Failure of aspirin to prevent incorporation of indium-111 labelled platelets into cardiac thrombi in man.
The in vitro and in vivo behaviour of platelets was studied in eleven patients with left ventricular aneurysms and mural thrombi. Five patients were on aspirin 300-2400 mg/day; the remaining six patients were controls. In vitro function was tested by the aggregation response of platelets to adenosine diphosphate (ADP) and collagen. In vivo function was assessed by the incorporation of indium-111-labelled platelets into cardiac thrombi as measured by scintigraphy. Platelets from patients on aspirin, whether tested before or after labelling, aggregated less with collagen than did those of controls (18 vs 52%; p less than 0.01 before labelling, 13 vs 49%; p less than 0.02 after labelling). Second wave aggregation, induced by ADP, was impaired in patients on aspirin. In all patients scintigraphy showed that the autologous labelled platelets were incorporated into ventricular thrombi. Thus, although in vitro the platelets from patients on aspirin aggregated subnormally, in vivo they took part in thrombosis.
D001241:Aspirin / Q000494:pharmacology* / Q000627:therapeutic use; D001792:Blood Platelets / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000378:metabolism; D006322:Heart Aneurysm / Q000150:complications; D006331:Heart Diseases / Q000517:prevention & control*; D006352:Heart Ventricles; D006801:Humans; D007204:Indium; D010974:Platelet Aggregation / Q000187:drug effects; D011868:Radioisotopes; D011877:Radionuclide Imaging; D013927:Thrombosis / Q000517:prevention & control*
D011868:Radioisotopes; D007204:Indium; D001241:Aspirin