Alcoholic Cardiomyopathy: Causes, Symptoms, and Diagnosis

Certain microscopic features may suggest damage secondary to alcohol causing cardiomyopathy. Commonly seen cellular structural alterations include changes in the mitochondrial reticulum, cluster formation of mitochondria and disappearance of inter-mitochondrial junctions. 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 conditions44. 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 ACM44.

ACKNOWLEDGMENTS

Distilled spirits, such as vodka, whiskey, rum, or tequila, are measured as 1.5 ounces (44 ml) per drink, with a typical ABV of around 40%. It is important to note that the size and strength of different alcoholic beverages can vary, so these definitions serve as general guidelines. It is always advisable to be mindful of individual tolerance and consume alcohol responsibly 4-6. The postulated mechanism includes mitochondria damage, oxidative stress injury, apoptosis, modification of actin and myosin structure, and alteration of calcium homeostasis. Studies have shown an increase in reactive oxygen species (ROS) level in myocytes following alcohol consumption and thus causes oxidation of lipids, proteins, and DNA leading to cardiac dysfunction. These changes are related to both direct alcohol toxicity on cardiac cells and the indirect toxicity of major alcohol metabolites such as acetaldehyde.

Metabolic: Thyroid Disease–Induced Cardiomyopathy

In conclusion, our study is unique in that we identified a downtrend in admissions among patients with AC in over a 13‐year period. Half the admissions occurred for cardiovascular etiologies and in‐hospital mortality among all admissions remained fairly unchanged in the absence of a clinically relevant trend. The commonest affected age group was patients in the 45 to 59‐year age group followed by the 60 to 74‐year age group. Comorbidities such as depression are often overlooked and many of these comorbidities could be potentially modifiable risk factors to help curb subsequent cardiovascular sequelae as a result of AC. Further studies are needed to address this subset of the heart failure population and validate the results. The diagnosis of alcohol-induced cardiomyopathy in our patient relied on the absence of known causes of dilated cardiomyopathy, the identification of excessive alcohol consumption and the improvement of cardiac function after the abstention from alcohol ingestion.

Recent Activity

• The authors examined the prevalence of cardiomegaly by means of chest x-rays and related it to alcohol consumption among a consecutive series of Japanese males of working age.
• As women typically have a lower BMI than men, a similar amount of alcohol would reach a woman’s heart after consuming smaller quantities of alcohol.
• Furthermore, Fernández-Solá et al30, when analysing a population of alcoholics, found a higher prevalence of DCM in alcoholics than among the general population.
• Once the 15 articles were selected (see Appendix Table 1 for the list of included articles), we extracted and organized relevant information from them.
• From the data provided in the available ACM studies, it appears that patients who received an ACEI globally showed improved prognosis.

For many decades, ACM has been considered one of the main causes of left ventricular dysfunction in developed countries. Specifically in the United States, ACM was declared the leading cause of non-ischemic DCM7; a fact related to the high consumption of alcoholic beverages worldwide, which is particularly elevated in Western countries26 . Unfortunately, it is well known that abstinence is difficult to achieve, and it is important to stress that alternative treatments are needed, including therapies to help with alcohol withdrawal, heart failure drugs, and other promising therapeutic approaches that focus on pathogenesis. Research has shown that the mortality rate for people with ACM is higher than that of the general population, with a five-year survival rate of around 50%.10 However, studies have also shown that people who stop drinking alcohol have a significantly better prognosis than those who continue to drink. 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. Alcoholic cardiomyopathy (ACM) is a disease in which the long-term consumption of alcohol leads to heart failure.1 ACM is a type of dilated cardiomyopathy.

The literature search was limited to publications written in the English language. While the overall admissions among patients with AC decreased over time, the proportion of patients with high‐risk characteristics such as smoking, depression, and drug abuse increased. Patients aged 45 and older were largely affected and cardiovascular etiologies predominated among causes for admission. New therapeutic strategies for AC are being developed with the support of animal models.

History and Physical

Besides, newer and better targeted therapies are required to be developed which will act on pathways involved in the loss of myocytes (apoptosis and necrosis) and cardiac fibrosis. Other than abstinence, very little is known about the treatment of cocaine-induced cardiac dysfunction. Indeed, there are case reports of reversibility of cardiac function after cessation of drug use. In patients who develop cardiomyopathy, the traditional therapy for LV dysfunction is appropriate. Two decades ago, the treatment of cocaine-induced cardiovascular effects favored the use of β-blockers, especially propranolol. As the clinical use of propranolol increased, reports of accentuation of cocaine-induced hypertension and myocardial ischemia began to surface, blaming the unopposed alpha effects of the β-blockers.

International Patients

This was questioned by other authors, who pointed out that these conclusions could not be drawn, as alcohol itself also induces changes in the pre-load and after-load conditions, which influence cardiac contractility35. However, in this context, experimental in vitro studies using cardiomyocytes have shown that alcohol depresses the contractile capacity of the myocardium, regardless of the sympathetic tone and the haemodynamic conditions36. Ethyl alcohol has several detrimental effects on myocardial metabolism; nevertheless, the pathogenetic mechanisms of alcoholic cardiomyopathy remain uncertain. Furthermore, the complete clinical picture of alcoholic cardiomyopathy seen in humans has not been reproduced in experimental animals by ethanol feeding, even though various morphological and functional changes have been observed in such animals. It appears likely that the toxic effect of ethanol on myocardium is modified by other factors and that the “alcoholic” cardiomyopathy observed clinically in human patients is a multifactorial disease. More specifically, atrial fibrillation with rapid ventricular response is a cause of arrhythmia-induced cardiomyopathy,61 which can potentially worsen LVEF in AC patients, on top of the direct toxic effect of ethanol, acetaldehyde damage, or the aforementioned genetic factors.

Heartache in a Bottle: Understanding Alcoholic Cardiomyopathy

Fortunately, there are several reversible CMs that have been proven to show a return to normal cardiac function with the appropriate management. 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 alcoholic cardiomyopathy symptoms recorded. The 6 subjects who experienced a clear improvement in their ejection fraction had fully refrained from drinking.

• There is a need for basic, observational and clinical trials to improve the knowledge of disease.
• Note that the heart walls are much thicker in the heart with hypertrophic cardiomyopathy.
• Moreover, myofibrils showed a progressively distorted structure, resulting in a homogeneous mass.
• It showed a significant increase in both acute and chronic alcohol intoxication.

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.

The first study, which specifically focused on the amount of alcohol necessary to cause ACM, was conducted by Koide et al20 in 1975. The authors examined the prevalence of cardiomegaly by means of chest x-rays and related it to alcohol consumption among a consecutive series of Japanese males of working age. They found that 2 of the 6 individuals (33%) whose alcohol consumption exceeded 125 mL/d had cardiomegaly. 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. The effect measure for each outcome was conducted using the mean differences effect measure, where the outcomes were assessed in identical units across the various literature reviews used in the study. Furthermore, for this review, certainty assessment was conducted by assessing the risk of bias, imprecision, inconsistency, and indirectness of the presented evidence.