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 evaluated whether primary percutaneous coronary intervention (pPCI) during off-hours is related to an increased incidence of contrast-induced nephropathy (CIN). We retrospectively analyzed the incidence of CIN mortality among 2552 patients with consecutive ST-segment elevation myocardial infarction treated with pPCI during regular hours (weekdays 8:00 am to 5:00 pm) and off-hours (weekdays 5:01 pm to 7:59 am, weekends and holidays). Patients in the off-hour group were more frequently admitted with acute heart failure symptoms (16.4% vs 7.8%, P < .001) and more contrast was injected during the procedure (235.2 ± 82.3 vs 248.9 ± 87.1 mL, P = .002). The frequency of CIN between on-hour and off-hour groups was similar (7.1% vs 6.2%, P = .453), but there was a trend toward higher in-hospital mortality when pPCI was performed during off-hours (1.9% vs 0.7%, P = .081). Off-hour pPCI was not associated with an increased risk of CIN (odds ratio: 1.051, P = .833). The incidence of CIN did not increase during off-hours, and off-hour pPCI is not a risk factor for CIN, despite an apparent increase in contrast media use during off-hour pPCI.

It is unclear whether changes in mean platelet volume (MPV) are associated with total mortality in acute coronary syndromes. We investigated whether the change in MPV predicts total mortality in patients with non-ST-segment elevation myocardial infarction (NSTEMI). We retrospectively analyzed 419 consecutive patients (19 patients were excluded). The remaining patients were categorized as survivors (n = 351) or nonsurvivors (n = 49). Measurements of MPV were performed at admission and after 24 hours. The difference between the 2 measurements was considered as the MPV change (ΔMPV). The end point of the study was total mortality at 1-year follow-up. During the follow-up, there were 49 deaths (12.2%). Admission MPV was comparable in the 2 groups. However, both MPV (9.6 ± 1.4 fL vs 9.2 ± 1.0 fL, P = .044) and ΔMPV (0.40 [0.10-0.70] fL vs 0.70 [0.40-1.20] fL, P < .001) at the first 24 hours were higher in nonsurvivors than survivors. In multivariate analysis, ΔMPV was an independent predictor of total mortality (odds ratio: 1.84, 95% confidence interval: 1.28-2.65, P = .001). An early increase in MPV after admission was independently associated with total mortality in patients with NSTEMI. Such patients may need more effective antiplatelet therapy.

A high admission RDW level in patients with acute AMI undergoing a primary percutaneous coronary intervention was associated with an increased risk for intrahospital cardiovascular mortality, but was not associated with worse postinterventional TIMI flow.

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.