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%). Conversely, those whose consumption remained in excess of 80 g/d showed an average decline of 3.8% in their ejection fraction. In spite of the high prevalence of excessive alcohol consumption and of its consideration as one of the main causes of DCM, only a small number of studies have analysed the long-term natural history of ACM.
Heart health support awaits
The process by which alcohol leads to an enlarged heart involves multiple mechanisms, each contributing to the deterioration of cardiac structure and function. This means that it has a toxic effect on heart muscle cells, damaging them at a cellular level. Over time, this damage accumulates and impairs the ability of the heart to contract and relax properly.
- Not all treatments or services described are covered benefits for Kaiser Permanente members or offered as services by Kaiser Permanente.
- Alcoholic cardiomyopathy is a type of heart disease caused by excessive alcohol consumption.
- The process by which alcohol leads to an enlarged heart involves multiple mechanisms, each contributing to the deterioration of cardiac structure and function.
- Data suggests patients with successful quitting of alcohol have improved overall outcomes with a reduced number of inpatient admissions and improvement in diameter size on echocardiogram.
Ways to stay healthy
In most patients, exercise or pharmacologic stress testing with echocardiographic or nuclear imaging is an appropriate screening test for heart failure due to coronary artery disease. The natural history of patients with AC depends greatly on each patient’s ability to cease alcohol consumption completely. 11 Multiple case reports and small retrospective and prospective studies have clearly documented marked improvement in or, in some patients, normalization of cardiac function with abstinence. The following reports and studies provide impressive data on the utility of abstinence and the confirmation of alcohol consumption as a cause of DC. Continued heavy alcohol use, on the other hand, will continue to make alcoholic cardiomyopathy worse.
Laboratory Studies
The natural history and long-term prognosis studies of Gavazzi et al10 and Fauchier et al11 compared the evolution of ACM patients according to their degree of withdrawal. These authors found a relationship between the reduction or cessation of alcohol consumption and higher survival rates without a heart transplant. Considering all the works conducted to date, it is clear that new studies on the natural history of ACM are needed, including patients treated with contemporary heart failure therapies. In light of the available data, new studies will help to clarify the current prognosis of ACM compared to DCM and to determine prognostic factors in ACM that might differ from known prognostic factors in DCM. One of the few papers analysing genetic susceptibility in ACM was published by Fernández-Solà et al64 in 2002.
This leads to reduced ejection fraction, a term that refers to the percentage of blood the left ventricle pumps out with each contraction. A healthy ejection fraction ranges from 55% to 70%, but in alcoholic cardiomyopathy, it may fall well below this, resulting in fatigue, shortness of breath, and fluid retention. Daily consumption of low to moderate amounts of alcohol has beneficial effects on cardiovascular Oxford House health among both ischemic and non-ischemic patients1-3. In contrast, chronic and excessive alcohol consumption could lead to progressive cardiac dysfunction and heart failure (HF)3. While alcoholic cardiomyopathy is a subtype of dilated cardiomyopathy, it has unique characteristics rooted in toxic exposure. Unlike hypertensive heart failure or ischemic cardiomyopathy caused by blocked arteries, alcoholic cardiomyopathy stems from the direct cellular toxicity of ethanol and its metabolites.
It is estimated, approximately 21-36% of all non-ischemic cardiomyopathies are attributed to alcohol. The prevalance of alcoholic cardiomyopathy in addiction units is estimated around %. Overall data with regards to alcohol induced cardiomyopathy is insuffienct and does not alcoholic cardiomyopathy is especially dangerous because illustrate significant available data.