Furthermore, subjects who had non-significant stenosis in the culprit vessel or their coronary anatomy was not eligible to perform coronary angioplasty. Patients either with a delayed diagnosis of STEMI or deferred arrival whose symptoms persisted longer than 12 h were excluded. Otherwise, 70-to 100-unit /kg bolus dose of UFH to achieve a therapeutic ACT had been considered. If use of a glycoprotein IIb/IIIa receptor antagonist was planned, 50-to 70-unit /kg IV bolus of unfractionated heparin to achieve therapeutic ACT (Activated clotting time) was administered. Thus, each participant received a loading dose of P2Y12 inhibitor (including 600 mg clopidogrel as the main agent and prasugrel 60 mg for a minority subgroup (1.2%)) accompanied with atorvastatin (80 mg), unfractionated heparin, and aspirin (300 mg). Coronary angiography was performed for all patients in addition to standard medical treatment of acute coronary syndrome. The median length of hospital stay determined as follow up period was six days. The secondary endpoint of the study was short-term in-hospital mortality of all cause. Angiographic results of reperfusion were inspected to evaluate the association of high CHA2DS2-VASc score and the likelihood of suboptimal TIMI flow. Then we compared these groups with respect to baseline characteristics. Patients were divided into two groups according to low and high CHA2DS2-VASc score. We have accomplished a retrospective cohort study among 1331 consecutive patients with STEMI diagnosis who underwent primary PCI in Tehran Heart Center between February 2016 and March 2018. Therefore, we have assessed prognostic yield of this clinical score to estimate the risk of no-reflow following primary PCI and stenting. Furthermore, such instruments have represented ample power in estimating major adverse cardiovascular outcomes in the setting of acute coronary syndrome. ĬHA2DS2 and CHA2DS2-VASc score models are widely applied to predict the risk of subsequent thromboembolic events in patients with atrial fibrillation. Thus, we need a reliable risk stratification tool, which properly predicts the incidence of no-reflow regarding its multifactorial pathogenesis. This entity involves about 5–15% of cases undergoing revascularization. The no-reflow phenomenon occurs because of heterogeneous factors including distal embolization of debris pertaining to ulcerated atherosclerotic plaques, microvascular damage, vasospasm, insults of oxidative stress, and reperfusion injury. One of the leading complications associated with primary PCI is suboptimal reperfusion of the endangered myocardium in the territory of corresponding epicardial coronary artery. In the era of revascularization, primary percutaneous intervention (PCI) is the mainstay of the treatment of acute ST segment elevation myocardial infarction (STEMI) owing to favorable efficacy rather than that of thrombolysis. Furthermore, incremental values are obtained by using both CHA2DS2-VASc and no-reflow regarding mortality risk assessment. Conclusions: Calculation of CHA2DS2-VASc score applied as a simple risk stratification tool before primary PCI affords great predictive power. We showed that using a cut off value of ≥ two in CHA2DS2-VASc model provides a sensitivity of 69.7% and specificity of 64.4% for discrimination of increased mortality hazards. Moreover, BMI, high thrombus grade, and cardiogenic shock were predictors of failed reperfusion (odds were 1.07 (1.01–1.35), 1.59 (1.28–1.76), and 8.65 (3.76–24.46), respectively). Results: The present study confirmed that CHA2DS2-VASc model enables us to determine the risk of no-reflow and all-cause in-hospital mortality independently. The study included 1331 consecutive patients with STEMI who underwent primary angioplasty. Materials and Methods: We designed a retrospective cohort study using the data of Tehran Heart Center registry for acute coronary syndrome. Background and objectives: We aimed to demonstrate the clinical utility of CHA2DS2-VASc score in risk assessment of patients with STEMI regarding adverse clinical outcomes particularly no-reflow phenomenon.
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