Understanding the pathogenesis and the pathology of hyperacute cardiac rejection

Abstract

The terminology of hyperacute rejection (HAR) has become outmoded and confusing due both to advances that have been made in delaying its onset and due to a proliferation of synonyms for the same pathologic process. Until such time as antibody-mediated xenograft rejection can be classified by the type of causative antibody, it is recommended that the term hyperacute rejection be applied to antibody-mediated rejection with classical HAR occurring within 24 h. Delayed HAR is the same pathologic process encountered after 24 h. Recognition of the key role that venous thrombosis plays in the pathogenesis of HAR allows the microscopist to intelligently interpret biopsies from various portions of a transplanted organ according to the pathologic effects of the obstructed venous drainage of the organ. Particularly in the heart, HAR often shows different pathologic features in the inner compared to the outer myocardium. Once xenografting becomes feasible, it will be possible to apply a grading system of HAR in clinical practice.