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Morphologische Befunde bei Herztransplantationen

Morphologic findings in heart transplantations

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Summary

The morphologic changes observed during the rejection of a transplanted heart take a principally similar course in experimental animals and in man. Hyperacute rejection of the transplanted heart is characterized by fibrin thrombi and aggregates of platelets which obstruct capillaries and arterioles. These changes are primarily the result of circulating antibodies. The acute rejection of a cardiac allotransplant is morphologically expressed in the myocardium by dense infiltrates consisting of mononuclear cells, monocytes or small lymphocytes, endothelial swelling, acute arteriitis, and disseminated cell necroses which can finally cause myocardial failure. The acute rejection crisis may be prevented by immunosuppressive therapy with cortisone derivatives, azathioprine, local irradiation and treatment with antilymphocytic globulin. The phase of chronic rejection is characterized by severe and usually obliterating intimal fibrosis of small and medium-size arteries as well as by interstitial fibrosis of the myocardium. Unspecific myocardial changes are ischemic and surgical-induced necroses and hemorrhages. In addition, the effects of denervation and interruption of the lymphatic vessels have to be considered. In cardiac transplants in man, severe atheromatous changes of the coronary arteries occur in the host. This severe atheromatosis of the coronary arteries is the result of immunologically induced endothelial processes and the influence of the persisting basic metabolic disease of the host as well as of long-term therapy with cortisone derivatives. Infections constitute the most serious complications of immunosuppressive therapy. Furthermore, the effects of cortisone, azathioprine and local irradiation on the myocardium are discussed.

Zusammenfassung

Die morphologischen Veränderungen bei der Abstoßung eines transplantierten Herzens verlaufen bei den verschiedenen Versuchstieren und beim Menschen prinzipiell in gleicher Weise. Bei der hyperakuten Abstoßung des Transplantates bilden sich Fibrinthromben und Thrombocytenaggregate, die die Capillaren und Arteriolen verschließen. Als Ursache kommen in erster Linie zirkulierende Antikörper in Betracht. Die akute Abstoßungsreaktion am transplantierten Herzen manifestiert sich morphologisch durch dichte Infiltration des Myokards mit mononucleären Zellen, Monocyten und kleinen Lymphocyten, Endothelzellschwellungen, eine akute Arteriitis und disseminierte Herzmuskelnekrosen, die schließlich die Insuffizienz des Herzens bedingen können. Durch eine geeignete immunsuppressive Therapie mit Cortisonderivaten, Azathioprin, lokaler Röntgenbestrahlung oder durch Behandlung mit Antilymphocytenserum kann die akute Abstoßungsreaktion unterdrückt werden. Die Phase der chronischen Abstoßung ist durch eine ausgeprägte, meist stenosierende Intimafibrose der kleinen und mittelgroßen Arterien und eine interstitielle Vernarbung des Myokards gekennzeichnet. Zu den unspezifischen Herzmuskelveränderungen gehören die ischämischen, operativ bedingten Herzmuskelnekrosen und Blutungen. Ferner sind die Einflüsse der Denervierung und der Unterbrechung der Lymphgefäße zu berücksichtigen. Bei den Herztransplantationen des Menschen wurden schwere atheromatöse Veränderungen an den Koronararterien des Empfängerherzens beobachtet. Diese schwere Atheromatose wird als Folge der immunbiologisch-induzierten Endothelprozesse und der persistierenden Grunderkrankung des Empfängers sowie der langdauernden Behandlung mit Cortisonderivaten aufgefaßt. Als Nebenreaktionen und Komplikationen der immunsuppressiven Therapie werden die Infektionen, die Wirkung von Cortison, Azathioprin und lokaler Röntgenbestrahlung auf den Herzmuskel erörtert.

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Knieriem, H.J., Meessen, H. & Schulte, H.D. Morphologische Befunde bei Herztransplantationen. Klin Wochenschr 49, 837–852 (1971). https://doi.org/10.1007/BF01513466

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