When it comes to alcohol consumption, long-term is defined as five to 15 years. Heavy drinking of alcohol is consumption that is above the recommended daily limits. For women, it means more than three drinks a day or more than seven drinks per week. Alcoholic cardiomyopathy (ACM) is a heart disease that occurs due to chronic alcohol consumption.
Alcohol addiction can impact your physical health as well as your mental well-being. One such potential risk of alcohol use disorder is alcoholic cardiomyopathy, a condition that can lead to heart failure. If you drink heavily and have unexplained fatigue or shortness of breath that worsens over time, you should schedule an appointment with a doctor right away.
What percentage of heavy drinkers develop cardiomyopathy?
Furthermore, 89% of the alcoholics with a DD genotype developed ACM, whereas only 13% of those with an II or ID genotype developed this condition. However, this individual susceptibility mediated by polymorphisms of the angiotensin-converting enzyme gene does not appear to be specific to ACM insofar as several diseases, including some that are not of a cardiologic origin, have been related to this genetic finding[65]. The suspicion that there may be an individual susceptibility to this disease is underscored by the finding that only a small group of alcoholics develop ACM, and that a proportional relationship between myocardial damage and alcohol intake has not been proven.
On physical examination, patients present with non-specific signs of congestive heart failure such as anorexia, generalized cachexia, muscular atrophy, weakness, peripheral edema, third spacing, hepatomegaly, and jugular venous distention. S3 gallop sound along with apical pansystolic murmur due to mitral regurgitation is often heard. Most common age population for ACM is males from age with significant history of alcohol use for more than 10 years. Females constitute roughly 14 % of cases of alcohol induced cardiomyopathy however lifetime exposure required for women to develop alcohol induced cardiomyopathy is less compared to men.
EFFECTS OF ALCOHOL WITHDRAWAL
Alcohol also can increase levels of co-enzymes or reducing equivalents (e.g., reduced nicotinamide adenine dinucleotide phosphate [NADPH]), which lead to increases in ROS formation and decreases in eNOS activity (Ceron et al. 2014). Several excellent reviews offer more detailed assessments of vascular cellular mechanisms (Cahill and Redmond 2012; Husain et al. 2014; Marchi et al. 2014; Toda and Ayajiki 2010). 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. However, very few studies have investigated the relationship between clinical characteristics and prognosis in ACM. Other findings may include cool extremities with decreased pulses and generalized cachexia, muscle atrophy, and weakness due to chronic heart failure and/or the direct effect of chronic alcohol consumption. Measuring blood alcohol concentration in an acute intoxication gives baseline information but does not permit deductions to chronic misuse.
These investigators also found decreases in peroxiredoxin 5, antioxidant protein 2, and glutathione transferase 5, important anti-oxidant enzymes. Proteins that were increased were signal transduction proteins such as tyrosine kinase (~2.1 fold increase) and mitogen-activated protein kinase phosphatase (~17.5 fold increase) (45). Investigators have used a variety of noninvasive tests to evaluate the acute effects of alcohol consumption on myocardial function and hemodynamics in healthy humans. As with isolated animal heart experiments, some investigators have found that acute alcohol exposure (blood alcohol levels 40 to 110 mg%) depresses myocardial systolic function in humans (Delgado et al. 1975; Lang et al. 1985; Timmis et al. 1975). For example, in one study, the ejection fraction decreased by 4 percent after alcohol consumption (Delgado et al. 1975).
The Pattern of Drinking and Other Mediating Factors
Assessing differences between various forms of alcoholic beverages it should be noted that resveratrol leads in vitro to platelet inhibition in a dose-dependent manner [100] and has shown effects on all-cause mortality in a community-based study [101]. Polyphenols of red barrique wines and flavonoids have been shown to inhibit endothelin-1 synthase [102] and PDGF-induced vasoproliferation thus also contributing to cardiovascular protection [103]. The natural history and long-term prognosis studies of Gavazzi et al[10] and Fauchier et al[11] compared the evolution of ACM patients according to their degree of withdrawal. These authors found a relationship between the reduction or cessation of alcohol consumption and higher survival rates without a heart transplant. 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. In light of the available data, new studies will help to clarify the current prognosis of ACM compared to DCM and to determine prognostic factors in ACM that might differ from known prognostic factors in DCM.
Keep in mind that with proper medications and lifestyle adjustments, which includes no alcohol, symptoms can be somewhat controlled. Most doctors encourage widespread education when it comes to alcohol consumption. The belief is that educating the public before they succumb to alcohol abuse is the best preventative measure. According to the National Institute on Alcohol Abuse and alcoholic cardiomyopathy Alcoholism (NIAAA), AUD is a brain disorder that doctors characterize by the inability to stop or control alcohol consumption. This inability occurs despite adverse effects on the person’s health, occupation, or relationships. The outlook for people with alcoholic cardiomyopathy varies depending on how long alcohol was abused and how much alcohol was consumed during that time.
This study included not only DCM, but also all causes of left ventricular dysfunction, including hypertensive heart disease, ischemic cardiomyopathy and heart valve disease. Furthermore, the inclusion criteria for ACM were very strict and required a minimum consumption of 8 oz of alcohol (200 g or 20 standard units) each day for over 6 mo. In contrast, European studies focusing on the prevalence of ACM included only subjects diagnosed with DCM and applied the consumption threshold of 80 g/d for ≥ 5 years, finding an ACM prevalence of 23%-47% among idiopathic DCM patients[9-12] (Figure (Figure11). Increased autophagy as a possible mechanism underlying the adverse myocardial effects of ethanol is intriguing.
Patients with alcoholic cardiomyopathy, therefore, usually present with symptoms of heart failure, i. Echocardiography may reveal a mild or severe depression of cardiac function and ejection fraction or even show hypertrophy in the beginning [109]. Heart failure symptoms may be due to early diastolic or to later systolic dysfunction.