Dilated Cardiomyopathy: Causes, Symptoms, and Treatment

The RCI is the ratio of state III/IV respiration, and a decrease indicates an uncoupling of oxidation and phosphorylation. Detailed study design and findings related to investigations reporting changes in oxidative phosphorylation are summarized in Table 2. Askanas et al21 found a significant increase in the myocardial mass and of the pre-ejection periods in drinkers of over 12 oz of whisky (approximately 120 g of alcohol) compared to a control group of non-drinkers. However, no differences were found in these parameters between the sub-group of individuals who had been drinking for 5 to 14 years and the sub-group of individuals who had a drinking history of over 15 years. Kino et al22 found increased ventricular thickness when consumption exceeded 75 mL/d (60 g) of ethanol, and the increase was higher among those subjects who consumed over 125 mL/d (100 g), without specifying the duration of consumption. In another study on this topic, Lazarević et al23 divided a cohort of 89 asymptomatic individuals whose consumption exceeded 80 g/d (8 standard units) into 3 groups according to the duration of their alcohol abuse.

Pathological Aspects of ACM

Efforts to control alcohol addiction have just 50%–60% positive results in specific cessation programs 8,9. Although the most common cause of heart failure is coronary artery disease, ischemic cardiomyopathy is unlikely in the absence of a clear history of prior ischemic events or angina and in the absence of Q waves on the ECG strip. In most patients, exercise or pharmacologic stress testing with echocardiographic or nuclear imaging is an appropriate screening test for heart failure due to coronary artery disease. 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. Palpitations, dizziness, and syncope are common complaints and are frequently caused by arrhythmias (eg, atrial fibrillation, flutter) and premature contractions.

• Increased cardiac output due to hyperdynamic circulation, left ventricular dysfunction (systolic and diastolic), and certain electrophysiological abnormal findings are pathophysiological features of the disease.
• Importantly however, remember that much of this information can be derived or inferred from the results of noninvasive testing.

Acute and Long-term Effects of Alcohol on the Myocardium

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. They try to control myocardial remodeling to avoid the progression of myocyte hypertrophy 39,148 or fibrosis 149 and ventricle dysfunction and dilatation, as well as to increase the degree of myocyte regeneration 150. Recently, new cardiomyokines (FGF21, Metrnl) and several growth factors (myostatin, IGF-1, leptin, ghrelin, miRNA, and ROCKs inhibitors) have been described as being able to regulate cardiac plasticity and decrease cardiac damage, improving cardiac repair mechanisms 112,119. They aim to control oxidative damage, myocyte hypertrophy, interstitial fibrosis, and persistent apoptosis.

• Alcohol-induced cardiomyopathy remains a relevant health problem, for which the mainstay of treatment is alcohol abstinence.
• Pathologically, ethanol induces myocytolysis, apoptosis, and necrosis of myocytes, with repair mechanisms causing hypertrophy and interstitial fibrosis.

What Are the Signs and Symptoms of Alcoholic Cardiomyopathy?

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. This induces a variety of effects, since more than 14 different sites in the myocyte can be affected by ethanol 19,98. 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. Ethanol-induced disruption of ribosomal protein synthesis also contributes to non-contractile protein depletion 104. Several aspects of mitochondrial function, including respiratory complex activities and mitochondrial-dependent oxidative damage and apoptosis, are also induced by ethanol 26,100.

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A repeat echocardiogram revealed normal left ventricular function, with an ejection fraction of 62% by modified Simpson’s biplane method. The end-systolic dimension was 3.3 cm and the end-diastolic dimension was 4.8 cm (Figure 2). An echocardiogram performed within 24 h of admission and reviewed by two independent echocardiographers demonstrated severe global left ventricular systolic dysfunction, with an ejection fraction of 20% by modified Simpson’s biplane method. The left ventricle was not dilated, and the right ventricle had normal function. The end-systolic dimension was 4.1 cm and the end-diastolic dimension was 5.0 cm (Figure 1).

Outlook for alcoholic cardiomyopathy

While some consider that this toxin alone is able to cause such a disease18,19, others contend that it is just a trigger or an agent favouring DCM3,21,22. An arrhythmia can come and go and can cause bouts of a ‘thumping heart’ (palpitations), dizziness and other symptoms. An arrhythmia called atrial fibrillation is the most common one that develops in people with dilated cardiomyopathy.

• Commonly seen cellular structural alterations include changes in the mitochondrial reticulum, cluster formation of mitochondria and disappearance of inter-mitochondrial junctions.
• The RCI is the ratio of state III/IV respiration, and a decrease indicates an uncoupling of oxidation and phosphorylation.
• Efforts to control alcohol addiction have just 50%–60% positive results in specific cessation programs 8,9.
• The prevalance of alcoholic cardiomyopathy in addiction units is estimated around %.
• The risk of ACM significantly increases with alcohol intake exceeding 80 g per day for a minimum of five years 3.
• Regional wall motion abnormalities are not uncommon, but they are usually less prominent than those observed in persons with ischemic heart disease.
• However, some reports indicate that alcohol-dependent women develop ACM after consuming less alcohol over a shorter period than do age-matched alcohol-dependent men (Fernández-Solà et al. 1997; Urbano-Marquez et al. 1989).

Markers such as ethyl sulphate, phosphatidyl ethanol, and fatty acid ethyl esters are not routinely done. For a comprehensive overview see Table 2 with combined data from 6, 8, 24, 28. 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. Apoptosis may be induced by ethanol through mitochondrial membrane permeabilization and the release of pro-apoptotic factors (cytochrome c) from the mitochondrial inter-membrane space to the cytosol.

Since myocardium requires a high energy supply to maintain persistent sarcomere contractions, it was supposed that alcohol could exert its damaging effect on the mitochondrial energy supply system, with the disruption of oxidative control mechanisms 26,100. In fact, mitochondrial structural changes have been described in chronic alcohol consumers, with swollen megamitochondria and the distortion of inner cristae 107,108. Functionally high ethanol produces disruptions in the myocyte oxidative pattern and decreases in Complex I, II, and IV of the mitochondrial respiratory chain 100,109,110.

What is Alcoholic Cardiomyopathy

This activity describes the pathophysiology of ACM, its causes, presentation and the role of the interprofessional team in its management.ACM is characterized by increased left ventricular mass, dilatation of the left ventricle, and heart failure (both systolic and diastolic). This activity examines when this condition should be considered on differential diagnosis. This activity highlights the role of the interprofessional team in caring for patients with this condition. Long-term heavy alcohol consumption induces adverse histological, cellular, and structural changes within the myocardium. These mechanisms contribute to the myocyte cellular changes that lead to intrinsic cell dysfunction, alcohol cardiomyopathy symptoms such as sarcoplasmic reticular dysfunction and changes in intracellular calcium handling and myocyte loss.

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. Some studies have suggested that even moderation of alcohol consumption similar outcomes as compared to abstinence.