Alcoholic Cardiomyopathy: Overview, Cardiac Effects of Alcohol, Quantity of Alcohol Intake in Cardiac Disease

Efforts to control alcohol addiction have just 50%–60% positive results in specific cessation programs [8,9]. The effect measure for each outcome was conducted using the mean differences effect measure, where the outcomes were assessed in identical units across the various literature reviews used in the study. Furthermore, for this review, certainty assessment was conducted by assessing the risk of bias, imprecision, inconsistency, and indirectness of the presented evidence. Through a thematic synthesis, we identified common trends, knowledge gaps, and emerging research areas related to ACM.

Cardiac Catheterization

For a comprehensive overview see Table 2 with combined data from [6, 8, 24, 28]. Among the many ethanol and heart studies, mitochondrial dysfunction or evidence of impaired bioenergetics has been a common finding. This is exemplified by either a change in mitochondrial ultrastructure and/or depressed indices of bioenergetics and oxidative phosphorylation. This is not surprising because mitochondria are a major target for free-radical injury; however, dysfunctional mitochondria are not only less alcoholic cardiomyopathy symptoms bioenenergetically efficient, they can also generate increased amounts of ROS and are more likely to initiated apoptosis (55). 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. In particular, mitochondrial DNA is highly susceptible to oxidative stress because of the close proximity to ROS generation and lack of protective histones and DNA repair mechanisms compared to nuclear DNA (55).

Проверка по РАМА Проверка по VIN

• There’s usually no cure for cardiomyopathy, but the treatments can be effective at controlling symptoms and preventing complications.
• In these patients, only early and absolute abstinence of alcohol can reverse myocardial dysfunction [56, 57, 126] which in a historic study by McDonald and Burch was achieved with prolonged bedrest for several months without further access to alcoholic beverages.
• 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.
• In patients with dilated cardiomyopathy, if additional questions remain after a history is obtained and noninvasive testing is performed, cardiac catheterization may be used to help exclude other etiologies of heart failure.
• It took almost 60 years before further attention was paid to the complex interaction between the heart and the peripheral vasculature in various cross-sectional and prospective epidemiologic studies, which have empirically confirmed this early report.

AMOUNT OF ALCOHOL REQUIRED TO PRODUCE ACM

• Patients with alcoholic cardiomyopathy, therefore, usually present with symptoms of heart failure, i.
• These authors found a relationship between the reduction or cessation of alcohol consumption and higher survival rates without a heart transplant.
• Since ethanol has multiple cell targets with different pathological mechanisms implicated, those different strategies to directly target alcohol-induced heart damage are only partially effective and can only be used as support medication in a multidisciplinary approach [112].
• Growth factors and cardiomyokines are relevant molecules that may modify this process.
• 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].
• Acetaldehyde is produced at a lower quantity in the heart as compared to the liver, and systemic acetaldehyde does not achieve toxic heart concentrations [77].

Acute or chronic right heart failure leads to elevation of liver enzymes most likely due to liver congestion, whereas  cirrhosis due to cardiac disease is infrequent. Chronic liver disease such as cirrhosis may in turn affect the heart and the whole cardiovascular system, leading to a syndrome named cirrhotic cardiomyopathy (CCM). Thus, CCM has been introduced as an new entity separate of the cirrhosis etiology. Increased cardiac output due to hyperdynamic circulation, left ventricular dysfunction (systolic and diastolic), and certain electrophysiological abnormal findings are pathophysiological features of the disease. The underlying mechanisms might include the impaired β‑receptor and calcium signaling, altered cardiomyocyte membrane physiology, elevated sympathetic nervous tone and increased activity of vasodilatory pathways [44].

Who is At Risk of Alcoholic Cardiomyopathy?

At later stages, due to atrial fibrillation, thrombi are not uncommon in the dilated atria. Atrial fibrillation and supraventricular tachyarrhythmias are common findings in 15–20 % of patients [111], whereas ventricular tachycardias are rare [112]. On ECG, unspecific abnormalities like complete or incomplete left bundle branch block, atrioventricular conduction disturbances, alterations in the ST segment, and P wave changes can be found comparable to those in idiopathic DCM [113].

In all three ethanol groups, compared to control groups there was a significant increase in heart weight-to-body weight ratios. In terms of cardiac function and structure, significant decreases in fractional shortening and ejection fraction were found in all ethanol groups, but no other changes were found in other echocardiography-derived parameters between the alcohol and control groups. Intra-myocardial lipid accumulation, which was direct contact with the mitochondria, was found in all ethanol-fed groups and was significantly correlated with increased myocardial triglyceride content. LCFA uptake was evaluated in isolated cardiomyocytes obtained from ethanol-fed rats and was increased in a dose-dependent manner (i.e., greatest in 18% ethanol group) (33). Among the LCFA transport genes examined in all ethanol groups, increases were found in Cd36 and Scd-1 expression.

Data Availability

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 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. Jugular venous distention, peripheral edema, and hepatomegaly are evidence of elevated right heart pressures and right ventricular dysfunction.

• In these studies there was also evidence of ethanol-induced collagen and fibronectin accumulation, apoptotic cell death and ventricular remodeling, all of which were blocked with the administration of the superoxide dismutase mimetic or not present in the AT1-KO ethanol-fed group (43).
• It can also be caused by other conditions, or risk factors, but for some people the cause is unknown.

Palpitations, dizziness, and syncope are common complaints and are frequently caused by arrhythmias (eg, atrial fibrillation, flutter) and premature contractions. In the setting of acute alcohol use or intoxication, this is called holiday heart syndrome, because the incidence is increased following weekends and during holiday seasons. In patients exhibiting chronic alcohol use, other causes of dilated cardiomyopathy need workup. Investigative work up such https://ecosoberhouse.com/ as mean corpuscular volume (MCV), gamma-glutamyl-transpeptidase (GGT), elevated transaminases (AST, ALT) and elevated INR usually are seen in liver injury can be helpful as supportive evidence of alcohol use.[14][15]. 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.

Acknowledgments