Alcoholic Cardiomyopathy: Causes, Symptoms, and Diagnosis

Therefore, the need to establish a more effective control on ethanol consumption has been repeatedly claimed [2]. 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. The mainstay of therapy for alcoholic cardiomyopathy (AC) is to treat the underlying cause, ie, to have the patient exercise complete and perpetual abstinence from all alcohol consumption. The efficacy of abstinence has been shown in persons with early disease (eg, prior to the onset of severe myocardial fibrosis) and in individuals with more advanced disease (see Prognosis). Results from serum chemistry evaluations have not been shown to be useful for distinguishing patients with alcoholic cardiomyopathy (AC) from those with other forms of dilated cardiomyopathy (DC).

Epidemiological studies

In addition, there is a relevant role on each organ, particularly on defense and adaptive mechanisms, with a clear induction of anti-oxidant, metabolic, and anti-inflammatory protective responses as a result of ethanol aggression [18,25,26]. This multi-factorial effect is attributed to genetic factors [27] and ethnic [28] variability. The final damage is an equilibrium between the intensity of damaging effects and the possibility of defense, plasticity, regeneration, and adaptation for every specific organ [29,30,31]. Thus, alcohol-dilated cardiomyopathy (ACM) is the result of dosage and individual predisposition [32]. As noted in text the exact amount and duration of alcohol consumption that results in ACM in human beings is variable.

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  • However, this individual susceptibility mediated by polymorphisms of the angiotensin-converting enzyme gene does not appear to be specific to ACM insofar as several diseases, including some that are not of a cardiologic origin, have been related to this genetic finding[65].
  • However, nutritional factors may worsen the natural course of ACM and should be avoided [18,19].
  • In his 1972 review article, Bridgen was the first to introduce the term alcoholic cardiomyopathy [27].
  • Some investigators have suggested that drinking wine may offer more protection against CV disease because it contains polyphenols, such as resveratrol and flavonoids, which are micronutrients with antioxidant activity (Tangney and Rasmussen 2013).

In his 1906 textbook The Study of the Pulse, William MacKenzie described cases of heart failure attributed to alcohol and first used the term “alcoholic heart disease” [26]. Regarding ICD and CRT implantation, the same criteria as in DCM are used in ACM, although it is known that excessive alcohol intake is specifically linked to ventricular arrhythmia and sudden cardiac death[71]. As it is not uncommon in ACM for patients to experience a significant recovery of systolic function, it is particularly challenging in this disease to decide the most appropriate time to implant an ICD and whether it is necessary to replace a previously implanted device. Future studies in ACM should also address this topic, which has important economic consequences.

1. The Natural Course of ACM

These mechanisms contribute to the myocyte cellular changes that lead to intrinsic cell dysfunction, such as sarcoplasmic reticular dysfunction and changes in intracellular calcium handling and myocyte loss. However, modulatory influences related to drinking patterns, genetic susceptibility, nutritional factors, ethnicity, and gender also many play a role alcoholic cardiomyopathy is especially dangerous because (Piano and Phillips 2014) (figure 4). The treatment of episodes of heart failure in ACM does not differ from that performed in idiopathic-dilated CMP [52,54]. A decrease in cardiac preload with diuretics and postload with angiotensin-converting-enzyme inhibitors or beta blockage agents allows for an improvement in signs of acute heart failure [19,131].

Treatment of ACM

New Research Finds Drinking Alcohol More Dangerous to the Heart Than Previously Thought – SciTechDaily

New Research Finds Drinking Alcohol More Dangerous to the Heart Than Previously Thought.

Posted: Sun, 22 May 2022 13:26:42 GMT [source]

One is aware today that alcohol may cause an acute but transient vasodilation, which may lead to an initial fall in blood pressure probably mediated by the atrial natriuretic peptide (ANP) [46]. But also short- and long-term pressor effects mediated by the renin–aldosterone system and plasma vasopressin have been described [47, 48]. Alcoholic cardiomyopathy (ACM) is a type of heart disease that can result from chronic alcohol consumption.

In fact, both molecules are directly cardiotoxic, decreasing structural protein synthesis and heart contractility and increasing oxidative and metabolic damage, leading to autophagy [20,75]. In experimental studies, acetaldehyde directly impairs cardiac contractile function [76], disrupts cardiac excitation–contraction coupling, and promotes oxidative damage and lipid peroxidation [20]. 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]. In addition, acetaldehyde is able to interact with proteins and produce protein-adduct compounds that are highly reactive and may induce additional inflammatory and immunologic heart damage [78]. Therefore, because of its multiple actions, acetaldehyde may influence ACM pathogenesis in addition to ethanol effect itself [20,76,77]. The onset of symptoms is usually insidious, but acute decompensations are also observed, especially in patients with asymptomatic left ventricular dysfunction who develop atrial fibrillation or other tachyarrhythmia and, because of this, are unable to increase their cardiac output.

Cardiac Effects of Alcohol

Through the process of oxidative phosphorylation, the mitochondria generate ~90 percent of cellular ATP. Common findings in alcohol studies from the 1970s and early 1980s included decreases in mitochondrial indices that reflected mitochondrial state III respiration, or ADP-stimulated respiration (Pachinger et al. 1973; Segel et al. 1981; Williams and Li 1977). The latter changes in these indices could be brought about by ethanol-induced imbalances in the reducing equivalents nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide hydrogen (NADH), an important chemical pathway involved in oxidative stress. In cardiomyocyte mitochondria as well as other mitochondrial types, such imbalances could lead to further decreases in cellular respiration and oxidative phosphorylation. In ACM, it is relevant to consider the treatment of the other alcohol-induced systemic damage, such as liver cirrhosis, malnutrition, and vitamin and electrolyte disturbances [2,11,52].

alcoholic cardiomyopathy is especially dangerous because