Alcohol-induced cardiomyopathy is a condition where your heart changes shape because of long-term heavy alcohol use. The changes to your heart’s shape cause long-term damage, leading to heart failure and severe problems. Abstaining from alcohol may help some people recover, but others will need medication or even surgery.
- Post-mortem biopsies from the hearts of human alcoholics revealed that the myocardial mitochondria is enlarged and damaged [1-9].
- A study in a rat model using an alcohol dehydrogenase transgene that results in elevated levels of acetaldehyde demonstrated a change in calcium metabolism at the intracellular level and a decrease in peak shortening and shortening velocity.
- This usually involves certain types of medications that treat heart rhythm problems or other symptoms of heart failure.
Laboratory Studies
In some cases, a pacemaker or other implantable device might be necessary to treat more severe heart rhythm problems. Treatment for this condition starts with helping you reduce your alcohol intake or stop drinking entirely. That also may involve supportive care that will help prevent — or at least reduce the impact of — any alcohol withdrawal symptoms.
Patient History
Animal studies have suggested a benefit from vitamins B-1 and B-12, speculated to be due to protective effects against apoptosis and protein damage. Anyone with concerns about alcohol consumption or heart health needs to consult a doctor for further advice and guidance. The primary treatment for ACM is complete abstinence from alcohol, which may require a combination of behavioral therapy and medication. Other treatments aim to treat the symptoms of ACM and prevent any disease complications. Alcoholic cardiomyopathy affects the heart’s ability to pump oxygen-rich blood around the body.
AMOUNT OF ALCOHOL REQUIRED TO PRODUCE ACM
Studies in experimental animals have demonstrated that both acute and chronic ethanol administration impairs cardiac contractility. Alcohol (ethanol) is contained in a number of beverages consumed all over the world since ancient times. The acute ingestion of large amount of alcohol as well as chronic alcohol abuse induce toxic effects to all organs and tissues [7], particularly to central nervous system, liver and heart [8,9]. The mainstay of therapy for alcoholic cardiomyopathy (AC) is to treat the underlying cause, ie, to have the patient exercise complete and perpetual abstinence from all alcohol consumption. The efficacy of abstinence has been shown in persons with early disease (eg, prior to the onset of severe myocardial fibrosis) and in individuals with more advanced disease (see Prognosis). Prior studies have investigated the impact of ethanol on changes in the activity and levels of oxidative enzymes.
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 alcoholic cardiomyopathy alpha effects of the β-blockers. Although these reports were isolated, the routine use of propranolol and subsequently all β-blockers were considered relatively contraindicated in treating cocaine-induced cardiovascular emergencies. As a result, benzodiazepines have been the drug of choice in treating the cerebrovascular and subsequent systemic hyperadrenergic complications of cocaine, and nitroprusside or phentolamine being advocated for peripheral vasodilatory effects.
- The latest two papers to be published, unlike previous papers, reported worse outcomes for ACM patients compared to DCM patients.
- Furthermore, in many of these reports, comorbid conditions, especially myocarditis and other addictions such as cocaine and nicotine, were not reported.
- Although these reports were isolated, the routine use of propranolol and subsequently all β-blockers were considered relatively contraindicated in treating cocaine-induced cardiovascular emergencies.
- Alcohol abuse has a toxic effect on many of your organs, including the heart.
- Segmental wall motion abnormalities usually suggest myocardial injury; however, approximately 18% to 20% of patients with cocaine abuse manifest global hypokinesia.
As a result, the body’s tissues and organs may not get enough nutrients and oxygen. Furthermore, there are conflicting data among studies regarding the prognosis of the condition, with some showing overall mortality near 60% and others showing a mortality rate of only 19% (Table https://ecosoberhouse.com/ (Table11). Finally, it should be noted that McKenna and co-workers, in one of the most frequently cited papers in the ACM field, reported an incidence of 40% in 100 individuals suffering from idiopathic DCM, but in this case the consumption threshold used was only g/d[8].
Heart Failure as a Consequence of Dilated Cardiomyopathy
- Jugular venous distention, peripheral edema, and hepatomegaly are evidence of elevated right heart pressures and right ventricular dysfunction.
- By following this methodology, we aim to contribute to the existing body of knowledge on ACM, providing a reliable and up-to-date understanding of its pathogenesis, clinical features, diagnostic approaches, treatment options, and potential preventive strategies.
- A 12-month observational study of 20 patients with AC noted smaller cavity diameters, better clinical evaluation findings, and fewer hospitalizations in the 10 patients who abstained from alcohol use.
- In conditions of acute alcohol toxicity, ethanol has been shown to increase circulating catecholamine, which may play a role in myocardial damage.
- At the end of the first year, no differences were found among the non-drinkers, who improved by 13.1%, and among those who reduced consumption to g/d (with an average improvement of 12.2%).
