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J Thorac Cardiovasc Surg 2001;121:400-401
© 2001 The American Association for Thoracic Surgery

Letters to the Editor

Why complement attacks cardiomyocytes in hyperacute heart rejection

Jiri T. Beranek, MD

4101 South Wappel Dr Columbia, MO 65203

To the Editor:

Being interested in cardiac hyperacute rejection (HAR),Go 1 I read with attention the article by Chen and associatesGo 2 about heart HAR in a pig-to-baboon model. The authors have overlooked large myocardial defects containing isolated damaged cardiomyocytes, remains of endomysial tubes, and "naked" cardiomyocyte nuclei in their Fig 2, A and B. In their previous article, also concerning cardiac HAR,Go 3 similar defects are present in Fig 1, C and D. In essence, their data have confirmed the recent conclusion that myocardial defects are formed in HAR.Go Go 1,4 In addition, it has been proposed that such defects are created by widespread cardiomyocyte apoptosis induced by complement.Go Go 1,4

According to conventional view, heart HAR starts with a reaction of primate natural antibodies with galactose {alpha}-1,3-galactose ({alpha}-Gal) epitopes located on porcine vascular endothelial cells. Newly formed antigen-antibody complexes fix complement and trigger the classical complement pathway. Resulting membrane attack complexes (MACs) damage vascular walls. The damaged vessels undergo thrombosis and lead to ischemic death and rejection.

A major drawback of the conventional view is that it does not explain myocardial defects that may develop in minutes in HAR.Go Go 1,4 In contrast, the hypothesis incorporating cardiomyocyte apoptosis elucidates their appearance reasonably well. When the reaction between host natural antibodies and porcine {alpha}-Gal epitopes takes place, newly formed MACs damage vascular walls and increase their permeability. This allows plasmatic proteins, including immunoglobulin M and MACs, to penetrate the extravascular space. Here, MACs react with any unprotected cell membranes, including those of cardiomyocytes without {alpha}-Gal epitopes. They will form channels in their sarcolemmas and induce their apoptosis.Go 5

The data of Chen and associatesGo 2 agree with this hypothesis. In their Fig 2, A,Go 2 immunoglobulin M is deposited not only on vascular endothelium but also on the surface of cardiomyocytes and on the remains of endomysial tubes present in myocardial defects. In Fig 2, B,Go 2 MACs are located not only on microvasculature but also on numerous cardiomyocytes manifesting gray color.

12/8/111202

doi:10.1067/mtc.2001.111202

References

  1. Beranek JT. Myocardial defects in hyperacute cardiac rejection: evidence of cardiomyocyte apoptosis. Transplantation 2000;70:697-8.[Medline]
  2. Chen RH, Kadner A, Mitchell RN, Adams DH. Fresh porcine cardiac valves are not rejected in primates. J Thorac Cardiovasc Surg 2000;119:1216-20.[Abstract/Free Full Text]
  3. Chen RH, Kadner A, Mitchell RN, Adams DH. Mechanism of delayed rejection in transgenic pig-to-primate cardiac xenotransplantation. J Surg Res 2000;90:119-25.[Medline]
  4. Beranek JT. Cardiac hyperacute rejection: a new look at an old problem. J Heart Lung Transplant 2000;19:716-7.[Medline]
  5. Beranek JT. Eosinophilic droplet formation, a morphologic manifestation of cardiomyocyte apoptosis, is present in the humoral (microvascular) rejection of human cardiac allografts. Transplantation 1998;66:404-5.[Medline]




This Article
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