A catecholamine-induced dilated cardiomyopathy is reported in a patient with multiple endocrine neoplasia, type 3. A histologic and ultrastructural study has been undertaken in cardiac biopsy samples, together with determination of myocardial Ca++ and cellular membrane fatty acids. Contraction band necrosis of cardiocytes with supercontraction of sarcomeres progressing to myofibrolysis and increased levels of myocardial Ca++ have been found as morphologic and biochemical abnormalities, respectively. No lipoperoxidation of cellular membranes or an alpha-adrenergic mediated reduction of coronary supply could be recognized in the study. We indicate a receptor-mediated intracellular Ca++ overload as the main abnormality responsible for myocardial impairment.
CATECHOLAMINE-INDUCED CARDIOMYOPATHY IN MULTIPLE ENDOCRINE NEOPLASIA - A HISTOLOGIC, ULTRASTRUCTURAL, AND BIOCHEMICAL-STUDY / Frustaci, Andrea; F., Loperfido; N., Gentiloni; M., Caldarulo; E., Morgante; Russo, Matteo Antonio. - In: CHEST. - ISSN 0012-3692. - 99:2(1991), pp. 382-385. [10.1378/chest.99.2.382]
CATECHOLAMINE-INDUCED CARDIOMYOPATHY IN MULTIPLE ENDOCRINE NEOPLASIA - A HISTOLOGIC, ULTRASTRUCTURAL, AND BIOCHEMICAL-STUDY
FRUSTACI, ANDREA;RUSSO, Matteo Antonio
1991
Abstract
A catecholamine-induced dilated cardiomyopathy is reported in a patient with multiple endocrine neoplasia, type 3. A histologic and ultrastructural study has been undertaken in cardiac biopsy samples, together with determination of myocardial Ca++ and cellular membrane fatty acids. Contraction band necrosis of cardiocytes with supercontraction of sarcomeres progressing to myofibrolysis and increased levels of myocardial Ca++ have been found as morphologic and biochemical abnormalities, respectively. No lipoperoxidation of cellular membranes or an alpha-adrenergic mediated reduction of coronary supply could be recognized in the study. We indicate a receptor-mediated intracellular Ca++ overload as the main abnormality responsible for myocardial impairment.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
