Catecholamine cardiomyopathy: review and analysis of pathogenetic mechanisms.
Catecholamines given in high concentrations produce myocardial damage in several mammalian species. The histological changes are similar to those found in patients given large amounts of pressor agents and in those who develop pheochromocytomas. They include myofiber necrosis, myofibrillar degeneration, and mononuclear leukocytic infiltration. Cardiac function is significantly impaired. Endogenous release of catecholamines can also induce myocardial injury in rabbits infused with tyramine. Anatomic and functional abnormalities described in various models of catecholamine cardiomyopathy are summarized. The several major theories regarding pathogenesis are reviewed. Recent data suggesting that O2-derived free radical generation is involved are discussed.
Jiang
J P
JP
Department of Pathology, Yale University School of Medicine, New Haven, CT 06510.
Downing
S E
SE
D000493:Allopurinol / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism; D009202:Cardiomyopathies / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D002395:Catecholamines / Q000494:pharmacology*; D005227:Fatty Acids / Q000378:metabolism; D005609:Free Radicals; D010974:Platelet Aggregation; D014661:Vasoconstriction
D002395:Catecholamines; D005227:Fatty Acids; D005609:Free Radicals; D000493:Allopurinol; D002118:Calcium