Local events in graft rejection.

It appears that allograft rejections can be considered as a series of cellular and molecular cascades of inflammation triggered by the immune response. In acute rejection, inflammatory changes with a prominent blast cell component dominate. The main result is toxic damage of several parenchymal components, particularly the microvascular endothelium, resulting in necrosis of the parenchyma and loss of the allograft within days after transplantation. In the chronic type of rejection, inflammation also exists, but the major manifestations are different. Adventitial inflammation and perivascular cuffing of leukocytes result in concentric intimal proliferation and atherosclerosis. Very little experimental data exist, at present, on the mechanisms of transplant atherosclerosis and chronic rejection.

Late results and prognosis after carotid artery surgery.

Carotid reconstruction was performed on 75 patients (84 operations) mainly because of transient ischemic attacks (TIA) and/or amaurosis fugax (67%) or TIA with incomplete recovery (20%). The operative mortality was 2.4%. The incidence of permanent postoperative neurologic deficit was 6.0%. The postoperative observation time was 1 year to 13 years 5 months (mean 66 months). At follow-up 87% of the survivors were symptom-free. Three new strokes, one of them not related to the operated side, occurred follow-up, and 26 more patients died. The relative cumulative 5-year survival was 87.3%. Of the total 28 deaths, 16 were due to myocardial infarction. Mortality was significantly heightened and cumulative 5-year survival reduced when preoperative ECG had indicated coronary heart disease. The high incidence of deaths from myocardial disease during long-term follow-up was directly related to preoperative presence of coronary heart disease.