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DOI 10.1016/0002-9149(88)90667-4

Медицинская библиотека · The American journal of cardiology · 1988

Patterns of evolution of myocyte damage after human heart transplantation detected by indium-111 monoclonal antimyosin.

Ballester-Rodés M, Carrió-Gasset I, Abadal-Berini L, Obrador-Mayol D, Bernà-Roqueta L, Caralps-Riera J M

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

The indium-111 labeled Fab fragment of antimyosin monoclonal antibody was used to study cardiac rejection and the time course of myocyte damage after transplantation. Fifty-three studies were performed in 21 patients, 17 men and 4 women, aged 19 to 54 years (mean 37 +/- 8), from 7 to 40 months after transplantation. Repeat studies were available in 8, and 10 were studied after the first year of transplantation. A heart-to-lung ratio was used for quantitation of uptake (normal 1.46 +/- 0.04). Differences between absent (1.69 +/- 0.29) and moderate (1.90 +/- 0.36) rejection were significant (p less than 0.03). Antimyosin ratio at 1 to 3 months (1.89 +/- 0.35) differed from that at greater than 12 months (1.65 +/- 0.2) (p less than 0.01). Repeat studies revealed a decrease in antimyosin ratio in 5 patients with uneventful clinical course; 2 had persistent activity after transplantation and suffered heart failure from rejection. After 1 year of transplantation uptake was within normal limits in 7 of 10 patients, and high uptake was associated with vascular rejection in 1. Because they can define evolving patterns of myocardial lesion activity, antimyosin studies could be useful both in patient management and in concentrating resources for those patients who most require them. The heart-to-lung ratio is suggested to monitor sequentially the degree of myocyte damage after transplantation.

Для цитирования: Ballester-Rodés M, Carrió-Gasset I, Abadal-Berini L, Obrador-Mayol D, Bernà-Roqueta L, Caralps-Riera J M. Patterns of evolution of myocyte damage after human heart transplantation detected by indium-111 monoclonal antimyosin.. The American journal of cardiology. 1988. DOI: 10.1016/0002-9149(88)90667-4.

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