The Impact of Baseline Platelet Count on Angiographic Finding and End-Points in St-Elevation Myocardial Infarction Managed With Percutaneous Coronary Intervention

Platelet counts on admission affect coronary flow, myocardial perfusion and left ventricular systolic function after primary percutaneous coronary intervention

“…A recent study reported that a higher platelet count on admission without any antithrombotic agent predicted total occlusion of the infarct-related artery before PPCI in patients with STEMI, 20 which is complementary to our observation that a lower platelet count on admission had a larger percentage of patients with TIMI III before PPCI. 21 Moreover, we found that baseline thrombus score was larger in the subgroup of patients with the highest platelet count, implying more erythrocyte content in these thrombi according to a recent study. 22 Another study found that a higher platelet count, even after multivariate adjustment, was independently associated with the presence of residual thrombus in the infarct-related artery after the administration of fibrinolytic therapy for STEMI.…”

Rapid on‐site evaluation of routine biochemical parameters to predict right ventricular dysfunction in and the prognosis of patients with acute pulmonary embolism upon admission to the emergency room

“…An increase in the PLR is caused by increased PLT and decreased LY counts, and an increase in PLT counts is reflective of the inflammatory condition and bleeding, which would stimulate megakaryocyte proliferation and induce thrombocytosis. 27 A decrease in LY counts is caused by reasons similar to those described for NLR. Although the PLR has a similar predictive ability for vascular disease in our regression model, it was not correlated with RVD.…”

Characterization of TCF21 Downstream Target Regions Identifies a Transcriptional Network Linking Multiple Independent Coronary Artery Disease Loci

“…Since the ChIPseq data was generated in HCASMC, a cell type found in the coronary artery, the results of CAD loci enrichment is consistent with the hypothesis that TCF21 regulates a greater than expected number of CAD genes in the vessel wall and that its effect on disease risk may be due in part to its regulation of the network of TCF21 target CAD associated genes. Consistent with TCF21 CAD target genes being active primarily in the vascular wall, we saw no difference in enrichment between the CAD analyses with and without lipid genes or SNPs being included in the analysis, and no enrichment was found for vascular risk factor traits “LDL cholesterol” and “Total cholesterol.” The enrichment for “Platelets” is not surprising given the known association of platelet number with vascular disease events, and this association could explain some portion of the TCF21 risk for CAD [ 41 – 43 ]. Human genetic epistasis studies are required to validate these putative gene-gene interactions between TCF21 and the other CAD genes in the network, but further study of the functional links among validated TCF21 target CAD genes should provide an opportunity for further dissecting the molecular basis of disease risk.…”