Cardiac pathology in chronic alcoholics

Abstract

Alcohol produces subclinical changes in the myocardium, with an increased iron content, which may be the forerunner for subsequent clinical cardiac dysfunction.

Cardiovascular risks and benefits of moderate and heavy alcohol consumption

“…Subendocardial and interstitial fibrosis is apparent in advanced cases ( Figure 3). 44,58,70 At an ultrastructural level, alcohol induces formation of myocardial cytoplasmic lipid droplets and glycogen deposits, swollen mitochondria and myofibrils with a progressively distorted structure, and disruption of Z lines. 77,79 Myocyte apoptosis is the main mechanism of alcohol-induced myocyte loss, and DNA fragmentation is evident in 1-2% of fibres, as determined by terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assays.…”

“…Repair mechanisms involving hypertrophy and a degree of myocyte regeneration can, to some extent, counteract the generation of lesions. 44 Eventually, irreversible structural damage develops, 15,44 with cell death by apoptosis. 45 The balance between mechanisms that either generate or repair lesions defines the degree and reversibility of the cardiac damage inflicted.…”

Myocardial structural and functional changes in patients with liver cirrhosis awaiting liver transplantation: a comprehensive cardiovascular magnetic resonance and echocardiographic study

“…Data regarding myocardial histopathological changes in cirrhosis are limited [37]. Most of earlier investigations were conducted in an autopsy setting of alcoholic etiology, and thus whether the findings are attributable to alcoholic cardiomyopathy and whether similar findings could be anticipated in an in vivo setting remain to be established.…”

Quercetin Attenuates Ethanol‐Induced Iron Uptake and Myocardial Injury by Regulating the Angiotensin II‐L‐Type Calcium Channel

“…[29,30] In the present study, excessive ethanol feeding or incubation resulted in iron accumulation and an LIP increase in the heart or cardiomyocytes concomitant with evident oxidative injury, which was in line with an autopsy-based prospective study that found that al-cohol produces subclinical changes in the myocardium with increased iron content. [8] Crucially, this type of injury was further aggravated by iron incubation, but was effectively attenuated by an iron chelator (DFO) or quercetin, suggesting that ethanolinduced iron deposition and uncontrolled LIP in cardiac tissue play important roles in the development and progression of alcoholic cardiomyopathy.…”

“…Nevertheless, both the liver and heart are susceptible to systematic iron overload. An autopsy‐based study revealed that alcohol produces subclinical changes in the myocardium, as well as increased iron content, suggesting that iron deposition may play a crucially pathological role in alcoholic myocardial injury by increasing the labile iron pool (LIP) and catalytic activity of the Fenton‐Haber ‐Weiss reaction . An understanding of the precise mechanisms by which ethanol induces iron overload and subsequently aggravated oxidative stress in cardiomyocytes, may therefore shed new light on the treatment and prevention of alcoholic cardiomyopathy.…”