Alcohol Use and Cardiovascular Disease Risk in Patients With Nonalcoholic Fatty Liver Disease

Abstract

Background & aims: Cardiovascular disease (CVD) is the leading cause of death among patients with nonalcoholic fatty liver disease (NAFLD). Moderate drinking (vs abstinence) is associated with lower risk of CVD in the general population. We assessed whether alcohol use is associated with CVD risk in patients with NAFLD.

Methods: We analyzed data from participants in the Coronary Artery Risk Development in Young Adults longitudinal cohort study of 5115 black and white young adults, 18-30 years old, recruited from 4 cities in the United States from 1985 through 1986. Participants self-reported alcohol use at study entry and then again after 15, 20, and 25 years. At year 25 (2010-2011), participants underwent computed tomography examination of the thorax and abdomen and tissue Doppler echocardiography with myocardial strain measured by speckle tracking. Coronary artery calcification was defined as an Agatston score above 0. NAFLD was defined as liver attenuation <51 Hounsfield Units after exclusions. Drinkers reported 1-21 (men) or 1-14 (women) standard drinks/week at years 15, 20, or 25. Nondrinkers reported no alcohol use at years 15, 20, and 25.

Results: Of the 570 participants with NAFLD (mean age, 50 years; 54% black; 46% female), 332 (58%) were drinkers; significantly higher proportions of drinkers were white, male, and with higher levels of education compared with nondrinkers (P < .05 for all). Higher proportions of drinkers had obesity, diabetes, and metabolic syndrome compared with nondrinkers (P < .01). There was no difference in liver attenuation between groups (P = .12). After multivariable adjustment, there was no association between alcohol use and CVD risk factors (diabetes, hypertension, hyperlipidemia) or subclinical CVD measures (coronary artery calcification, early transmitral velocity/late (atrial) transmitral velocity (E/A) ratio, global longitudinal strain).

Conclusions: In a population-based sample of individuals with NAFLD in midlife, prospectively assessed alcohol use is not associated with significant differences in risk factors for CVD or markers of subclinical CVD. In contrast to general population findings, alcohol use may not reduce the risk of CVD in patients with NAFLD.

Keywords: CARDIA Study; Heart Disease; NAFLD; NASH.

Figure 1

Study sample—Abbreviations: CAC, coronary artery calcification; CT, computed tomography; HIV, human immunodeficiency virus; IV, intravenous; NAFLD, nonalcoholic fatty liver disease; Y25, year 25 ^*Heavy alcohol use was defined as > 14 standard drinks/week in women, > standard 21 drinks/week in men at Y25 ^†Medications = valproic acid, methotrexate, tamoxifen and amiodarone.

Figure 2. Alcohol exposure assessment

Primary analyses included 332 drinkers compared with 238 nondrinkers. Binge drinkers were included in the primary analysis only if they met moderate drinking thresholds (women ≤ 14; men ≤ 21 standard drinks/week). In sensitivity analysis, those participants with heavy alcohol use at any prior exam (n=19) or reported binge drinking behavior during the 10 years prior to liver fat assessment (n=92) were excluded. Thus, sensitivity analysis included comparisons between lifetime never-drinkers and drinkers without binge drinking behavior. ^*NAFLD was defined as CT liver attenuation < 51 Hounsfield units after exclusions for secondary causes of liver fat (heavy alcohol/medications/HIV/hepatitis/cirrhosis). ^**Heavy alcohol use was defined as > 14 standard drinks/week in women, > 21 standard drinks/week in men ^By “occasion” we mean at the same time or within a couple of hours of each other