Platelet function and composition in heart transplant recipients compared with nontransplanted coronary patients.

Abstract

Accelerated coronary artery disease seems to be the main condition limiting long-term survival after heart transplantation. Ninety-one heart transplant recipients were compared with 94 nontransplanted coronary artery disease patients in an attempt to identify the factors responsible for the accelerated form of coronary artery disease occurring after heart transplantation. Among the parameters examined, heart transplant recipients exhibited a higher plasma level of insulin (8.5±0.5 versus 62±03 mIU/1, p=0.002), a lower plasma level of vitamin E (14.8±0.4 versus 16.9±0.7 mg/1, p=0.03), a higher platelet cholesterol-to-phospholipid ratio (8.9±0J versus 7.6±0«3, p=0.007), and an increased response to ADP-induced platelet aggregation (for the first wave, 29.1±0.9% of maximal aggregation versus 25.1±1.0%, />=0.002; for the second wave, 21.4±1.4% versus 15.9±1.1%, p=0.002, after adjustment for hematocrit), but no untoward changes in the level of fibrinogen, plasminogen activator inhibitor-1, antithrombin III, or lipoprotein(a). In addition, platelet aggregation in patients who required retransplantation as a result of severe coronary artery disease was similar before and after retransplantation. This suggests that severe coronary artery disease is not the cause of platelet hyperaggregability. In multiple-regression analysis, ADP-induced platelet aggregation in heart transplant recipients was significantly positively related to blood glucose (r=0.50, p<0Ml) and inversely related to n-3 fatty acids from platelet phospholipids (r=0.40,p<0.01). These results are consistent with the view that a platelet disorder associated with or responsible for the increased thrombotic tendency could play a role in the pathogenesis of the disease. However, further studies are needed to investigate the mechanism of this platelet hyperaggregability, which is possibly related to a lipid peroxidation process (low plasma vitamin E) and/or to a diabetes-associated platelet lipid disorder (high insulin level). (Arteriosclerosis and Thrombosis 1992;12:222-230)

Increased Platelet Aggregation Response in Cavalier King Charles Spaniels with Mitral Valve Prolapse

“…Increase in serum factors inducing platelet aggregation has been seen in acute pancreatitis in dogs, and changes in platelet plasma membrane lipid composition have been suggested to increase aggregability in humans with diabetes mellitus and some cardiovascular disorders. [40][41][42] A shortened platelet life span can explain findings of platelet hyperaggregability because young platelets are more active than older platelets. 43 The high prevalence of macrothrombocytosis could indicate an increased thrombocytopoiesis in CKCS, 21 but in this study, an increased platelet aggregation was found only in CKCS with Ͼ100,000 platelets/Lwhich are not the ones that usually have macrothrombocytosis.…”

Modified Cretan Mediterranean Diet in the Prevention of Coronary Heart Disease and Cancer

“…In the accelerated form of CHD typical of the posttransplantation patient, higher levels of lipid peroxidation [53][54][55] and of oxidized LDL [56] were found compared with the stable form of CHD in the nontransplanted patients. Reactive oxygen metabolites and oxidants influence thrombus formation [57], and platelet reactivity is significantly higher in transplanted patients than in nontransplanted CHD patients [58]. However, platelet phospholipid fatty acids (which partly determine platelet function) are different from those of the nontransplanted CHD patients [58] which may explain, at least partly, the high platelet reactivity of the transplanted.…”

“…Reactive oxygen metabolites and oxidants influence thrombus formation [57], and platelet reactivity is significantly higher in transplanted patients than in nontransplanted CHD patients [58]. However, platelet phospholipid fatty acids (which partly determine platelet function) are different from those of the nontransplanted CHD patients [58] which may explain, at least partly, the high platelet reactivity of the transplanted. As the effects of reactive oxygen metabolites on platelet function are quite complex [59], further studies are warranted to definitely answer the question of the relations between lipid peroxidation and platelet function in CHD.…”

Cardiac Allograft Vasculopathy and Insulin Resistance—Hope for New Therapeutic Targets

“…28 Since long ago, it has been demonstrated that heart transplant recipients have elevated levels of hemostatic and proinflammatory markers, mirroring the findings in non-transplant insulin resistant individuals. 29 The published data confirms that heart transplant recipients are insulin resistant, and suggests that this state of impaired insulin action accelerates CAV.…”