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Alcoholic Cardiomyopathy: Causes, Symptoms, and Diagnosis

2021年02月26日

Apoptosis occurs mainly as a consequence of lipid peroxidation and oxidative stress in various body organs. There is also an established link between the development of ACM and apoptosis because of myocardial cell death, which contributes to heart pathology and dysfunction. They found that there is about 14% loss of myocardial cells in the left ventricle of those rats. All previous mechanisms can induce myocyte apoptosis through the induction of mitochondrial damage and oxidative stress 12. Since ethanol consumption of the global population is not currently under control 2, the incidence of alcoholic cardiomyopathy is expected to be maintained in the future, especially in specific population groups, such as adolescents and young people 3.

Echocardiographic and haemodynamic studies in alcoholics

Also, low to moderate daily alcohol intake was proved to be a predictor of better prognosis for both ischemic cardiomyopathy and heart failure regardless of the presence of coronary disease1,2. Unfortunately Lazarević et al23, as in most of these studies, systematically excluded patients with a history of heart disease or with HF symptoms. It is therefore possible that most of these studies may have also consistently omitted most alcohol abusers in whom alcohol had already caused significant ventricular dysfunction. A diverse variety of arrhythmias appear early and may worsen the course of ACM, atrial fibrillation being the most frequent 60 and ventricular tachycardia the most deleterious 61. These arrhythmias are usually related to episodes of binge drinking 43,62 and are more frequent in established ACM than in subjects with normal cardiac function 52. In chronic alcoholics, arrhythmia may frequently appear in relation to episodes of ethanol abstinence because of the increased release of catecholamines and electrolyte deficiencies 19.

2. Is ethanol the Real Cause of ACM

Alcoholic cardiomyopathy can present with signs and symptoms of congestive heart failure. Symptoms include gradual onset worsening shortness of breath, orthopnea/paroxysmal nocturnal dyspnea. Palpitations and syncopal episodes can occur due to tachyarrhythmias seen in alcoholic 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 alcoholic cardiomyopathy symptoms 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.

• Dilated cardiomyopathy secondary to alcohol use does not have a pre-defined exposure time.
• Prior studies have investigated the impact of ethanol on changes in the activity and levels of oxidative enzymes.
• A second set of studies that are quoted when addressing this topic are those conducted in individuals who started an alcohol withdrawal program21-24.
• For many decades, ACM has been considered one of the main causes of left ventricular dysfunction in developed countries.
• On both occasions, she had normal cardiac enzyme levels and no evidence of cardiac dysfunction, and a chest x-ray revealed no cardiomegaly or pulmonary edema.

Alcohol consumption and risk of cardiovascular disease among hypertensive women

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. The authors highlighted the presence of an extensive intracellular accumulation of neutral lipids, principally in the form of small cytoplasmic droplets. 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 ischemia43.

Patient History

Finally, it is worth stressing that a large majority of studies on the physiopathology and prognosis of ACM were conducted some years ago, prior to the development of our current understanding regarding the role of genetics in DCM67. According to recent data, a genetic form of DCM could be present in up to 50% of idiopathic DCM cases, and other specific forms of DCM such as peripartum cardiomyopathy have been shown to have a genetic basis in a significant number of cases68. It is therefore possible that patients with ACM could also harbour a genetic substrate that predisposes them to this form of cardiomyopathy. One of the few papers analysing genetic susceptibility in ACM was published by Fernández-Solà et al64 in 2002. He compared the prevalence of different polymorphisms of the angiotensin-converting enzyme gene in 30 ACM patients and in 27 alcoholics with normal ventricular function.

Alcohol and the heart

Finally, it should be noted that a large majority of studies on the long-term prognosis of ACM used the cut-off point of 80 g/d for a minimum of 5 years to consider alcohol as the cause of DCM. In this review, we evaluate the available evidence linking alcohol consumption with HF and DCM. Before recognizing that ethanol itself is the etiological factor of ACM, different theories and hypotheses emerged 1,66.

• Goal-directed heart failure therapy, as utilized in idiopathic DCM with low ejection fraction, should be a part of pharmaceutical therapy.
• This causes a decrease in sarcolemmal contraction and also disturbance in other intercellular organelles dependent of i.c.
• In the ESC consensus document on the classification of cardiomyopathies, ACM is classified among the acquired forms of DCM19.
• Our study has several limitations due to the administrative nature of the database and reliance on accuracy of coding.

From the data provided in the available ACM studies, it appears that patients who received an ACEI globally showed improved prognosis. In contrast, beta-blockers, similar to aldosterone inhibitors, however beneficial they may be, have thus far not yielded sufficient data on their efficacy in relation to this disease. Basic research studies have described an abundance of mechanisms that could underscore the functional and structural alterations found in ACM.