Alcoholic cardiomyopathy is a type of cardiomyopathy which is caused by a prolonged and heavy consumption of alcohol. It is a disease of the heart muscle in which the walls of the ventricles of the heart become thickened, leading to a decrease in the ability of the heart to pump blood. Before this medical admission, the patient had two previous admissions for acute pancreatitis due to ethanol abuse. On both occasions, she had normal cardiac enzyme levels and no evidence of cardiac dysfunction, and a chest x-ray revealed no cardiomegaly or pulmonary edema. Her most recent admission with pancreatitis had occurred four months before the present admission.
- In that study, zinc supplementation suppressed some of the ethanol-induced changes in both the metallothionein knock-out mouse model and wild-type; however, ethanol-induced mitochondrial swelling and disorganization remained in both mouse groups.
- Additionally, cardiac markers may be also elevated due to underlying myocardial injury 32, 33.
- The end-systolic dimension was 4.1 cm and the end-diastolic dimension was 5.0 cm (Figure 1).
Systolic Vs Diastolic: What Is the Difference
Patients who consume more than two drinks per day have a 1.5- to 2-fold increase in hypertension compared with persons who do not drink alcohol, and this effect is most prominent when the daily intake of alcohol exceeds five drinks. Because hypertension may directly contribute to left ventricular (LV) dysfunction, this may be a confounding comorbidity in persons who abuse alcohol, and it should be differentiated from pure forms of alcoholic cardiomyopathy. Hypertension due to alcohol may be a confounding comorbidity in that it may contribute to LV dysfunction; therefore, LV dysfunction due to hypertension must be differentiated from pure AC. The diagnosis of alcohol-induced cardiomyopathy in our patient relied on the absence of known causes of dilated cardiomyopathy, the identification of excessive alcohol consumption and the improvement of cardiac function after the abstention from alcohol ingestion. Specifically, there was no evidence of a preceding viral infection or presence of another toxin. Several case studies and clinical trials highlight the potential for reversal of alcoholic cardiomyopathy.
- Alcohol-induced cardiomyopathy treatment includes a combination of lifestyle modifications, pharmacological treatment, management of arrhythmia, and supportive care.
- Although analytical markers of alcohol consumption, such as average erythrocyte volume and serum gamma-glutamyltranspeptidase levels, could be an aid to establish abstinence or persistence of alcohol intake in patients, the quantity of alcohol intake is dependent on the patients’ report.
- We then proceeded with screening and selection based on the titles and abstracts of the initial search results.
- Interestingly, ischemic cardiomyopathy is responsible for about half of these patients.
Acetaldehyde damage
- The Scd-1 gene encodes for stearoyl-CoA desaturase 1, an enzyme that catalyzes the rate-limiting step in mono-unsaturated fatty acid synthesis.
- Long-term alcohol abuse weakens and thins the heart muscle, affecting its ability to pump blood.
- This primary CM occurs, in its typical form, when the contractile function of the mid and apical segments of the LV are depressed and there is hyperkinesis of the basal walls, producing a balloon-like appearance of the distal ventricle with systole.
- Alcohol-induced cardiomyopathy is a condition where your heart changes shape because of long-term heavy alcohol use.
- Because hypertension may directly contribute to left ventricular (LV) dysfunction, this may be a confounding comorbidity in persons who abuse alcohol, and it should be differentiated from pure forms of alcoholic cardiomyopathy.
- Interestingly, with continuous positive airway pressure (CPAP) treatment, levels of endothelin and circulating nitric oxide invariably return to normal 77.
The exact physiopathology is not completely understood but the role of cytokines and endotoxins is thought to have an important role in the myocardial depression found in this condition. Other factors that are also related are metabolic disturbances, hypoxia, coagulopathies, and oxygen deprivation https://ecosoberhouse.com/ leading to myocardial injury 26. Another theory is the high consumption of oxygen by the mitochondria creating an energy imbalance. Pro-inflammatory factors from infectious agents cause a release of cytokines and endotoxins that accelerate the oxygen consumption in a low oxygen environment eventually leading to the production of e metabolites such as free radicals and nitrogen species 27.
A Look At Alcoholic Cardiomyopathy: Causes & Treatment
Notably, the response to evidence-based therapies is variable, and reverse remodeling is not evident in all cases. However, they are partially related to the variable etiology of DCM that encompasses both non-genetic and genetic variants. They may also use diuretics to help your body remove excess fluid and reduce swelling. Although lab tests aren’t useful in diagnosing the condition, they can help check the severity of your heart condition. 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/d8. At present ACM is considered a specific disease both by the European Society of Cardiology (ESC) and by the American Heart Association (AHA)18,19.
How should I change my diet if I have this condition?
Histologically, light microscopy reveals interstitial fibrosis (a finding that has been shown to be prevented by zinc supplementation in the mouse model), myocyte necrosis with hypertrophy of other myocytes, and evidence of inflammation. Electron microscopy reveals mitochondrial enlargement and disorganization, dilatation of the sarcoplasmic reticulum, fat and glycogen deposition, and dilatation of the intercalating discs. Cardiac percussion and palpation reveal evidence of an enlarged heart with a laterally displaced and diffuse point of maximal impulse. Auscultation can help to reveal the alcoholic cardiomyopathy 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.
Medical History Assessment
- These include damaging factors such as acetaldehyde or ROS, cardiac fibrosis, or apoptosis.
- Patients with CKD usually continue to have abnormal myocardial remodeling despite improvements made to dialysis and advancements in the treatment of CKD, hypertension, hypervolemia, anemia.
- In another study on this topic, Lazarević et al23 divided a cohort of 89 asymptomatic individuals whose consumption exceeded 80 g/d (8 standard units) into 3 groups according to the duration of their alcohol abuse.
From the data provided in the available ACM studies, it appears alcoholism symptoms that patients who received an ACEI globally showed improved prognosis. In contrast, beta-blockers, similar to aldosterone inhibitors, however beneficial they may be, have thus far not yielded sufficient data on their efficacy in relation to this disease. The first paper to assess the natural history and long-term prognosis of ACM was published by McDonald et al69 in 1971. He recruited 48 patients admitted to hospital with cardiomegaly without a clear aetiology and severe alcoholism.