We investigated 2 hypotheses: (1) a relationship between platelet indices and stable coronary artery disease (CAD) and acute ST-segment elevation myocardial infarction (STEMI) and (2) a relationship between platelet indices on admission and thrombolysis outcomes in patients with STEMI. A total of 260 patients were enrolled. The white blood cell (WBC) and platelet distribution width (PDW) were found to be increased in patients with STEMI (P for both < .001). White blood cell and PDW were independent predictors of acute STEMI. Mean platelet volume (MPV) and PDW were significantly higher in the thrombolysis failure group than in the thrombolysis success group (9.9 ± 1.8 vs 9.2 ± 1.5 fL, P = .021 and 17.7 ± 1.0 vs 16.4 ± 2.1 fL, P < .001, respectively). Mean platelet volume and PDW were independent predictors of thrombolysis failure. Patients with acute STEMI had higher PDW than did patients with stable CAD. In addition, higher PDW and MPV seem to correlate with thrombolysis failure in patients with STEMI.

Preprocedural high-thrombus burden (HTB) of infarct-related artery (IRA) is a harbinger of procedural complications following primary percutaneous coronary intervention (PCI) in patients with ST-elevation myocardial infarction (STEMI). The HTB of IRA can lead to poor outcomes by various mechanisms, including no-reflow phenomenon, increased myocardial necrosis and with subsequent reduced survival benefit at follow-up. In this study, we investigated the relationship between all platelet indices on admission and thrombus burden and the no-reflow phenomenon after primary PCI of IRA in patients with STEMI. We retrospectively enrolled 475 patients with STEMI undergoing primary PCI. Study population was divided into two groups according to the thrombolysis in myocardial infarction thrombus grade of IRA as low-thrombus burden or HTB. There were no statistically significant differences in platelet indices, including platelet count, platelet-large cell ratio (P-LCR), mean platelet volume (MPV) and platelet distribution with (PDW) among the groups. However, in the subgroup analysis, P-LCR, MPV and PDW were significantly higher in the no-reflow patients than reflow patients despite similar platelet count (P for all < 0.001). The cutoff value of P-LCR for predicting no-reflow was 26.5% with a sensitivity of 67.0% and a specificity of 62% (area under the curve, 0.689; 95% confidence interval, 0.614-0.765; P < 0.001). Furthermore, P-LCR, MPV and PDW had similar AUC (0.689, P < 0.001; 0.688, P < 0.001; and 0.677, P < 0.001; respectively) for predicting no-reflow phenomenon after primary PCI. As a result, all of the platelet indices have no effect on thrombus load of IRA, however, these parameters seem to impair epicardial perfusion after primary PCI.

In patients with CTO, a poor coronary collateral status and multivessel disease may further impair electrical homogeneity. Our results indicate that successful CTO PCI reduces the arrhythmic vulnerability of the myocardium on the basis of an analysis of the TpTe, the TpTe/QT ratio, and QTc dispersion.

N/L ratio can be used to predict poor FC in patients with CHF.

: Serum resistin, mainly secreted by the bone marrow, monocytes, and macrophages, contributes to many processes, including endothelial dysfunction, vascular smooth muscle cell (VSMC) proliferation, and atherothrombosis demonstrating effects on the development of hypertension and coronary artery disease (CAD). Previously published clinical studies have shown that plasma resistin levels are significantly associated with cardiovascular disease risk factors and adverse clinical outcomes associated with the condition. Resistin is associated with vascular smooth muscle cell dysfunction in vitro, most plausibly due to its relationship with oxidative stress in advanced atherosclerosis, whereas in vivo studies have shown resistin to be associated with intimal hyperplasia. We aimed to summarize the role of resistin on cardiovascular disease (CVD), as we could not find any review focused on the role of resistin on CVD.