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A D Sniderman

Publications and source records attributed to A D Sniderman.

129 records · Page 8Linked to original sources

Dyslipoproteinemias after heart and heart-lung transplantation: potential relation to accelerated graft arteriosclerosis.

Plasma lipid, lipoprotein lipid, and low-density lipoprotein (LDL) apolipoprotein B (Apo B) levels were measured in 34 patients who had undergone heart transplantation and in two patients who had undergone heart-lung transplantation. In contrast to initial reports, atherogenic dyslipoproteinemias were common, with 14% of patients having increased LDL cholesterol levels, 16.7% increased triglyceride levels, 8.3% decreased high-density lipoprotein (HDL) cholesterol levels, and 22.2% increased LDL Apo B levels. Of interest, 14% of patients had an HDL cholesterol level greater than the 95th percentile of the general population. In four patients coronary arteriosclerosis developed after transplantation. All had an atherogenic dyslipoproteinemia. One had type II hypercholesterolemia, and one had isolated low HDL cholesterol levels. Two had hyperapobetalipoproteinemia, one of whom also had low HDL cholesterol levels. The results establish that atherogenic dyslipoproteinemias are frequent in patients after heart transplantation and suggest that these dyslipoproteinemias, along with rejection, may play a role in the pathogenesis of arteriosclerosis after transplantation.

Adult↗

Pulmonary edema induced by fluid administration in acquired immune deficiency syndrome patients with cardiac autonomic dysfunction.

Two patients with the acquired immune deficiency syndrome developed acute pulmonary edema following intravenous fluid administration. Both recovered with diuretic therapy. In neither case was there evidence of persistent severe left ventricular dysfunction, nor was there evidence (either clinically or by thallium study) of flow limiting coronary lesions or of cardiac uptake of iodine-123 meta-iodobenzylguanidine, pointing to ventricular sympathetic neuropathy. It is hypothesized that destruction of the cardiac sympathetics contributed importantly to the development of pulmonary edema following the intravenous fluid load.

3-Iodobenzylguanidine↗