Biopsy specimens from 80 cardiac allografts were studied immunocytochemically with nine antibodies selected to identify cellular, immunologic, and vascular aspects of rejection. Results from these experiments were converted to a numeric base and used to calculate rejection indexes for each of these aspects of rejection. Pretransplantation biopsy specimens of donor hearts were studied to determine normal values, and clinical, catheterization, and conventional biopsy findings were used to classify patients as stable or unstable. The standard deviation of cellular and immunologic reaction indexes were overlapping for stable and unstable patients, but the vascular indexes for these patient groups were significantly different, suggesting that vascular damage defines clinical instability in cardiac allograft recipients. To study the vascular index in the absence of cellular infiltrates, biopsy specimens from 80 allografted hearts were selected to represent 40 patients with cellular infiltrates and 40 patients devoid of infiltrates. The results of this analysis revealed no difference in the vascular index between hearts that contained or did not contain infiltrates; the spectrum of vascular damage between the groups ranged from trivial to severe, suggesting that vascular damage was not dependent on cellular infiltrates. Concluding that these were independent events was not possible, however, because none of the hearts continuously were devoid of cellular infiltrates. Two groups of patients with significantly different vascular indexes then were studied for a systemic manifestation of coagulation by measurement of their thrombin times. The group with low vascular index was found to have significantly prolonged thrombin times compared to the group with high vascular index, and a trend to less prolongation of thrombin times was observed in another group with high cellular index. The relation of these results with cardiac allograft vasculopathy is not established, but the results suggest hitherto unexplored roles for quantitative expressions of hemostasis, fibrinolysis, and anticoagulation in the pathophysiology of vascular disease in allografts.