Alcoholic Cardiomyopathy: Causes, Symptoms, and Diagnosis

It’s not known how commonly dogs develop DCM, but the increase in reports to FDA signal a potential increase in cases of DCM in dogs not genetically predisposed. When it can’t pump out enough blood, the heart starts to expand to hold the extra blood. Eventually, the heart muscle and blood vessels may stop functioning properly due to the damage and strain. It’s important to note that alcoholic cardiomyopathy may not cause any symptoms until the disease is more advanced. 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.

• Echocardiography is perhaps the most useful initial diagnostic tool in the evaluation of patients with heart failure.
• As you reduce your alcohol intake, your provider will also treat your symptoms.
• CVCA will repeat collection of urine, blood, and feces at 1 to 2 months, and at 6 months after the initial diagnosis and document any treatment or dietary changes, if any, that were recommended by the cardiologist.
• All patients with severe ventricular dysfunction, regardless of cause, should avoid alcohol because of the risk for worsening of their heart failure.
• Alcohol-related cardiomyopathy is a type of dilated cardiomyopathy, which is when your heart’s shape changes because its muscles are stretching too much.
• In particular, prolongation of conduction times and heterogeneous increases in refractory period have been reported, especially in patients with cardiomyopathy.

This expansion causes the walls of the heart to become thinner as the heart itself becomes larger, eventually affecting the muscles’ and the vessel’s ability to function. If you are short of breath or have other symptoms of dilated cardiomyopathy, see your health care provider as soon as possible. Call 911 or your local emergency number if you have chest pain that lasts more than a few minutes or have severe difficulty breathing. Some people with dilated cardiomyopathy don’t have any signs or symptoms in the early stages of the disease. There is some evidence that moderate amounts of alcohol might help to slightly raise levels of “good” HDL cholesterol. Researchers have also suggested that red wine, in particular, might protect the heart, thanks to the antioxidants it contains.

Taurine & Amino Acids

You should also follow your doctor’s guidance and advice on any treatments you receive. If you have any questions about how to do either of these, your healthcare provider can answer them and offer you help and resources along the way. The only way to completely prevent alcohol-induced cardiomyopathy is not to drink alcohol at all.

• However, in patients admitted to the hospital, the prevalence of alcoholic cardiomyopathy was 0.08% in women and 0.19% in men.
• Ask any patient presenting with new heart failure of unclear etiology about their alcohol history, with attention to daily, maximal, and lifetime intake and the duration of that intake.
• To diagnose this condition, healthcare providers will typically use several of the following methods.
• We did not include in these numbers the many general cardiac reports submitted to the FDA that did not have a DCM diagnosis.

Auscultation can help to reveal the apical murmur of mitral regurgitation and the lower parasternal murmur of tricuspid regurgitation secondary to papillary muscle displacement and dysfunction. Third and fourth heart sounds can be heard, and they signify systolic and diastolic dysfunction. Pulmonary rales signify pulmonary congestion secondary to elevated left atrial and left ventricular end-diastolic pressures. Jugular venous distention, peripheral edema, and hepatomegaly are evidence of elevated right heart pressures and right ventricular dysfunction.

Gender Differences in Alcohol Pathology

Overall, the risks of continued alcohol consumption outweigh this small benefit of this lipid improvement. The risk of atrial and ventricular dysrhythmias and sudden cardiac death are also increased in this population already prone to these adverse events [36, 37]. Consequently, alcohol consumption should be avoided in all patients with substantial heart failure and in those whose cardiomyopathy is suspected to be primarily from alcohol regardless of severity. https://ecosoberhouse.com/article/alcoholics-heart-problems-cardiomyopathy/ accounts for about one-third of all the nonischemic, dilated cardiomyopathies [29].

Your heart’s shape is part of how that timing works, and when parts of your heart stretch, it can disrupt that timing. If it takes too long — even by tiny fractions of a second— that delay can cause your heart to beat out of sync (a problem called dyssynchrony). Similarly, alcohol can have a toxic effect on your heart and cause scar tissue to form. That scar tissue can also cause potentially life-threatening arrhythmias (irregular heart rhythms). The muscles that control the lower chambers of your heart, the left and right ventricle, are especially prone to this kind of stretching.

How does this condition affect my body?

Manhattan Cardiology is the premier facility for cardiac testing and preventive treatment in New York. Our cardiologists practice under a guiding principle that early detection is the best form of prevention. The Heart Failure Association (HFA) is a branch of the European Society of Cardiology (ESC). Its aim is to improve quality of life and longevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research. A total of 201 (27%) patients reported no alcohol usage, while 356 (48%) were low users and 187 (25%) had moderate or high intake.

To our knowledge, our study determined prognostic factors for ACM outcome in the largest cohort of ACM patients described to date. Our data show that the variables most closely predicting a poor outcome in ACM are QRS duration, SBP and NYHA classification at admission. The status of all patients was followed up by telephone interview, outpatient clinic attendance, or hospitalization during the follow-up period. Despite the key clinical importance of alcohol as a cause of DCM, little information has been published on the long-term outcome of patients with ACM in China. The aims of the present study were to define the long-term outcome of ACM, to compare the patient characteristics between the death and survival groups, and to determine prognostic markers.

How is alcoholic cardiomyopathy treated?

Alcohol-induced cardiomyopathy, especially when more severe, leads to deadly problems like heart attack, stroke or heart failure. Individuals with this condition who don’t stop drinking heavily are at the greatest risk. Between 40% to 80% of people who continue to drink heavily will not survive more than 10 years after receiving this diagnosis.

Among the ACM patients, no differences between the patients in the death and survival groups were observed at baseline with respect to age, disease duration, smoking status, presence of syncope, heart rate, gender, and blood test results. The frequencies of a high New York Heart Association (NYHA; class III/IV) classification, atrial fibrillation (AF) and atrioventricular block were higher in the death group than those in the survival group. Alcoholic cardiomyopathy can present with signs and symptoms of congestive heart failure. Symptoms include gradual onset worsening shortness of breath, orthopnea/paroxysmal nocturnal dyspnea.

This was interpreted by the authors as suggesting that acetaldehyde plays a key role in the cardiac dysfunction seen after alcohol intake. Others have suggested that an acute decrease in mitochondrial glutathione content may play a role in mitochondrial damage and implicate oxidative stress as a contributor in this process. During the first half of the 20th century, the concept of beriberi heart disease (ie, thiamine deficiency) was present throughout the medical literature, and the idea that alcohol had any direct effect on the myocardium was doubted. Epidemics of heart failure in persons who had consumed beer contaminated with arsenic in the 1900s and cobalt in the 1960s also obscured the observation that alcohol could exhibit a direct toxic effect. The postulated mechanism includes mitochondria damage, oxidative stress injury, apoptosis, modification of actin and myosin structure, and alteration of calcium homeostasis.