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[Congenital alcoholic cardiomyopathy in 3 children]
Insights
Congenital alcoholic cardiomyopathy in infants results from maternal heavy alcohol consumption during pregnancy. Histological analysis revealed unique toxic and hypotrophic changes in heart muscle cells, differing from adult alcoholic cardiomyopathy.
Area of Science:
- Cardiology
- Pediatrics
- Toxicology
Background:
- Alcoholic cardiomyopathy is a known condition in adults resulting from chronic alcohol abuse.
- Congenital heart defects can arise from various prenatal exposures.
- The effects of heavy maternal alcohol consumption on fetal cardiac development are not fully understood.
Observation:
- Three infants born to mothers with heavy alcohol consumption presented with congenital heart defects.
- These infants were diagnosed with ventricular septal defect and Tetralogy of Fallot, requiring surgical intervention.
- Left-ventricular myocardial biopsies were obtained during open-heart surgery.
Findings:
- Histological and electronmicroscopic examination of myocardial biopsies revealed primary toxic and hypotrophic changes.
- Observed cellular alterations included reduced diameters of cells, nuclei, and myofibrils.
- Mitochondrial damage, myofibril disarray with contraction bands, sarcoplasmic reticulum dilation, and cell surface invagination into interstitial tissue were noted.
Implications:
- These findings suggest that alcohol exposure during pregnancy can cause distinct forms of cardiomyopathy and cardiac defects in children.
- The observed changes indicate inhibited embryofetal cell growth and direct cytotoxic damage by alcohol.
- Alcoholic cardiomyopathy in children appears to be associated with extreme maternal alcohol abuse, with an unknown long-term prognosis.
Abstract:
Three cases of congenital alcoholic cardiomyopathy and cardiac defects in children are described. The mothers were heavy spirits drinkers. One child had a ventricular septal defect, two had Fallot's tetralogy, all requiring operation. At open-heart surgery left-ventricular myocardial biopsies were obtained in all three children. Histological and electronmicroscopic examination revealed primary toxic and hypotrophic changes, which differed from those seen in alcoholic cardiomyopathy of the adult. The cells, their nuclei and the myofibrils had reduced diameters. The mitochondria were damaged to differing extent. The myofibrils were arranged in parallel and some had contraction bands and ruptures. The sarcoplasmic reticulum was dilated and had vacuoles. The cell surface penetrated into the interstitial tissue. All these changes could have resulted from inhibited embryofetal cell growth and cytotoxic damage by alcohol during pregnancy. It would seem that alcoholic cardiomyopathy occurs only in extreme forms of alcohol abuse during pregnancy. The prognosis is as yet unknown.