Alcohol's Effects on the Cardiovascular System

Abstract

Alcohol use has complex effects on cardiovascular (CV) health. The associations between drinking and CV diseases such as hypertension, coronary heart disease, stroke, peripheral arterial disease, and cardiomyopathy have been studied extensively and are outlined in this review. Although many behavioral, genetic, and biologic variants influence the interconnection between alcohol use and CV disease, dose and pattern of alcohol consumption seem to modulate this most. Low-to-moderate alcohol use may mitigate certain mechanisms such as risk and hemostatic factors affecting atherosclerosis and inflammation, pathophysiologic processes integral to most CV disease. But any positive aspects of drinking must be weighed against serious physiological effects, including mitochondrial dysfunction and changes in circulation, inflammatory response, oxidative stress, and programmed cell death, as well as anatomical damage to the CV system, especially the heart itself. Both the negative and positive effects of alcohol use on particular CV conditions are presented here. The review concludes by suggesting several promising avenues for future research related to alcohol use and CV disease. These include using direct biomarkers of alcohol to confirm self-report of alcohol consumption levels; studying potential mediation of various genetic, socioeconomic, and racial and ethnic factors that may affect alcohol use and CV disease; reviewing alcohol-medication interactions in cardiac patients; and examining CV effects of alcohol use in young adults and in older adults.

Figure 1

Incidence of hypertension in men and women. NOTE: * Indicates data significantly different from nondrinkers. For females, data at higher alcohol consumption levels (>40 g/day) were not analyzed. SOURCE: Data from Briasoulis et al. 2012.

Figure 2

Relative risks (95% confidence intervals) for cardiovascular (CV), coronary heart disease (CHD), and stroke outcomes. SOURCE: Data used from Ronksley et al. 2011.

Figure 3

Mechanisms related to the positive and adverse effects of alcohol on cardiovascular conditions, such as coronary heart disease and stroke as well as cardiomyopathy. Different mechanisms may be in effect depending on the dose, duration, and pattern of alcohol consumption. NOTE: BP = blood pressure, Ca²⁺ = calcium, CRP = C-reactive protein, DM = diabetes mellitus, HDL = high-density lipoprotein, LDL = low-density lipoprotein, PAI-1 = plasminogen activator inhibitor-1. SOURCE: Adapted from Krenz and Korthuis 2012.

Figure 4

Pathophysiologic schema for the development of alcoholic cardiomyopathy (ACM). As noted in the text, the exact amount and duration of alcohol consumption that results in ACM in human beings varies. The exact sequence of the development of ACM remains incompletely understood. Data from animal models and human beings with a history of long-term drinking suggest that oxidative stress may be an early and initiating mechanism. Many cellular events, such as intrinsic myocyte dysfunction, characterized by changes in calcium homeostasis and regulation and decreased myofilament sensitivity, can come about due to oxidative stress. Variables in gray ovals represent potential mediating factors. NOTE: LV = left ventricle, RAAS = renin–angiotensin–aldosterone system. SOURCE: Adapted from Piano and Phillips 2014.

Figure 5

Summary of potential cellular changes related to ethanol. Ethanol-induced changes may be related to oxidative or nonoxidative pathways of ethanol metabolism. More than one mechanism may be activated and may lead to the multitude of ethanol-induced changes in cellular proteins and cell function. As reviewed in the text, data from pharmacologic and transgenic approaches revealed an important role for oxidative stress and the hormone angiotensin II. NOTE: Ang II = angiotensin II, ATG = atrogin, ATI = angiotensin I receptor, ATP = adenosine triphosphate, CYP2E1 = cytochrome P450 2E1, FAEE = fatty ethyl esters, mTOR = mammalian (or mechanistic) target of rapamycin, NADPH oxidase/NOX = nicotinamide adenine dinucleotide phosphate-oxidase, ROS = reactive oxygen species. SOURCE: Adapted from Piano and Phillips 2014.