Markers for chronic alcohol consumption rely on liver enzymes such as gamma-glutamyltransferase (GGT) [119], glutamic oxalacetic transaminase (GOT), and glutamic pyruvic transaminase (GPT). Elevations of the transaminases (GOT, GPT), especially a ratio of GOT/GPT higher than 2 might be indicative of alcoholic liver disease instead of liver disease from other etiologies [120, 121]. An excellent marker is carbohydrate deficient transferrin (CDT), which best detects chronic alcohol consumption alone [122, 123] or in combination with the other markers such as GGT [8, 124]. Markers such as ethyl sulphate, phosphatidyl ethanol, and fatty acid ethyl esters are not routinely done.
6. The Effect of Low-dose Ethanol on ACM
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. Previous studies were conducted on rats that are fed alcohol for about eight months. They found that there is about 14% loss of myocardial cells in the left ventricle of those rats. It showed a significant increase in both acute and chronic alcohol intoxication. All previous mechanisms can induce myocyte apoptosis through the induction of mitochondrial damage and oxidative stress [12]. Since ethanol consumption of the global population is not currently under control [2], the incidence of alcoholic cardiomyopathy is expected to be maintained in the future, especially in specific population groups, such as adolescents and young people [3].
- It should be noted that a moderate drinker included in this latter group showed an improvement of his ejection fraction.
- Clinical overview, pathogenesis, treatment and prognosis of alcoholic cardiomyopathy.
- At ultrastructural level, dysfunction on the transition pore in the inner membrane is related to ethanol exposure [111].
- The RCI is the ratio of state III/IV respiration, and a decrease indicates an uncoupling of oxidation and phosphorylation.
Mitochondrial Bioenergetics/Stress
Prognosis in individuals with low or moderate consumption up to one or two drinks per day in men and one drink in women is not different from people who do not drink at all. In CAD, diabetes, and stroke prevention the J‑type mortality curves even indicate some benefit apart from the social ”well-being“. In patients with chronic alcohol use disorders and severe heart failure prognosis is poor, since continued alcohol abuse results in refractory congestive heart failure. Death might also be sudden due to arrhythmias, heart conduction block, and systemic or pulmonary embolism.
- Because the cardiac myocyte relative to other cell types, including the hepatocyte, contains the highest volume of mitochondria, the critical mass of mitochondria negatively impacted by ethanol before significant mitochondrial dysfunction occurs may be higher than other tissues.
- Mortality in ACM is related to the progression of heart failure and malignant arrhythmias [58,65].
- For instance, healthcare professionals can carry out a stress test or heart catheterization to rule out coronary artery disease (CAD), which is another cause of cardiomyopathy.
- It’s important that people with or at risk of ACM discuss this in detail with their heart specialist (cardiologist).
- As the pathogenesis of AC is complex, specific treatments focus on different targets.
4. Ethanol Disruption of Transients and SR Activation
Therefore, complete abstinence from ethanol is the most useful measure to control the natural course of ACM [51,56,135]. In fact, patients with ACM who abstain from alcohol have a better long-term prognosis than subjects with idiopathic dilated CMP [54]. Out of end-stage cases, the majority of subjects affected https://ecosoberhouse.com/ by ACM who achieve complete ethanol abstinence functionally improve [33,82,135]. 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.
Dietary Factors
The most important unresolved question, however, relates to the primary injury/mechanism by which ethanol stimulates or initiates this array of adverse changes within the myocardium. Several inter-related mechanisms may include oxidative stress, apoptotic cell death, impaired mitochondrial bioenergetics/stress, alcoholic cardiomyopathy symptoms derangements in fatty acid metabolism and transport, and accelerated protein catabolism. In this review, we discuss these mechanisms, as well as the potential importance of drinking patterns, genetic susceptibility, nutritional factors, ethnicity, and sex in the development of ACM.
Treatment of ACM
Enlarged heart, in heart failure
- The findings were analysed taking into account the amount and chronicity of intake and they were compared with the same parameters measured in a control group of non-drinkers.
- Therefore, the need to establish a more effective control on ethanol consumption has been repeatedly claimed [2].
- In the ESC consensus document on the classification of cardiomyopathies, ACM is classified among the acquired forms of DCM[19].
- As reviewed below, it is possible that mitochondria serve as a site for ethanol-induced ROS generation, but also may be a target of ethanol-induced ROS injury.