Alcoholic cardiomyopathy is a result of direct cardiotoxic effects from heavy alcohol consumption resulting in left ventricular (LV) systolic dysfunction.⁸ Up to 40% of dilated cardiomyopathy in western countries has been attributed to excess alcohol use, although what constitutes excess alcohol consumption varies among studies.⁸,⁹ Few clinical or histological characteristics are specific to alcoholic cardiomyopathy, but it shares characteristics with other forms of dilated cardiomyopathy including a dilated left ventricle and a reduced LV ejection fraction (EF).⁸ In a cohort study of 52 patients with alcohol abuse, Urbano-Marquez et al found a significant decrease in the LVEF that was directly proportional to the patients’ lifelong cumulative alcohol intake.¹⁰ Some studies suggest worse outcomes in alcoholic cardiomyopathy compared with other forms of dilated cardiomyopathy. Fauchier et al studied 50 patients with alcoholic cardiomyopathy and 84 patients with dilated cardiomyopathy over a follow-up period of 47 months, finding a significantly higher survival rate in patients with dilated cardiomyopathy compared to their counterparts with alcoholic cardiomyopathy.¹¹ Gavazzi et al studied 79 patients with alcoholic cardiomyopathy and 259 patients with dilated cardiomyopathy over a mean follow-up period of 59 months and found that transplant-free survival was significantly worse among patients with alcoholic cardiomyopathy than among those with dilated cardiomyopathy (41% vs 53%, respectively).¹² Guzzo-Merello et al examined alcoholic cardiomyopathy in a cohort study, finding that one-third of these patients had a poor prognosis while two-thirds remained clinically stable.⁹ Out of the clinically stable patients, one-half recovered LV systolic function (ie, an absolute increase in LVEF >10% to a final value of >40%). In contrast, no significant difference in clinical outcomes was identified between patients with alcoholic cardiomyopathy who completely abstained from alcohol compared with those who reduced their intake to moderate.

Alcohol is a well-known trigger of atrial fibrillation, so much so that patients who present with atrial fibrillation after alcohol consumption are commonly referred to as having ‘holiday heart syndrome’. Heavy alcohol consumption may be a stronger risk factor for atrial fibrillation than hypertension or obesity.¹³ Multiple meta-analyses suggest that even moderate alcohol consumption increases the risk of atrial fibrillation.¹⁴,¹⁵ Infrequent binge drinking has also been implicated in the development of atrial fibrillation. Atrial fibrillation has been shown to occur even in infrequent and nondrinkers after a binge. Even though atrial fibrillation typically terminates after 24 hours, it will recur in about a quarter of patients with subsequent binges. Liang et al found that binge drinking among individuals who consumed a moderate amount of alcohol conferred a risk of atrial fibrillation similar to habitual heavy consumption.¹⁶

It has been postulated that alcohol may increase the risk of arrhythmias by inducing electrical atrial remodeling.¹⁷ Patients who drink alcohol have a higher recurrence of atrial fibrillation after ablation. In one study, 1-year arrhythmia-free survival post circumferential pulmonary vein isolation was found in 81% of patients who abstained from alcohol, 69% patients with light-moderate consumption, and only 35% in patient with heavy consumption.¹⁸ Patients with heavy alcohol consumption were also more likely to have adverse outcomes such as thromboembolism, even after adjusting for anticoagulation use and the CHA₂DS₂Vasc score.¹⁸ Importantly, abstinence from alcohol appears to reduce the risk of atrial fibrillation recurrence, with a recent randomized controlled trial showing that patients with a history of atrial fibrillation who previously consumed more than 10 drinks per week and subsequently abstained from alcohol significantly reduced their risk of arrhythmia recurrence and overall burden.¹⁹

