Alcoholic Cardiomyopathy: Overview, Cardiac Effects of Alcohol, Quantity of Alcohol Intake in Cardiac Disease

Other findings may include cool extremities with decreased pulses and generalized cachexia, muscle atrophy, and weakness due to chronic heart failure and/or the direct effect of chronic alcohol consumption. The onset of symptoms is usually insidious, but acute decompensations are also observed, especially in patients with asymptomatic left ventricular dysfunction who develop atrial fibrillation or other tachyarrhythmia and, because of this, are unable to increase their cardiac output. A 1- and 4-year follow-up study of 55 men with alcoholism showed that abstinence and controlled drinking of up to 60 g/day (4 drinks) resulted in comparable improvement in left ventricular (LV) ejection fraction. Ten patients who continued to drink higher amounts of alcohol all died during the follow-up period. Long-term alcohol abuse weakens and thins the heart muscle, affecting its ability to pump blood. When your heart can’t pump blood efficiently, the lack of blood flow disrupts all your body’s major functions.

It’s important to be honest with your doctor about the extent of your alcohol use, including the number and amount of drinks you have each day. This will make it easier for them to make a diagnosis and develop a treatment plan. When it can’t pump out enough blood, the heart starts to expand to hold the extra blood. Eventually, the heart muscle and blood vessels may stop functioning properly due to the damage and strain.

Clinical work-up for alcoholic cardiomyopathy

For many people, abstaining from alcohol can lead to a full recovery, especially when your case is less severe. However, for others, the effects of alcohol-induced cardiomyopathy may be life-long. Even in cases where people can undergo a heart transplant, individuals with a history of alcohol-induced cardiomyopathy are more likely to face other health problems down the road. As you reduce your alcohol intake, your provider will also treat your symptoms. This usually involves certain types of medications that treat heart rhythm problems or other symptoms of heart failure. Those who don’t fully recover are also likely to need this kind of treatment indefinitely.

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. S3 gallop sound along with apical pansystolic murmur due to mitral regurgitation is often heard. Dilated cardiomyopathy secondary to alcohol use does not have a pre-defined exposure time.


During the first half of the 20th century, the concept of beriberi heart disease (ie, thiamine deficiency) was present throughout the medical literature, and the idea that alcohol had any direct effect on the myocardium was doubted. Epidemics of heart failure in persons who had consumed beer contaminated with arsenic in the 1900s and cobalt in the 1960s also obscured the observation that alcohol could exhibit a direct toxic effect. In the 1950s, evidence began to emerge that supported the idea of a direct toxic myocardial effect of alcohol, and research during the last 35 years has been particularly productive in characterizing the disease entity of alcoholic cardiomyopathy (AC).

alcoholic cardiomyopathy

To address the high morbidity of surgical myectomy and the limitations in anatomical feasibility with alcohol septal ablation, radiofrequency ablation has emerged as a potential alternative. Additionally, alcohol septal ablation may not be feasible in cases involving small or mismatched septal perforator arteries, and inadvertent injection or extravasation of alcohol into adjacent arteries can result in an unexpectedly extensive area of infarction. Our patients tell us that the quality of their interactions, our attention to detail and the efficiency of their visits mean health care like they’ve never experienced.

Dilated cardiomyopathy

On histological examination, various degrees of fibrosis, patchy areas of endocardial fibroelastosis, intramural blood clots and focal collections of swollen cells in both the epicardium and endocardium were found. Also, there were significant size variations in the myofibrils and they showed a relative decrease in the number of striations, in addition to swelling, vacuolisation and hyalinisation. Cell nuclei were larger than normal, morphologically difficult to define and they occasionally showed hyperpigmentation.

These factors may internally drive the DCM susceptibility of anthracycline drugs and alcohol intolerance patients [64••]. Studies that have assessed the prevalence of ACM among IDCM patients have found high alcohol consumption in 3.8% to 47% of DCM patients. The lowest prevalence of ACM among DCM (3.8%) was obtained from a series of 673 patients admitted to hospital consecutively due to HF in the state of Maryland[27].


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