Alcohol-Induced Cardiomyopathy: Causes, Symptoms and Treatment

Elevated systemic blood pressure may reflect excessive intake of alcohol, but not AC per se. In addition, people who receive early treatment for ACM, including medication and lifestyle modifications, have a better chance of improving their heart function and overall health. Abnormal heart sounds, murmurs, ECG abnormalities, and enlarged heart on chest x-ray may lead to the diagnosis.

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. The latest two papers to be published, unlike previous papers, reported worse outcomes for ACM patients compared to DCM patients. In the first of these studies, Fauchier et al[11] studied 50 patients with ACM and 84 patients with DCM between 1986 and 1997. Although up to 81% of ACM patients received an ACEI, none received beta-blockers and the use of spironolactone was not specified, although it was probably quite low.

Cardiovascular Research

Alcoholic cardiomyopathy is a disorder in which excessive, habitual use of alcohol weakens the heart muscle. The heart cannot pump blood efficiently, and this in turn affects the lungs, liver, brain, and other body systems. However, if alcoholic cardiomyopathy is caught early and the damage isn’t severe, the condition can be treated. It’s very important to stick with the treatment plan and to stop drinking alcohol during recovery.

For that reason, transplant programs have very strict list requirements to qualify for a transplant and abstaining from alcohol is almost always on those lists. An electrical current travels through your entire heart with every heartbeat, causing each part of the heart to squeeze in a specific sequence. Your heart’s shape is part of how that timing works, and when parts of your heart stretch, it can disrupt that timing. If it takes too long — even by tiny fractions of a second— that delay can cause your heart to beat out of sync (a problem called dyssynchrony).

How is alcoholic cardiomyopathy diagnosed?

Also, current common cardiac therapies such as ICD and CRT devices were not used because of the period when the study was conducted. After a follow-up period of 47 mo, a significantly higher survival rate was observed among patients with DCM compared to patients with ACM. In this study, the only independent predictor of cardiac death was alcohol abstinence. Alcoholic cardiomyopathy (ACM) is considered one of the main causes of left ventricular dysfunction and is the leading cause of nonischemic dilated cardiomyopathy (DCM) in developed countries.

• Further research is required to determine the definitive role of genetics on ACM pathophysiology.
• Excessive drinking can also contribute to cardiomyopathy, a disorder that affects the heart muscle.
• In contrast, chronic and excessive alcohol consumption could lead to progressive cardiac dysfunction and heart failure (HF)[3].
• Analogous to the sarcoplasmic reticulum, the mitochondria were swollen or oedema was present, with crest alterations and intra-mitochondrial inclusions suggesting degenerative processes (Figure 2).

Basic research studies have described an abundance of mechanisms that could underscore the functional and structural alterations found in ACM. Because of this, their origin could be multifactorial and linked both to the alcohol molecule and to its main metabolite, acetaldehyde. Despite these features, the structural changes do not seem to be specific, furthermore, they are not qualitatively different from those found in idiopathic DCM and they do not allow us to differentiate between the two conditions[44]. It also appears that the changes emerging in ACM patients only differ from idiopathic DCM in quantitative terms, with histological changes being more striking in idiopathic DCM than in ACM[44]. Data on the amount of alcohol consumption required to cause ACM are limited and controversial. At present ACM is considered a specific disease both by the European Society of Cardiology (ESC) and by the American Heart Association (AHA)[18,19].

ICD-10-CM Diagnosis Code I42.6

Palpitations, dizziness, and syncope are common complaints and are frequently caused by arrhythmias (eg, atrial fibrillation, flutter) and premature contractions. In the setting of acute alcohol use or intoxication, this is called holiday heart syndrome, because the incidence is increased following weekends and during holiday seasons. Echocardiography is perhaps the most useful initial diagnostic tool in the evaluation of patients with heart failure. Because of the ease and speed of the test and its noninvasive nature, it is the study of choice in the initial and follow-up evaluation of most forms of cardiomyopathy.

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Alcoholic cardiomyopathy in women compared to men

For example, a slight increase in the pre-ejection period/left ventricular ejection time ratio (PEP/LVET) was found by some authors, suggesting a sub-clinical impairment of systolic function[21,33]. Mathews and Kino found a small, but significant increase in left ventricular mass in individuals consuming at least 12 oz of whisky during 6 years and 60 g of ethanol per day, respectively[22,40]. Finally, only Urbano-Márquez et al[24] found a clear decrease in the ejection fraction, in a cohort of 52 alcoholics, which was directly proportional to the accumulated alcohol intake throughout the patients’ lives. The signs and symptoms of alcoholic cardiomyopathy (ACM) can vary depending on the severity of the condition.

• Alcohol consumption may also lead to deficiencies in magnesium, potassium, phosphorus, and thiamine, which may further exacerbate existing dysfunction.
• Studies that have assessed the prevalence of ACM among IDCM patients have found high alcohol consumption in 3.8% to 47% of DCM patients.
• Researchers have also suggested that red wine, in particular, might protect the heart, thanks to the antioxidants it contains.
• As animal lovers and pet owners, FDA employees understand that the sudden onset of a life-threatening disease in a previously healthy pet can be devastating.

In a subsequent study using electron microscopy, the authors found histological features that could be superimposed onto those found in hearts that had suffered hypoxia, anoxia or ischemia[43]. Analogous to the sarcoplasmic reticulum, the mitochondria were swollen or oedema was present, with crest alterations and intra-mitochondrial inclusions suggesting degenerative processes (Figure 2). Moreover, myofibrils showed a progressively distorted structure, resulting in a homogeneous mass. Although our hospital is the largest cardiovascular disease hospital that admits patients from all areas of China, the data described herein cannot be extrapolated to the entire ACM population. In addition, because the present study was a retrospective analysis, we did not collect precise information on medication use and alcohol abstinence in the patients with 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. Indeed, the first account of the possible harmful effects of alcohol specifically on heart muscle was reported in the latter half of the 19th century. Expressions referring to “the heart of a wine drinker in Tubingen” and particularly a “Munich beer heart” were used and known in Germany during this time[13].

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The Mayo Clinic experience and patient stories

A second set of studies that are quoted when addressing this topic are those conducted in individuals who started an alcohol withdrawal program[21-24]. In these studies, the authors estimated the amount and chronicity of alcohol intake and subsequently related the https://ecosoberhouse.com/article/alcoholics-heart-problems-cardiomyopathy/ figures to a number of echocardiographic measurements and parameters. Although all of the studies reported an increase in left ventricular mass and volume, it cannot generally be stated that they provided the alcohol consumption dosage required to cause ACM.

Alcohol in excessive quantities has a directly toxic effect on heart muscle cells. In all ACM studies, inclusion of patients is based on patients’ self-reported alcohol drinking habits, which may lead to an underestimation of the prevalence of ACM together with problematic identification of patients who abstain and those who continue drinking. Furthermore, in many of these reports, comorbid conditions, especially myocarditis and other addictions such as cocaine and nicotine, were not reported.