Alcohol abuse and/or heavy alcohol use, including binge drinking, have been associated with an increased risk of myocardial infarction.²⁰ The effects of habitual light to moderate alcohol consumption on the risk of atherosclerotic cardiovascular disease (CVD) are not clear. Several epidemiological studies have suggested that light to moderate alcohol consumption confers a protective effect compared to both abstinence and heavy alcohol consumption. In the Physician’s Health Study, a prospective cohort of 89,299 US men, alcohol consumption appeared to be inversely associated with CVD mortality at any level of consumption, although at the highest consumptions levels the benefit seemed to be balanced by an increased risk of non-CVD mortality.²¹ However, the conclusions regarding cardioprotective effects arise from cohort studies and observational data rather than randomized, controlled trials. These studies tend to recruit populations that are more likely to be health conscious, have stable access to care, and may therefore have confounding characteristics.²² Results from Mendelian randomization studies (“nature’s randomized trials”), suggest higher CVD risk due to alcohol consumption. In a study of a large cohort of European descent, the presence of a variant in the gene for alcohol dehydrogenase was associated with lower alcohol consumption and lower odds of both coronary heart disease and ischemic stroke.²³ Given inherent challenges in performing traditional randomized trials of alcohol consumption—such as participant recruitment and blinding, long- term adherence to assigned intervention, and ethical considerations,—the effects of light to moderate alcohol consumption on atherosclerotic CVD are likely to remain uncertain.

There is a long-established link between alcohol and hypertension.²⁴ Up to 16% of hypertension cases may be attributed to
alcohol consumption. A meta-analysis of 15 randomized controlled trials showed that alcohol reduction significantly lowered systolic and diastolic blood pressures in a dose-dependent fashion.²⁵ Notably, blood pressure does not appear to acutely rise after alcohol exposure, and has been shown to decrease for up to 8 hours after heavy evening drinking.²⁶ Rather, hypertension related to alcohol consumption develops subacutely over days to weeks.²⁷

Tobacco has been a leading cause of CVD for decades.³⁰ One large prospective study by Banks et al looked at 188,167 CVD- and cancer-free individuals aged greater than or equal to ≥45 years in Australia and examined cardiovascular effects associated with cigarette smoking.³¹ The study demonstrated that tobacco abuse increases the risk of all CVD subtypes, with current tobacco smokers having at least double the risk of developing the most significant types of CVD, including over five times the risk of developing peripheral arterial disease, and three times the risk of mortality from CVD compared to people who have never smoked.³¹

Complete smoking cessation has been shown to substantially reduce the excess risk of tobacco-related CVD, and should be reinforced in every clinical encounter. Banks et al showed that former smokers aged greater than 45 years reduced their excess smoking-related risk by 90% if they had quit by age 35 to 44 years.³¹ These findings are consistent with other studies, such as a prospective study conducted by Pirie et al who found a risk reduction of over 90% for patients who quit by the age of 40 years and 97% for those who quit by the age of 30 years.³²

Younger recreational smokers may be prone to incorrectly assuming that light smoking carries low harm. One study surveying 24,658 adolescents showed that a tenth of them thought light smoking was not harmful, and that 65% of light smokers did not associate this behavior with significant harm.³³ However, a meta-analysis of 141 cohort studies and 55 case reports that examined low cigarette consumption and the risk of CVD found that reduction in cigarette smoking did not proportionally correlate to a reduction in cardiovascular risk; even smoking only one cigarette a day still carried half the risk of smoking 20 cigarettes a day.³⁴

E-cigarette use has exponentially risen in recent years, in part due to its marketing as a healthier alternative or bridge to smoking cessation. With the growing popularity of e-cigarettes, one question more and more patients may ask is whether switching to e-cigarettes may reduce cardiovascular risk. One randomized trial found that the use of e-cigarettes resulted in a 1-year rate of abstinence from cigarettes of only 18%, though this was significantly higher than those randomized to other nicotine replacement products.³⁵

A prospective, randomized control trial by George et al with chronic smokers without known coronary artery disease who switched to e-cigarettes compared with those who continued traditional cigarettes found a significant improvement in endothelial function within one month of switching to e-cigarettes, especially for female participants, suggesting a potential in risk reduction for select patients.³⁶ While the use of e-cigarettes may be a useful harm reduction strategy among select adults who abuse cigarettes, the increasing penetration of e-cigarette use among adolescents is a public health concern, made all the more pressing by widespread reports of e-cigarette related acute lung injury in the US associated with vitamin E acetate.³

Growing evidence also suggests that e-cigarette use may confer cardiovascular risk. One study showed exposure of human-induced pluripotent stem cell-derived endothelial cells to flavored e-cigarettes exacerbated endothelial dysfunction.³⁷ Another study found that daily e-cigarette use, adjusted for smoking conventional cigarettes as well as other risk factors, was associated with increased risk of myocardial infarction.³⁸