This study included not only DCM, but also all causes of left ventricular dysfunction, including hypertensive heart disease, ischemic cardiomyopathy and heart valve disease. Furthermore, the inclusion criteria for ACM were very strict and required a minimum consumption of 8 oz of alcohol (200 g or 20 standard units) each day for over 6 mo. In contrast, European studies focusing on the prevalence of ACM included only subjects diagnosed with DCM and applied the consumption threshold of 80 g/d for ≥ 5 years, finding an ACM prevalence of 23%-47% among idiopathic DCM patients9-12 (Figure 1). Electrocardiogram may reveal increased QRS voltage, early repolarization, ischemic or nonspecific ST-T changes, or pathologic Q waves.
- On physical examination, patients present with non-specific signs of congestive heart failure such as anorexia, generalized cachexia, muscular atrophy, weakness, peripheral edema, third spacing, hepatomegaly, and jugular venous distention.
- By following this methodology, we aim to contribute to the existing body of knowledge on ACM, providing a reliable and up-to-date understanding of its pathogenesis, clinical features, diagnostic approaches, treatment options, and potential preventive strategies.
- Two independent reviewers assessed each article for relevance and eligibility for full-text review.
- Various studies have shown that alcohol exerts a negative inotropic effect on the myocardium.
Acknowledgments
You will receive the first heart failure and transplantation email in your alcoholic cardiomyopathy symptoms inbox shortly. When seeking answers, people often look to experts for clear and accurate information. By subscribing to heart failure content from Mayo Clinic, you have taken an important first step in gaining knowledge and using it for your overall health and well-being. Treatment includes medicines and sometimes surgically implanted devices and heart surgery. In the second study, Gavazzi led a multicentre study in which, from 1986 to 1995, 79 patients with ACM and 259 patients with DCM were recruited10. Transplant-free survival after 7 years was worse among patients with ACM than among those with DCM (41% vs 53%).
- People with alcoholic cardiomyopathy often have a history of heavy, long-term drinking, usually between five and 15 years.
- Meanwhile, we excluded duplicates, case reports, letters, editorials, and reviews not specifically addressing ACM.
- In contrast, an enlarged heart was found in only 1 of 25 subjects with moderate consumption (4%), in 6 of 105 very mild consumers (5.7%), and in 4.5% of non-drinking individuals.
- Certain microscopic features may suggest damage secondary to alcohol causing cardiomyopathy.
Table 1. List of literature articles reviewed in this study.
If you have the condition, your healthcare professional might recommend that your family members be checked. Call 911 or your local emergency number if you faint, have trouble breathing or have chest pain that lasts for more than a few minutes. To date, none of the ACM studies have proposed a treatment for ACM other than that recommended for DCM in current HF guidelines. Further research is required to determine the definitive role of genetics on ACM pathophysiology. Furthermore, Fernández-Solá et al30, when analysing a population of alcoholics, found a higher prevalence of DCM in alcoholics than among the general population. Specifically, among alcoholics they found a prevalence of DCM of 0.43% in women and 0.25% in men, whereas the described prevalence of DCM in the general population is 0.03% to 0.05%18,19.
Alcoholic cardiomyopathy: incidence, clinical characteristics, and pathophysiology
Daily alcohol consumption of 80 g per day or more for more than 5 years significantly increases the risk, however not all chronic alcohol users will develop Alcohol-induced cardiomyopathy. For tens of years, the literature has documented many clinical cases or small series of patients who have undergone a full recovery of ejection fraction and a good clinical evolution after a period of complete alcoholic abstinence. Finally, it is worth stressing that a large majority of studies on the physiopathology and prognosis of ACM were conducted some years ago, prior to the development of our current understanding regarding the role of genetics in DCM67. According to recent data, a genetic form of DCM could be present in up to 50% of idiopathic DCM cases, and other specific forms of DCM such as peripartum cardiomyopathy have been shown to have a genetic basis in a significant number of cases68. It is therefore possible that patients with ACM could also harbour a genetic substrate that predisposes them to this form of cardiomyopathy.
Additionally, echocardiographic data suggest that subjects who do not fully withdraw from alcohol consumption, but who reduce it to moderate amounts recover LVEF in a similar manner to strict non-drinkers. Thus, Nicolás et al73 studied the evolution of the ejection fraction in 55 patients with ACM according to their degree of withdrawal. The population was divided into 3 groups according to their intake volume during the follow-up period. At the end of the first year, no differences were found among the non-drinkers, who improved by 13.1%, and among those who reduced consumption to g/d (with an average improvement of 12.2%).