Next, we established inclusion and exclusion criteria to determine the eligibility of articles. Inclusion criteria encompassed articles that focused on ACM or the relationship between alcohol abuse and cardiac dysfunction, involved human subjects or relevant animal models, were written in the English language, and were published within the last 10 years. Meanwhile, we excluded duplicates, case reports, letters, editorials, and reviews not specifically addressing ACM.
Authors
Results from serum chemistry evaluations have not been shown to be useful for distinguishing patients with alcoholic cardiomyopathy (AC) from those with other forms of dilated cardiomyopathy (DC). Results from evaluations of mean cell volume, aspartate aminotransferase levels, alanine aminotransferase levels, lactate dehydrogenase (LDH) levels, and gamma-glutamyltransferase levels have been shown to be similar in persons with AC to those in persons with other forms of DC. However, results from tissue assays have been shown to be potentially helpful in distinguishing AC from other forms of DC. Physical examination findings in alcoholic cardiomyopathy (AC) are not unique compared with findings in dilated cardiomyopathy from other causes.
Prognosis
As a cardiologist and HCM specialist, here are my insights on how to treat the condition. Numerous studies have shown conflicting results regarding the natural history and outcomes with alcoholic cardiomyopathy (AC). This review revisits our past and deals with our current thinking on the epidemiology, pathophysiology, clinical characteristics, and treatments available for alcoholic cardiomyopathy. As pointed out before, the current accepted definition of ACM probably underestimates the number of women affected by the disease. Alcohol affects heart function and is dependent on the quantity of alcohol that the heart is exposed to.
ACKNOWLEDGMENTS
- I first talk with patients about symptoms, asking if they have any of the symptoms previously mentioned.
- With the obstructive form of HCM, the heart is too contractile, meaning it pumps extra vigorously.
- They found that high concentrations of alcohol (150 mmol to 180 mmol) administered acutely inhibited calcium binding to troponin-tropomyosin protein complexes in vitro.
- Specifically in the United States, ACM was declared the leading cause of non-ischemic DCM7; a fact related to the high consumption of alcoholic beverages worldwide, which is particularly elevated in Western countries26 .
- Moreover, ranolazine prevents ethanol-induced atrial arrhythmias both in vitro and in vivo by blocking the late sodium current, which is activated by CaMKII.112 Its effect on preventing the decrease of LVEF in AC is currently unknown.
If your heart is severely damaged, your doctor may recommend an implantable defibrillator or pacemaker to help your heart work. Most major academic medical centers have at least one person who sees many patients with HCM. The right doctor should actively review the most up-to-date HCM literature because it evolves dramatically every year. Someone who treats people with the same therapies from the 1970s is probably not going to provide optimal care.
TREATMENT
For tens of years, the literature has documented many clinical cases or small series of patients who have undergone a full recovery of ejection fraction and a good clinical evolution after a period of complete alcoholic abstinence. One of the few papers analysing genetic susceptibility in ACM was published by Fernández-Solà et al64 in 2002. He compared the prevalence of different polymorphisms of the angiotensin-converting enzyme gene in 30 ACM patients and in 27 alcoholics with normal ventricular function. 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 finding65.
Dilated Cardiomyopathy: A Genetic Journey from Past to Future
There are several factors that I consider to determine if someone is at high, alcoholic cardiomyopathy symptoms medium, or low risk for sudden death. Studies of alcohol and stroke are complicated by the various contributing factors to stroke. Heavier drinkers are apparently at a higher risk of hemorrhagic stroke, whereas moderate drinking might be neutral or even result in a reduced risk of ischemic stroke.
Furthermore, in contrast to nuclear DNA, mitochondrial DNA is susceptible to oxidative stress due to its close proximity to the formation of ROS and the limited protective mechanisms in place to safeguard DNA integrity. Post-mortem biopsies from the hearts of human alcoholics revealed that the myocardial mitochondria is enlarged and damaged 1-9. Apoptosis occurs mainly as a consequence of lipid peroxidation and oxidative stress in various body organs. There is a significant association between cardiovascular disorders and apoptosis. There is also an established link between the development of ACM and apoptosis because of myocardial cell death, which contributes to heart pathology and dysfunction.
They also have not established how long a person would need to consume alcohol before developing ACM. Some studies have suggested that even moderation of alcohol consumption similar outcomes as compared to abstinence. They commonly include fatigue, shortness of breath, and swelling of the legs and feet. These complications affect several bodily systems, including the GI, neurological, cardiovascular, and endocrine systems. Usually, if people with HCM don’t feel well enough to exercise, they become sedentary and can develop diabetes, high cholesterol, or coronary artery disease.
