PubMed Health⌕ Search

Biomedical subjects

Philip Hornick

Publications and source records attributed to Philip Hornick.

3 recordsLinked to original sources

Tuberculous pericardial effusion after coronary artery bypass graft.

We describe a case of a recurrent pericardial effusion after coronary artery bypass grafting. This was initially considered to be due to post-pericardiotomy syndrome, but was later treated empirically as tuberculosis. After definitive surgery for this condition, pericardial histology and immunohistochemistry confirmed the diagnosis of tubercular pericarditis. At 4-months follow-up, while continuing anti-tuberculous therapy and corticosteroids, the patient showed consistent improvement without further recurrence of his pericardial effusion. Local reactivation of tuberculosis after pericardiotomy has not been previously reported and merits careful consideration in population groups in which tuberculosis is highly endemic.

Antitubercular Agents↗

Chronic rejection in the heart.

The dramatic improvements in 1-yr survival following cardiac transplantation have not been matched by similar improvements in long-term graft survival. Long-term survival of allografted hearts is limited by a progressive fibroproliferative disease, resulting in intimal thickening and occlusion of the grafted coronary vessels. This disease, variously known as accelerated transplant coronary artery disease or cardiac graft vasculopathy, is also known as chronic rejection. The histology and clinical sequelae are briefly described. The disease can be thought of as a model for non-transplant atherosclerosis, postangioplasty restenosis, and vein graft atherosclerosis. There is compelling evidence that it is driven by alloantigen-dependent mechanisms. The evolution of the disease consists of three phases, an antibody-mediated phase, a cell-mediated phase, and a phase of tissue remodeling that is dependent on cytokines and growth factors. Experimental studies show that adoptive transfer of immunoglobulin can transfer features of intimal hyperplasia to transplanted arteries in immunodeficient recipients. Damage to donor endothelium is likely to be an important initiating factor in this disease because it exposes a thrombogenic subendothelial matrix. Whether T cells of antibody are most important in damaging the endothelium is currently the subject of much research. Although T cells are sometimes present in atherosclerotic lesions, an association with acute rejection has never been consistently shown.

Animals↗

Direct and indirect allorecognition.

The design and effectiveness of strategies to promote long-term graft acceptance requires a fundamental understanding of the mechanisms underlying acute and chronic rejection. This chapter discusses the two pathways of allorecognition--direct and indirect--and suggests that the direct pathway plays a major role in the early weeks after transplantation and that the indirect pathway may contribute to the process of chronic rejection. The results of in vitro and in vivo experimental models are discussed, together with clinical data.

Animals↗