Cardiomyopathy Symptoms and causes

Studies are also warranted to identify whether concomitant polysubstance use influences the risks (for instance, whether there is any interaction between cocaine use, smoking, and alcohol use disorder). Finally, pharmacoepidemiological studies (and ideally randomized clinical trials) are warranted to understand the relative benefit of conventional heart failure therapy to prevent heart failure development and progression of alcoholic cardiomyopathy in patients at risk. Until more robust evidence exists, caution is warranted before labeling patients as having alcoholic cardiomyopathy due to a risk of neglecting other contributors, such as genetic causes for disease. First, we devised a search strategy to retrieve relevant articles from PubMed.

Myocardial Storage–Related Cardiomyopathy

• In contrast, an enlarged heart was found in only 1 of 25 subjects with moderate consumption (4%), in 6 of 105 very mild consumers (5.7%), and in 4.5% of non-drinking individuals.
• Measurement of multiple viral titers in the blood is expensive and has not proven to be very useful over the years.
• The left ventricular end-diastolic diameters show a significant increase in such patients compared to healthy individuals in the same age and weight.

Although all of the studies reported an increase in left ventricular mass and volume, it cannot generally be stated that they provided the alcohol consumption dosage required to cause ACM. A study in a rat model using an alcohol dehydrogenase transgene that results in elevated levels of acetaldehyde demonstrated a change in calcium metabolism at the intracellular level and a decrease in peak shortening and shortening velocity. This was interpreted by the authors as suggesting that acetaldehyde plays a key role in the cardiac dysfunction seen after alcohol intake. Others have suggested that an acute decrease in mitochondrial glutathione content may play a role in mitochondrial damage and implicate oxidative stress as a contributor in this process. Diastolic dysfunction is the earliest sign of ACM and is usually seen in approximately 30% of patients with a history of chronic alcohol abuse with no evidence of systolic dysfunction nor left ventricle hypertrophy. In alcoholic cardiomyopathy, similar to idiopathic dilated cardiomyopathy (DCM), beta 1‑adrenergic and muscarinic receptors are reduced in the myocardium itself and reduced responsiveness of the adenyl cyclase was shown, whereas catecholamine levels in the circulation may be elevated [104].

Signs and symptoms

The common denominator is the reduced power output of the heart, because it has been compromised. A normal heart produces myocardial shortening of about 30 percent, resulting in an EF of around 60 percent. Normal coronary perfusion favors the endocardium and blood flow is about 1 ml/min/gram at rest. However, cardiac apoptosis may also develop independently of the mitochondrial pathway [115] through the extrinsic pathway, which involves cell surface death receptors [116]. In addition to inducing apoptosis, ethanol inhibits the effect of anti-apoptotic molecules such as BCL-2 [101]. Ethanol-induced myocyte apoptosis may be regulated by growth factors [117,118] and cardiomyokines [119].

• The most striking finding from observing the gene-edited mice was that nuclear envelope ruptures triggered by the lack of Lamin A/C proteins began occurring before any other signs of heart disease, and ultimately involved surprisingly high numbers of muscle cells.
• Although analytical markers of alcohol consumption, such as average erythrocyte volume and serum gamma-glutamyltranspeptidase levels, could be an aid to establish abstinence or persistence of alcohol intake in patients, the quantity of alcohol intake is dependent on the patients’ report.
• 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.
• Several pathophysiological mechanisms have been proposed at the basis of alcohol-induced damage, most of which are still object of research.

Alcoholic Cardiomyopathy and Your Health

The heart output is progressively lower in a dose-dependent relationship with the lifetime accumulated total dose of alcohol consumed [38]. Several growth factors and cardiomyokines exert an autocrine or paracrine effect that tries to compensate for this heart damage [119,133]. Antioxidant, anti-inflammatory, anti-apoptotic, and antifibrogenic mechanisms try to avoid myocyte necrosis and heart fibrosis [14,30,58]. The final result is that achieved from the equilibrium between the degree of damage and the capacity of heart repair mechanisms in each specific individual [31,56]. Myocyte apoptosis, based on assessment of TUNEL staining and caspase activity, has been demonstrated to be an active phenomenon leading to myocyte loss in diverse cardiomyopathies [113,114] and also in chronic high-dose ethanol consumption both in experimental [109] and clinical models [101].

Cardiac Catheterization