versus 1.2 [1.1-1.4], odds ratio for coronary artery calcification>0 of 1.8 [1.5-2.1] versus 1.4 [1.2-1.6], respectively). Similar associations were seen for interleukin-6, fibrinogen, carotid intima-media thickness, and ankle-brachial index. A monotonic association was also found between higher pack-year quartiles and increasing inflammatory markers. Furthermore, current smokers with hsCRP>2 mg/L were more likely to have increased carotid intima-media thickness, abnormal ankle-brachial index, and coronary artery calcification>75th percentile for age, sex, and race (relative to smokers with hsCRP<2 mg/L, interaction P<0.05 for all 3 outcomes). In contrast, time since quitting in former smokers was independently associated with lower inflammation and atherosclerosis (eg, odds ratio for hsCRP>2 mg/L of 0.91 [0.88-0.95] and odds ratio for coronary artery calcification>0 of 0.94 [0.90-0.97] for every 5-year cessation interval). Conclusions - These findings expand our understanding of the harmful effects of smoking and help explain the cardiovascular benefits of smoking cessation. © 2015 American Heart Association, Inc.

Tison G.H.,University of California at San Francisco | Tison G.H.,Johns Hopkins Hospital | Blaha M.J.,Johns Hopkins Hospital | Nasir K.,Johns Hopkins Hospital | And 4 more authors.
American Journal of Cardiology | Year: 2015

We hypothesized that anthropometric measures of abdominal obesity would have a stronger positive association with nonalcoholic fatty liver disease (NAFLD) measured by noncontrast computed tomography versus general measures of obesity. The Multiethnic Study of Atherosclerosis comprised participants aged 45 to 84 years free of known cardiovascular disease. We studied 4,088 participants with adequate liver and spleen computed tomography imaging and no previous use of oral steroids, class 3 antiarrhythmics, moderately heavy alcohol use, or cirrhosis. Prevalent NAFLD was defined as a liver:spleen Hounsfield attenuation ratio of <1. Multivariable log-linear regression modeled the association of 4 obesity measures - weight, body mass index (BMI), waist circumference, and waist-to-hip ratio - with prevalent NAFLD. Receiver-operator curve analysis compared NAFLD discrimination. Median age was 63 years, and 55% were women. For each obesity measure, adjusted prevalence ratios for NAFLD were fourfold to fivefold greater in the highest versus the lowest quartile (p <0.001). Waist circumference and BMI had the highest prevalence ratios, and waist circumference had the best discrimination, for NAFLD in the total population, although an abnormal BMI categorized subjects with NAFLD as well if not better than waist circumference. In ethnic-specific analysis, whites and Chinese had the strongest association of obesity and NAFLD compared with other ethnicities. In conclusion, although waist circumference provided the best discrimination for NAFLD, BMI may perform similarly well in clinical settings to screen for NAFLD. © 2015 Elsevier Inc. All rights reserved.

Martin S.S.,Center for Wellness and Prevention | Blaha M.J.,Center for Wellness and Prevention | Blankstein R.,Brigham and Womens Hospital | Agatston A.,University of Miami | And 10 more authors.
Circulation | Year: 2014

BACKGROUND-: Worldwide clinical practice guidelines for dyslipidemia emphasize allocating statin therapy to those at the highest absolute atherosclerotic cardiovascular disease (CVD) risk. METHODS AND RESULTS-: We examined 5534 Multi-Ethnic Study of Atherosclerosis (MESA) participants who were not on baseline medications for dyslipidemia. Participants were classified by baseline coronary artery calcium (CAC) score (>0, ≥100) and the common clinical scheme of counting lipid abnormalities (LA), including low-density lipoprotein cholesterol ≥3.36 mmol/L (130 mg/dL), high-density lipoprotein cholesterol <1.03 mmol/L (40 mg/dL) for men or <1.29 mmol/L (50 mg/dL) for women, and triglycerides ≥1.69 mmol/L (150 mg/dL). Our main outcome measure was incident CVD (myocardial infarction, angina resulting in revascularization, resuscitated cardiac arrest, stroke, cardiovascular death). Over a median follow-up of 7.6 years, more than half of events (55%) occurred in the 21% of participants with CAC ≥100. Conversely, 65% of events occurred in participants with 0 or 1 LA. In those with CAC ≥100, CVD rates ranged from 22.7 to 29.5 per 1000 person-years across LA categories. In contrast, with CAC=0, CVD rates ranged from 2.7 to 5.9 per 1000 person-years across LA categories. Individuals with 0 LA and CAC ≥100 had a higher event rate compared with individuals with 3 LA but CAC=0 (22.7 versus 5.9 per 1000 person-years). Similar results were obtained when we classified LA using data set quartiles of total cholesterol/high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, or low-density lipoprotein particle concentration and guideline categories of low-density lipoprotein cholesterol or non-high-density lipoprotein cholesterol. CONCLUSIONS-: CAC may have the potential to help match statin therapy to absolute CVD risk. Across the spectrum of dyslipidemia, event rates similar to secondary prevention populations were observed for patients with CAC ≥100.© 2013 American Heart Association, Inc.

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