Acute reversible left ventricular dysfunction secondary to alcohol PMC

alcoholic cardiomyopathy decreased ast

Finally, we analyzed and presented the synthesized literature, along with relevant findings and conclusions from the included studies, in a coherent manner. We identified main themes and sub-themes to provide a comprehensive overview of the current state of knowledge regarding ACM. 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. However, if alcoholic cardiomyopathy is caught early and the damage isn’t severe, the condition can be treated. It’s very important to stick with the treatment plan and to stop drinking alcohol during recovery. It’s important to note that alcoholic cardiomyopathy may not cause any symptoms until the disease is more advanced.

Enzymes and signal pathways in the pathogenesis of alcoholic cardiomyopathy

  • A case of rapid reversal of alcohol-induced cardiomyopathy with abstinence is reviewed.
  • Data suggests patients with successful quitting of alcohol have improved overall outcomes with a reduced number of inpatient admissions and improvement in diameter size on echocardiogram.
  • Also, acute alcohol administration in a rat model significantly raised plasma cardiac troponin T level after 2.5 h (11).
  • Several growth factors and cardiomyokines exert an autocrine or paracrine effect that tries to compensate for this heart damage [119,133].

Dysregulated excessive autophagy, together with other factors such as oxidative stress, neurohormonal activation, and altered fatty acid metabolism, contributes to cardiac structural and functional damage following alcoholism. This influences the maintenance of cardiac geometry and contractile function, increasing the development of ACM [121]. In ACM, protein degradation with sarcomere disarray and contractile protein loss has been suggested to be a key point of autophagy induction [18]. Different pathogenic hypotheses have been suggested, such as the pivotal role of acetaldehyde [122], the role of oxidative stress and stress signaling cascades [109], and the translocation of NFkB into the nucleus [106]. The cardiovascular system is, after the liver and gastrointestinal system, the second most affected system by global ethanol toxicity [1,33,34]. The effect of a low dose of alcohol consumption on the cardiovascular system has been also extensively evaluated with evidence of a dual effect, beneficial for coronary artery disease at low doses [44] but reversing to a damaging effect at moderate to high doses [19].

Clinical Characteristics and Prevalence

alcoholic cardiomyopathy decreased ast

Depression of LV ejection fraction (EF) is the hallmark of this period that also occurs with a reduction in LV shortening fraction, increase in LV diameter, and mass indices that may be measured by echocardiography or cardiac MR spectroscopy [40,52]. Congestive symptoms, such as the expression of right ventricular failure, with peripheral edema or anasarca, are characteristic of advanced cases of ACM [42,56]. The pathologic and histologic findings of alcoholic cardiomyopathy (AC) are essentially indistinguishable from those of other forms of dilated cardiomyopathy (DC). Findings from gross examination include an enlarged heart with 4-chamber dilatation and overall increased cardiac mass.

4. Ethanol Disruption of Transients and SR Activation

In skeletal muscle, ubiquitin E3 ligases, such as atrogin-1 and muscle RING Finger 1 (MuRF1), accelerate protein breakdown and lead to muscle atrophy (67,68). Recently, Lang and Korzick (65) reported that 20 weeks of alcohol consumption in female Fischer 344 rats increased myocardial atrogin-1 and MuRF1 expression (e.g., messenger ribonucleic acid levels). In this same study, investigators found increased markers of alcoholic cardiomyopathy autophagy, such as LC3B and autophagy-related gene 7 proteins and tumor necrosis factor α, along with a reduction in mTOR activity. Autophagy is a catabolic mechanism carried out by lysosomes and is important for the degradation of unnecessary or damaged intracellular proteins, therefore keeping the cell healthy. This mechanism is also important for cell and organism survival during stress and nutrient deprivation.

  • In this section, we briefly discuss the patterns of drinking, specifically binge, as well as genetic variants in certain proteins/enzymes and variability in nutrition or dietary nutrients that may influence the occurrence of ACM.
  • To diagnose this condition, healthcare providers will typically use several of the following methods.
  • Ethanol abstinence allows for recovery in the majority of cases, including in those with previous severe depression of LV EF [81,88,135].
  • Although anticoagulation may be of benefit to patients with profound LV dysfunction and atrial fibrillation, the risks must be weighed heavily in this patient population.

How common is this condition?

What tests will be done to diagnose this condition?

alcoholic cardiomyopathy decreased ast

  • These arrhythmias are usually related to episodes of binge drinking [43,62] and are more frequent in established ACM than in subjects with normal cardiac function [52].
  • Alternatively, studies have analysed its effect by combining ethanol with cyanamide.
  • Investigating the mechanisms, consequences, and potential treatment options for ACM remains a very important area of research.
  • A healthcare provider can also connect you with available resources and refer you to other specialists and experts who can help you reduce or stop your alcohol intake.

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