Clopidogrel alone or in combination with aspirin markedly inhibited adenosine diphosphate (ADP)-mediated platelet aggregation compared with monotherapy with aspirin (24.6 +/- 3.3% or 26.6 +/- 2.7% vs. 44.7 +/- 2.9%; p < 0.001). Combined treatment significantly inhibited collagen-induced aggregation compared with aspirin and clopidogrel (16.4 +/- 2.4%, 36.5 +/- 4.2% and 59.3 +/- 5.1%, respectively;, p < 0.001) and resulted in considerable inhibition of aggregation induced by thrombin receptor agonist peptide (TRAP, p < 0.03). Clopidogrel with or without aspirin significantly suppressed expression of platelet activation markers CD 62p, CD 63 and PAC-1 after stimulation with ADP or thrombin (p < 0.001). In addition, the combined treatment was more effective than either agent alone after activation with low dose thrombin (p < 0.05). Both doses of aspirin equally potentiated the platelet inhibitory effects of clopidogrel. CONCLUSIONS In this prospective clinical ex vivo platelet study, clopidogrel was more effective than aspirin in inhibiting ADP-mediated platelet aggregation and activation. Clopidogrel in combination with aspirin showed synergistic inhibitory effects after stimulation with collagen and thrombin compared with monotherapies. Thus, this dual antiplatelet treatment strategy deserves further evaluation in clinical trials for secondary prevention of acute myocardial infarction or unstable angina.

These data clearly indicate that in children ABO major-mismatched PLT transfusions result in inferior transfusion efficacy, with the only exception of group A(2) PLTs. ABO minor-mismatched PLTs showed comparable efficacy to identical transfusions.

To investigate a possible association of ABO blood group alleles with myocardial infarction, a case-control study comprising 177 patients (median age 57.0 years; range 32-72 years) and 89 controls was performed. The distributions of the ABO blood-genotype O1, O2, A1, A2 and B alleles were assessed by analysis of genomic DNA, using the sequence-specific primer-polymerase chain reaction (PCR-SSP) technique to investigate exons VI and VII on chromosome 9. The prevalence of the B allele was 2.5 times higher amongst patients with a history of myocardial infarction than amongst controls (16.3 vs. 6.7%; P = 0.034, Fisher's exact test). There was an association between patients carrying the B allele and myocardial infarction, with an odds ratio (OR) of 2.7 (95% confidence interval 1.1-6.8). The B allele remained an independent risk factor for myocardial infarction (P = 0.038) when classical risk factors were adjusted for by unconditional logistic regression. In conclusion, the ABO blood group B allele was found to be an independent risk factor for myocardial infarction.

Functional thrombin receptors are present on endothelium and SMCs of IMA and SV. Endothelial thrombin receptors mediate relaxation in IMA but not SV. Thrombin causes much more pronounced contraction and proliferation in SMCs of SV than IMA independent of tethered receptors, suggesting other thrombin receptors exist. These differences of thrombin receptor activation in IMA and SV may be important in the development of and therapy for graft disease.