Coexistence of prothrombic risk factors and its relation to left ventricular thrombus in acute myocardial infarction.

OBJECTIVE: Within the last few years a number of thrombophilic mutations have been identified. Pre-symptomatic testing for these established genetic risk factors identifies individuals predisposed to a disease and often allows to select suitable prophylactic interventions in time. We investigated whether or not the prothrombin G20210A allele, the factor V Leiden G1691A, and MTHFR C677T allele are risk factors for left ventricular thrombus (LV) in patients with myocardial infarction (AMI) or not. METHODS AND RESULTS: We analysed clinical, echocardiographic and biochemical data in 183 consecutive patients (aged 58 +/- 12 years; 34 women) with a first anterior acute myocardial infarction. Two-dimensional echocardiographic examination was performed on days 1, 3, 7, 15, and 30. LV thrombi were detected in 42 (23%) of the 183 patients with acute myocardial infarction. We have used multiplex assays based on PCR and DNA hybridization in microtitre plates for the simultaneous analysis of three mutations (FV Leiden G1691A, prothrombin G20210A, and MTHFR C677T). No significant differences in allele frequencies of FV Leiden G1691A (9.5% vs. 8.5%, p = 0.75), prothrombin G20210A (9.5% vs 7.1%, p = 0.74) and MTHFR C677T (47.6% vs. 50.3%, p = 0.74) were found in patients with LV thrombus when compared with those without LV thrombus. No significant differences in haemostatic factor levels were found in patients with LV thrombus when compared with those without LV thrombus. CONCLUSION: FV Leiden, prothrombin 20210 variant, and MTHFR mutation are no risk factors for left ventricular thrombus in patients with myocardial infarction.The presence of multiple mutations did not influence the development and outcome of LV thrombus in patients with myocardial infarction

Flow cytometric assay of platelet glycoprotein receptor numbers in hypercholesterolemia.

In this study, platelet glycoprotein (Gp) receptor numbers were measured by a flow cytometric assay using Cytoquant Gp in seven hypercholesterolemic and five normal subjects. Thrombin receptor agonist peptide (TRAP) was used to activate platelets. In hypercholesterolemia the Gp receptor numbers per resting platelet were found to be: 38,629 +/- 8,538 (GpIIb/IIIa), 22,269 +/- 5,628 (GpIb), 37,037 +/- 9,810 (GpIIIa), 224 +/- 504 (CD62-P). After activation, receptor numbers were determined to be: 56,399 +/- 9,003 (GpIIb/IIIa), 10,970 +/- 5,319 (GpIb), 50,715 +/- 7,904 (GpIIIa), 1,222 +/- 687 (P-selectin). In the normal group before the activation, receptor numbers were: 43,828 +/- 8,862 (GpIIb/IIIa), 22,166 +/- 3,847 (GpIb), 42,351 +/- 1,049 (GpIIIa), 62 +/- 139 (CD62-P), After activation, receptor numbers were determined to be: 60,573 +/- 4,294 (GpIIb/IIIa), 13,003 +/- 4,118 (GpIb), 52, 067 +/- 1,039 (GpIIIa), 3,608 +/- 1,508 (CD62-P). In hypercholesterolemic subjects, GpIIb/IIIa and GpIIIa receptor numbers on activated platelets increased significantly, whereas P-selectin numbers remained unchanged. However, the GpIb levels decreased significantly. In the control group, after activation, GpIIb/IIIa and P-selectin receptors increased significantly, GpIIIa receptor numbers did not change significantly, whereas GpIb receptor numbers decreased significantly. When the GpIIb/IIIa, GpIb, GpIIIa receptor numbers of the control group and hypercholesterolemic group were compared before and after activation, no significant changes were observed (P > 0.05). But P-selectin receptor numbers were significantly decreased in hypercholesterolemic patients compared to normals following TRAP activation (P < 0.05). In this study, the effect of hypercholesterolemia on platelet function was observed. The striking observation about present study was the marked decrease in P-selectin expression after activation in the hypercholesterolemics compared to normals. This finding suggests some sort of platelet dysfunction in these individuals.