We aimed to investigate the relationship between platelet-to-lymphocyte ratio (PLR) and contrast-induced acute kidney injury (CI-AKI) in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (pPCI). A total of 2563 patients diagnosed with STEMI and underwent primary pPCI were retrospectively included in the study. Levels of PLR and creatinine were measured before and at 72 hours after pPCI. Patients were divided into 2 groups: non-CI-AKI group and CI-AKI group. Contrast-induced acute kidney injury occurred in 6.4% of the overall study population. Patients in the CI-AKI group had significantly higher PLR than those in the non-CI-AKI group (169.18 ± 81.01 vs 149.49 ± 74.54, P < .001). In logistic regression analysis, PLR was an independent predictor of CI-AKI (odds ratio [OR]: 1.774, 95% CI: 1.243-2.532, P = .002), along with age, use of angiotensin-converting enzyme inhibitor/angiotensin receptor blocker prior to the procedure, preprocedural creatinine level, amount of contrast material used during the procedure, and hypertension. Increased PLR levels are independently associated with a greater risk of CI-AKI in patients undergoing primary PCI for STEMI.

We retrospectively analyzed short- and long-term outcomes of patients who received bailout tirofiban during primary percutaneous intervention (pPCI). A total of 2681patients who underwent pPCI between 2009 and 2014 were analyzed; 1331 (49.6%) out of 2681 patients received bailout tirofiban. Using propensity score matching, 2100 patients (1050 patient received bail-out tirofiban) with similar preprocedural characteristics were identified. Patients who received bailout tirofiban had a significantly higher incidence of acute stent thrombosis, myocardial infarction, and major cardiac or cerebrovascular events during the in-hospital period. There were numerically fewer deaths in the bailout tirofiban group in the unmatched cohort (1.7% vs 2.5%, P = .118). In the matched cohort, in-hospital mortality was significantly lower (1.1% vs 2.4%, P = .03), and survival at 12 and 60 months were higher (96.9% vs 95.2%, P = .056 for 12 months and 95.1% vs 92.0%, P = .01 for 60 months) in the bailout tirofiban group. After multivariate adjustment, bailout tirofiban was associated with a lower mortality at 12 months (odds ratio [OR]: 0.554, 95% confidence interval [CI], 0.349-0.880, P = .012) and 60 months (OR: 0.595, 95% CI, 0.413-0.859, P = .006). In conclusion, bailout tirofiban strategy during pPCI is associated with a lower short- and long-term mortality, although in-hospital complications were more frequent.

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IntroductionThe primary goal in the management of acute ST segment elevation myocardial infarction (STEMI) is to open the occluded artery at an early stage. The development of no-reflow is multifactorial, and the etiology is not fully understood. There is accumulating evidence that anemia is related to a series of severe complications in cardiovascular disease (CVD) such as thromboembolic events, bleeding complications, uncontrolled hypertension, and inflammation characterized by elevated levels of inflammatory cytokines.AimWe investigated the relationship between hemoglobin level and the no-reflow of infarct-related artery (IRA) in patients with STEMI undergoing primary percutaneous coronary intervention (PPCI).Material and methodsA total of 3804 patients with acute STEMI who underwent PPCI were enrolled. The patients were divided into two groups according to thrombolysis in myocardial infarction (TIMI) flow grades after PPCI. Hematological parameters were measured on admission. Univariate and multivariate logistic regression analyses were conducted to assess the association between hemoglobin level and no-reflow.ResultsIn the current study, 471 (12.4%) patients presented with no-reflow after PPCI. The patients in the no-reflow group had a significantly lower hemoglobin level (12.1 ±1.9 g/dl vs. 13.8 ±1.8 g/dl, p < 0.001). The multivariate logistic regression models revealed that hemoglobin level (OR = 0.564, 95% CI: 0.526–0.605; p < 0.001) was an independent predictor of development of no-reflow. The cutoff value for hemoglobin level was 11.5 g/dl with sensitivity of 83.0% and specificity of 80.0% (AUC = 0.844, 95% CI: 0.821–0.867; p < 0.001).ConclusionsOur results suggest that hemoglobin level showed a moderate diagnostic performance regarding the prediction of no-reflow in patients with STEMI undergoing PPCI.

Introduction: In-stent restenosis (ISR) still constitutes a major problem after percutaneous vascular interventions and the inflammation has a pivotal role in the pathogenesis of such event. The C-reactive protein/albumin ratio (CAR) is a newly identified inflammatory biomarker, and it may be used as an indicator to predict ISR in subjects with coronary artery stenting. In light of these data, our main objective was to investigate the relationship between the preprocedural CAR and ISR in patients undergoing successful iliac artery stent implantation. Methods: In total, 138 consecutive patients who had successful iliac artery stent implantation in a tertiary heart center between 2015 and 2018 were enrolled in the study. The study population was categorized into two groups; patients with ISR and those without ISR during follow-up. The CAR was determined by dividing CRP by serum albumin. Results: In the multivariable regression analysis; the CAR (HR: 2.66, 95% CI: 1.66-4.25, P < 0.01), stent length (HR: 1.01, 95% CI: 0.99-1.02, P = 0.04), and HbA1c levels (HR: 1.22, 95% CI: 0.99-1.51, P = 0.04) were independently related with ISR. A receiver operating curve analysis displayed that the CAR value of >0.29 predicted ISR with sensitivity of 97.5% and specificity of 88.8% (AUC 0.94, P < 0.01). Conclusion: Our findings provide evidence that the CAR may be an applicable inflammatory biomarker in predicting ISR in subjects undergoing iliac artery stenting for the treatment of peripheral artery disease (PAD). Also, the stent length and poor glycemic control were found to be associated with ISR.