The prevalence of chronic pulmonary diseases among patients with AC was approximately 30% and has remained unchanged through the years studied. This possibly reflects concomitant maladaptive coping behaviors and cocausation with depression precipitating alcohol use and vice versa.19 Rates of hypertension, however, have doubled from 30% to 60% over the studied timeframe. This requires close attention, considering the ill effect of high blood pressure on the cardiovascular system. The rate of liver disease including but not limited to cirrhosis in our cohort was between 15% and 19%.

Risk factors

Chronic alcohol consumption can cause multi-organ damage including myocardial dysfunction. There are no specific targeted histological or immunological biomarkers for alcoholic cardiomyopathy symptoms 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.

• Alcoholic cardiomyopathy (ACM) is a cardiac disease caused by chronic alcohol consumption.
• We used search terms, such as “alcoholic cardiomyopathy,” “alcohol-induced cardiomyopathy,” “alcohol-related heart disease,” “alcohol abuse and heart failure,” and “alcohol and cardiac dysfunction.” By combining these terms using Boolean operators, we aimed to enhance the search precision and coverage.
• This will make it easier for them to make a diagnosis and develop a treatment plan.
• Alcoholic cardiomyopathy is most common in men between the ages of 35 and 50, but the condition can affect women as well.
• 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.
• Although some authors contend that the initial event is the appearance of hypertrophy, the majority accept that the core event is the loss of cardiomyocytes.

Alcohol and the heart: to abstain or not to abstain?

She admitted to an eight-year history of the ingestion of more than 600 mL of vodka per day. Within the month before presentation, she had increased her alcohol intake by drinking a large glass of 70% ethanol per day. In patients exhibiting chronic alcohol use, other causes of dilated cardiomyopathy need workup. Investigative work up such as mean corpuscular volume (MCV), gamma-glutamyl-transpeptidase (GGT), elevated transaminases (AST, ALT) and elevated INR usually are seen in liver injury can be helpful as supportive evidence of alcohol use.1415. When it can’t pump out enough blood, the heart starts to expand to hold the extra blood.

Authors and Affiliations

• Some studies have suggested that even moderation of alcohol consumption similar outcomes as compared to abstinence.
• Management of PPCM includes the standard CHF regimen, but careful consideration must be made to avoid all teratogenic drugs, including angiotensin-converting enzyme inhibitors (ACE-Is) and angiotensin-receptor blockers (ARBs).
• An echocardiogram performed within 24 h of admission and reviewed by two independent echocardiographers demonstrated severe global left ventricular systolic dysfunction, with an ejection fraction of 20% by modified Simpson’s biplane method.
• ACM represents one of the leading causes of non-ischemic dilated cardiomyopathy.
• This study included not only DCM, but also all causes of left ventricular dysfunction, including hypertensive heart disease, ischemic cardiomyopathy and heart valve disease.

There is a need for basic, observational and clinical trials to improve the knowledge of disease. Alcoholic cardiomyopathy is best managed with an interprofessional approach with the involvement of primary care physician and cardiology. Other deficiencies including nutritional such as thiamine or other toxic materials ingested may lead to additional concomitant complications. To make a diagnosis, your doctor will perform a physical examination and ask you about your medical history.

• A 48-year-old woman presented to the emergency department with confusion and shortness of breath.
• Abnormal heart sounds, murmurs, ECG abnormalities, and enlarged heart on chest x-ray may lead to the diagnosis.
• Our study has several limitations due to the administrative nature of the database and reliance on accuracy of coding.
• Myocardial depression secondary to alcohol is initially reversible however prolonged sustained alcohol use leads to irreversible dysfunction.
• The addition of zinc to the diet prevented the occurrence of cardiac fibrosis but not hypertrophy.
• Fauchier et al11 found that after 47 mo of follow-up, the transplant-free survival of DCM patients was better than that of patients with ACM, but these differences were no longer significant when comparing the DCM group with the alcoholics who refrained from drinking or significantly reduced their alcohol consumption11.

Long-term prognosis in patients with alcoholic cardiomyopathy and severe heart failure after total abstinence

• Prior studies have investigated the impact of ethanol on changes in the activity and levels of oxidative enzymes.
• The guidelines typically define one drink as specific quantities for different types of alcoholic beverages.
• However, during the time that these haemodynamic changes appeared, some researchers identified a possible decrease in the ejection fraction and other parameters related to systolic function32-39.
• It is unclear whether it was the cumulative dose or the increased daily dose of alcohol that precipitated the left ventricular dysfunction.
• In a small study conducted in South Africa, it was shown to improve the LVEF by more than 100%.29 Larger trials and further studies are required to establish its efficacy, but initial data have shown promising results.

The clinical features of ACM develop when the injury is irreversible and advanced. Therefore, based on the existence or absence of congestive heart failure symptoms and signs, individuals may be classified as asymptomatic (preclinical phase) or symptomatic (clinical phase). The left ventricular end-diastolic diameters show a significant increase in such patients compared to healthy individuals in the same age and weight.

A dipyridamole stress test performed seven days after admission revealed no myocardial ischemia. The patient’s ejection fraction was calculated at 58%, and she was discharged on a diuretic, an ACE inhibitor and a beta-blocker. An echocardiogram performed within 24 h of admission and reviewed by two independent echocardiographers demonstrated severe global left ventricular systolic dysfunction, with an ejection fraction of 20% by modified Simpson’s biplane method. The left ventricle was not dilated, and the right ventricle had normal function.

Diagnosis

It has been difficult to reproduce experimentally, except for the pig, until recent studies using a liquid alcohol-containing diet in a metallothionen (MT) knockout mouse. The addition of zinc to the diet prevented the occurrence of cardiac fibrosis but not hypertrophy. 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 that may include malnutrition, cigarette smoking, systemic hypertension and additives used in production of alcoholic beverages. Apoptosis occurs mainly as a consequence of lipid peroxidation and oxidative stress in various body organs. There is a significant association between cardiovascular disorders and apoptosis.