Kaye, M. P.

In right-sided extracardiac conduits inserted for surgical correction of certain congenital heart defects, obstruction is a significant late complication requiring conduit replacement in about 5% of the patients. Our histopathologic study indicates a significant role of platelets in the pathogenesis. This study was designed to evaluate the feasibility of imaging procedure with 111-Indium-labeled platelets to localize and later quantify platelet accumulation in the conduits. Four patients with pulmonary atresia and 1 with truncus arteriosus underwent conduit placement, 2 with and 3 without porcine valve. Autologous platelets collected.from 43 ml of blood drawn prior to surgery were labeled with 111-Indium-oxine in ACD-saline medium (labeling efficiency 50-60%). 400-500 μCi of autologous 111-Indium-labeled platelets were administered intravenously immediately after surgery in 4, and five days after surgery in 1 patient. Imaging was performed at 6 hours and daily for 1-4 days using a portable gamma camera interfaced with a computer and fitted with medium-energy parallel hole collimator. Platelet deposition was noted at the site of the conduit in all 5 patients. Maximum accumulation (0.1-0.3% of dose) of platelets was seen within the first 24 hours. Activity over blood pool and lungs declined and over liver and spleen increased in a predictable manner over the imaging period. This technique has potential use as a noninvasive quantitative tool to study the effect of platelet inhibitor drugs in preventing conduit obstruction.

The effect of hypercholesterolemia on the transverse wall properties of the upper descending thoracic aorta was studied in canines. Hypothyroid animals were fed a free diet supplemented with cholesterol, propylthiouracil, and saturated fat (lard) for 11 mo. The mechanical properties of the wall showed marked changes following experimental pathology. The failure stress, failure elongation, and energy to failure decreased following hypercholesterolemia. The tensile response was bilinear in both the pathological and control tissues. In the initial region, which is controlled by elastic fibers, the response was left unchanged by the experimental pathology. In the secondary region, which is controlled by stretching of the collagen fibers, the intercept with the strain axis and the slope were decreased by the pathology. This indicates that there are changes in the strength-bearing collagen and its interaction with the amorphous matrix. However, no significant parallel histological changes were observed in the structure of collagen and elastic fibers. Although this phenomenon precedes the development of atherosclerotic plaques which are charateristic of a diagnosed human disease, the aortic wall is already “hardened” because of its reduced compliance resulting from the shift in the onset of secondary (collagenous) response.