We searched for mitral-valve prolapse by two-dimensional echocardiography in 15 patients with von Willebrand syndromes to test the hypothesis that this bleeding disorder is actually a mesenchymal dysplasia that resembles the heritable disorders of connective tissue. This valvular abnormality was found in nine (60 per cent) of these patients, as compared with four (13.3 per cent) of 30 sex-matched and age-matched healthy controls. This difference was statistically significant (P less than 0.01). The association between these two disorders encourages a search for mitral-valve prolapse in persons with a von Willebrand syndrome. The complex of a von Willebrand syndrome and mitral-valve prolapse may be an example of a newly recognized category of related coagulation and cardiovascular disorders.

Peripheral blood lymphocyte subsets were quantified by immunofluorescence in nine patients undergoing open heart surgery for coronary artery, valvular, and congenital heart disease. Compared with normal preoperative values, all patients developed an absolute lymphopenia, a reduction in T4 (helper) lymphocytes, and a statistically significant reversal of the T4/T8 ratio two hours after cardiopulmonary bypass (CPB). These changes could be caused by mechanical or immunogenic injury. A return to normal of the T4 subset and T4/T8 proportion occurred 24 hours after surgery. Whereas transient inactivation of immunoreactive lymphocyte clones may prevent unwanted immunization to blood products received during surgery, such temporary immune dysfunction could make certain patients liable to infectious sequelae. Viral-induced postperfusion syndromes, transmission of human T lymphotropic virus (HTLV) III by blood products, and reports of acquired immune deficiency syndrome after CPB foster a concern regarding postoperative infections under these circumstances.

The purpose of this study was to examine the recognized ability of interleukin-1 alpha (IL-1 alpha) to alter the functional properties of endothelial cells and to induce replication of smooth muscle and fibroblasts. Such changes could potentially link IL-1 alpha pathogenetically to the myointimal proliferation of vascular sclerosis. Using a peroxidase-immunoperoxidase immunohistochemical method, saphenous veins and internal mammary arteries were examined for the presence of IL-1 alpha before their implantation as aortocoronary bypass grafts. Occluded saphenous vein grafts requiring replacement because of recurrent angina pectoris also were similarly examined. Interleukin-1 alpha, deposited as a scarlet immunoprecipitate, was seen on the luminal surface, in the subintima, and on the spindle cells and infiltrating macrophages in the media of 13 phlebosclerotic veins before surgical insertion. The remaining 30 unchanged veins did not contain IL-1 alpha. Similarly, IL-1 alpha was not identified in any of the 43 sampled internal mammary arteries that were all considered structurally intact. All the 55 bypass grafts, which were examined by biopsy during revascularization and demonstrated diverse histopathologic abnormalities consisting of reduced luminal patency, myointimal proliferation, mononuclear cell infiltration, mural collagenization, and luminal-mural hemorrhage, also contained widely distributed IL-1 alpha. The observation that IL-1 alpha was absent in all of the internal mammary arteries concomitant with maintenance of normal microanatomic structure may help explain, in part, their recognized resistance to reduction in luminal patency and their improved clinical survival when used as coronary artery bypass grafts. Alternatively, the consistent presence of IL-1 alpha in all vessels with sclerotic histopathologic changes suggests that this cytokine may be an important in situ indicator of and a potential participant in vascular injury. Interleukin-1 alpha may be a pathogenetic factor in the complex processes leading to vascular occlusion.

Plasma levels of factor VIII-related antigen (fVIIIRA) and factor XIII S and A subunits (fXIIIS, fXIIIA) were assayed by counterimmunoelectrophoresis before, during, and after cardiopulmonary bypass (CPB) in patients with coronary artery and valvular heart disease to define the basis for clinical and laboratory abnormalities of hemostasis occurring in this form of surgery. During CPB, concentrations of fXIIIA dropped in both patient groups but returned to preoperative levels promptly after pump removal. In contrast, fVIIIRA and fXIIIS, which are not incorporated into the clot, remained unchanged even during fluid administration. These data provide evidence of a transient consumption coagulopathy as a feature of CPB. Hemodilution probably plays a secondary role in these changes.