The risk of ACM significantly increases with alcohol intake exceeding 80 g per day for a minimum of five years 3. According to the American Heart Association (AHA) and other US-based guidelines, alcohol intake recommendations are provided to promote responsible drinking habits and maintain overall health. The AHA suggests moderate alcohol consumption for those who choose to drink, defining moderation as up to one drink per day for women and up to two drinks per day for men.
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There are no specific targeted histological or immunological biomarkers for the diagnosis of alcohol-induced cardiomyopathy. Various pathophysiological mechanisms have been postulated in the development of cardiomyopathy however one key factor undergoing active research is the role of genetic mutation and susceptibility to develop cardiomyopathy. One interesting aspect of the present case is that although the patient had been a heavy user of alcohol for many years, there had been no previous evidence of cardiomyopathy. It was only after the recent significant increase in alcohol intake that the myocardial dysfunction became apparent.
Figure 1. Alcohol-induced dilated cardiomyopathy.
- The AHA suggests moderate alcohol consumption for those who choose to drink, defining moderation as up to one drink per day for women and up to two drinks per day for men.
- From the data provided in the available ACM studies, it appears that patients who received an ACEI globally showed improved prognosis.
- However, if alcoholic cardiomyopathy is caught early and the damage isn’t severe, the condition can be treated.
- We conducted our analysis on discharge data from the Healthcare Cost and Utilization Project‐Nationwide Inpatient Sample (HCUP‐NIS) from 2002 through 2014.
- This eventually limits the heart’s ability to pump oxygen-rich blood around the body.
It is characterized by ventricular dilation and impairment in cardiac function. ACM represents one of the leading causes of non-ischemic dilated cardiomyopathy. The major risk factor for developing ACM is chronic alcohol use; however, there is no cutoff value for the amount of alcohol consumption that would lead to the development of ACM.
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It’s important to note that alcoholic cardiomyopathy may not cause any symptoms until the disease is more advanced. In patients with alcohol-induced cardiomyopathy, the mainstay and goal of therapy is abstinence from alcohol. As with all patients with congestive heart failure, ACE inhibitors and beta-blockers should be prescribed as initial therapy. The association between alcohol-induced cardiomyopathy and myocarditis is controversial. In one six-patient study (12) focusing alcoholic cardiomyopathy symptoms on alcoholic cardiomyopathy, the surprising histological findings on endomyocardial biopsy of two patients was found to be myocarditis with lymphocytic infiltration in association with myocyte degeneration or focal necrosis. However, no other biopsy study of patients with presumed alcohol-induced cardiomyopathy has found this.
Guillo et al17 in 1997 described the evolution of 9 ACM patients who had been admitted. He divided this cohort into two groups according to the evolution of the ejection fraction during 36 mo in which no deaths were recorded. The 6 subjects who experienced a clear improvement in their ejection fraction had fully refrained from drinking. Conversely, the 3 subjects recording a less satisfactory evolution had persisted in their consumption of alcohol. It should be noted that a moderate drinker included in this latter group showed an improvement of his ejection fraction. 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.
