This review will provide an updated view of this condition, including its epidemiology, pathogenesis, diagnosis, and treatment (Graphical Abstract). Certain microscopic features may suggest damage secondary to alcohol causing cardiomyopathy. Commonly seen cellular structural alterations include changes in the mitochondrial reticulum, cluster formation of mitochondria and disappearance of inter-mitochondrial junctions. The patient came to the emergency room with a decreased level of consciousness, hallucinations and convulsions after 24 h to 48 h of abstinence from alcohol.
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On physical examination, patients present with non-specific signs of congestive heart failure such as anorexia, generalized cachexia, muscular atrophy, weakness, peripheral edema, third spacing, hepatomegaly, and jugular venous distention. S3 gallop sound along with apical pansystolic murmur due to mitral regurgitation is often heard. Most common age population for Oxford House ACM is males from age with significant history of alcohol use for more than 10 years.
Acute reversible left ventricular dysfunction secondary to alcohol
- Β-adrenoceptor blockers may also be used during pregnancy, but β1–selective agents are generally preferred as they do not interfere with uterine relaxation.
- In patients exhibiting chronic alcohol use, other causes of dilated cardiomyopathy need workup.
- The ‘Quebec beer drinkers’ cardiomyopathy’ was related to cobalt supplementation to beer that was made in the past.
- However, its modern clinical report was delayed until the 19th century, where specific ACM cases were clinically described in Germany and England 1.
At ultrastructural level, dysfunction on the transition pore in the inner membrane is related to ethanol exposure 111. In addition, ethanol induces mitochondrial-dependent apoptosis pathways with Bax and caspase activation 101. 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 https://ecosoberhouse.com/ century, there was no scientific evidence on the direct and dose-dependent effect of ethanol on the heart as cause of ACM 6,38. This is a longstanding accumulated effect that usually appears when a subject has, in their lifetime, consumed more than 7 Kg of ethanol per Kg of body weight in men (equivalent to 60 drinks per month), and 5 Kg of ethanol per Kg of body weight in women (equivalent to 43 drinks per month) 19,46.
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- Before recognizing that ethanol itself is the etiological factor of ACM, different theories and hypotheses emerged 1,66.
- Notably, in patients with a history of chronic alcohol consumption complicated by significant myocardial dysfunction and chronic malnutrition, re-feeding syndrome may increase the cardiac dysfunction.
- An endomyocardial biopsy based on the Dallas classification system37 is one of the prime methods of diagnosing IC.
- These authors found a relationship between the reduction or cessation of alcohol consumption and higher survival rates without a heart transplant.
- In fact, mitochondrial structural changes have been described in chronic alcohol consumers, with swollen megamitochondria and the distortion of inner cristae 107,108.
- In addition, contractile sarcomere proteins such as Myosin, Actin, and Troponin are also affected by ethanol, causing the functional progressive depression of myocyte contractility, inducing progression to heart failure 56,104,131.
In long-term follow-up studies, a mortality rate of 10% of patients/year has been observed in the group of patients with persistent high-dose ethanol consumption 19,52. Acute can be defined as large volume acute consumption of alcohol promotes myocardial inflammation leading to increased troponin concentration in serum, tachyarrhythmias including atrial fibrillation and rarely ventricular fibrillation. Dilated cardiomyopathy secondary to alcohol use does not have a pre-defined exposure time. Daily alcohol consumption of 80 g per day or more for more than 5 years significantly increases the risk, however not all chronic alcohol users will develop Alcohol-induced cardiomyopathy. 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 alcoholic cardiomyopathy alcoholics with normal ventricular function.
Associated Data
- At present, ACM is defined as a dilated cardiomyopathy of toxic origin with low left-ventricle ejection fraction, chamber dilatation, and progression to congestive heart failure 18,52,53.
- Specifically, ethanol disturbs the ryanodine Ca2+ release, the sarcomere Ca2+sensitivity 102,103, the excitation–contraction coupling and myofibrillary structure, and protein expression, decreasing heart contraction 86.
- New strategies to improve the natural course of ACM have been proposed as promising agents in this field 112,147.
- Due to its significant toxicity, studies have avoided its direct instillation, as it produces indiscriminate cell damage even at low doses.
- In addition, ethanol has a widespread diffusion because of the potential for distribution though biological membranes, achieving targets not only in the membrane receptors and channels but also in endocellular particles and at the same nuclear compartment 29,99,100.
The percentage of effective abstinence achievement on these patients submitted to specific programs ranges from 50% to 60% 8,9. Therefore, many ACM subjects are not able to effectively control their alcohol-consumption rates. Therefore, any decrease in the previous quantity of alcohol consumption may improve, to some degree, cardiac health 51. Since ACM is related to frequent perioperative events and high postoperative morbidity 139, detection and treatment of ACM is compulsory to avoid anesthetic and surgical complications 140. Studies that have assessed the prevalence of ACM among IDCM patients have found high alcohol consumption in 3.8% to 47% of DCM patients. The lowest prevalence of ACM among DCM (3.8%) was obtained from a series of 673 patients admitted to hospital consecutively due to HF in the state of Maryland27.
