Based on these data, acute ethanol-induced injury appears to be mediated by ethanol and acetaldehyde; the latter may play a more important role. Some studies have suggested that a genetic vulnerability exists to the myocardial effects of alcohol consumption. Individuals with certain mitochondrial deoxyribonucleic acid (DNA) mutations and angiotensin-converting enzyme (ACE) genotypes (DD genotype) may be particularly susceptible to the damaging effects of alcohol. 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. It’s important to be honest with your doctor about the extent of your alcohol use, including the number and amount of drinks you have each day.
Those materials, such as contrasts or tracers, are helpful because they can reveal blood flow blockages that would be very hard to see otherwise. The muscles that control the lower chambers of your heart, the left and right ventricle, are especially prone to this kind of stretching. These chambers are important as they do the majority of the work of your heart, with the right ventricle pumping blood to your lungs and the left ventricle pumping blood to your entire body. Weakening in the muscles around the ventricles means they can’t pump as hard, which negatively affects your entire body.
This test will assess the ejection fraction (EF), a measurement that expresses how much blood the LV pumps out with each contraction. Once doctors have found this, they will look for the cause of the weakened heart. This can cause heart inflammation, leading to an atypically fast heart rhythm, such as atrial fibrillation (AF).
The review concludes by suggesting several promising avenues for future research related to alcohol use and CV disease. Long-term alcohol abuse can cause alcohol-related liver injury (acute alcoholic hepatitis, acute liver failure, hepatic steatosis, fibrosis, or cirrhosis), as well as cardiac injury. Incidence of alcoholic cardiomyopathy ranges from 1-2% of all heavy alcohol users. In the United States, excess alcohol consumption contributes to more than 10% of cases of heart failure.
Given the heart’s almost complete dependence upon aerobic metabolism maintaining mitochondrial function is critical to the well being of the heart. Although a small number relative to the more than 1000 proteins localized to the mitochondria, they are critical in the formation and stability of the five complexes that perform oxidative phosphorylation [69]. Chronic alcohol consumption produces a myriad of structural and biochemical alterations in the alcoholic cardiomyopathy heart, that are observed both intracellular and extracellular [41-44]. Those intracellular studies have centered predominantly on the contractile elements and mitochondrial dysfunction, but also calcium deregulation and the presence of cellular inclusions. For many people, abstaining from alcohol can lead to a full recovery, especially when your case is less severe. However, for others, the effects of alcohol-induced cardiomyopathy may be life-long.
This suggests a direct or indirect role for ethanol-mediated oxidative stress in the heart (Jiang et al. 2012; Tan et al. 2012). Several studies and meta-analyses have been conducted to determine the relationship between alcohol consumption and the risk of developing heart failure in healthy subjects, as well as in those with a history of MI or CHD. Studies also have examined the “safety” of alcoholic beverage consumption in subjects with heart failure.
Overall, your healthcare provider is the best source of information and answers when it comes to your recovery. 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. In addition, it provides information not only on overall heart size and function, but on valvular structure and function, wall motion and thickness, and pericardial disease. In the course of ethanol-induced cardiac damage, one of the more relevant findings is that ethanol exerts its deleterious effects on cardiac myocytes at multiples sites (membrane, receptors, mitochondria, ribosomes, sarcolemma, DNA, or cytoskeleton) [18,19,98] (Table 1). Until the second part of the 20th century, there was no scientific evidence on the direct and dose-dependent effect of ethanol on the heart as cause of ACM [6,38].
