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.

The relationship between epicardial adipose tissue (EAT) and coronary artery disease has been predominantly demonstrated in the last two decades. The aim of this study was to investigate the predictive value of EAT thickness on ST-segment resolution that reflects myocardial reperfusion in patients undergoing primary percutaneous coronary intervention (pPCI) for acute ST-segment elevation myocardial infarction (STEMI). The present study prospectively included 114 consecutive patients (mean age 54 ± 10 years, range 35-83, 15 women) with first acute STEMI who underwent successful pPCI. ST-segment resolution (ΔSTR) <70 % was accepted as ECG sign of no-reflow phenomenon. The EAT thickness was measured by two-dimensional echocardiography. EAT thickness was increased in patients with no-reflow (3.9 ± 1.7 vs. 5.4 ± 2, p = 0.001). EAT thickness was also found to be inversely correlated with ΔSTR (r = -0.414, p = 0.001). Multivariate logistic regression analysis demonstrated that EAT thickness independently predicted no-reflow (OR 1.43, 95 % CI 1.13-1.82, p = 0.003). Receiver operating characteristic curve analysis demonstrated good diagnostic accuracy for EAT thickness in predicting no-reflow [area under curve (AUC) = 0.72, 95 % CI 0.63-0.82, p < 0.001]. In conclusion, increased EAT thickness may play an important role in the prediction of no-reflow in STEMI treated with pPCI.

No abstract

Superwarfarins (brodifacoum, difenacoum, bromodialone and chlorphacinone) are anticoagulant rodenticides that were developed in 1970s to overcome resistance to warfarin in rats. A 26-year-old previously healthy man was admitted to the emergency department with epigastric pain, severe upper and lower gastrointestinal haemorrhage, gingival bleeding and melena. The patient stated that he had been healthy with no prior hospital admissions and no personal or family history of bleeding diathesis. The patient, who later admitted attempted suicide, stated that he had taken 400 g rodenticide including brodifacoum orally for five days prior to admission to hospital. He had oral mucosal bleeding, numerous bruises over the arms, legs and abdomen, and an abdominal tenderness, together with melena. Laboratory tests revealed a haemoglobin level of 12.3 g/dl, leucocyte count of 9.1 × 10(9) /l, haematocrit of 28% and platelet count of 280 × 10(9) /l. The prothrombin time (PT) was > 200 s (normal range 10.5-15.2 s) and the activated partial thromboplastin time (aPTT) was 91 s (normal range 20-45 s). The INR (International normalised ratio) was reported to be > 17 (normal range 0.8-1.2). The thrombin time and plasma fibrinogen levels were in the normal range. The results showed the presence of brodifacoum at a concentration of 61 ng/ml, detected by reversed-phase liquid chromatography.

Background: Development of contrast-induced acute kidney injury (CI-AKI) in patients with ST-elevation myocardial infarction (STEMI) treated via primary percutaneous coronary intervention (PCI) is a major cause of morbidity and mortality worldwide. The neutrophil-to-lymphocyte ratio (NLR), which is a marker of inflammation, has been demonstrated to be associated with the development of major adverse cardiovascular outcomes in many studies. From this point of view, in this study, we aimed to evaluate the predictive value of the NLR as regards the occurrence of CI-AKI in patients with STEMI undergoing primary PCI. Methods: This study was conducted at Dr. Siyami Ersek Training and Research Hospital from May 2008 to June 2016. A total of 2000 patients with STEMI treated via primary PCI were enrolled in the study. The NLR was calculated as the ratio of the number of neutrophils to the number of lymphocytes. All venous blood samples were obtained within 8 hours after admission. CI-AKI was the primary end point of the study. Then, the relationship between CI-AKI and the NLR was assessed. Results: CI-AKI was detected in 148 (7.4%) patients. The patients who developed CI-AKI had a significantly higher NLR than those who did not (7.08±4.43 vs. 6.18±3.98; P=0.011). In the multivariate logistic regression analyses, the NLR remained a significant independent predictor of CI-AKI (OR: 1.78, 95% CI: 1.21–2.61, and P=0.003). Conclusion: The NLR may be a significant independent predictor of CI-AKI in patients with STEMI treated via primary PCI and higher NLR values could be independently associated with a greater risk for CI-AKI.   J Teh Univ Heart Ctr 2019;14(2):59-66   This paper should be cited as: Tanık VO, Çınar T, Velibey Y, Öz A, Kalenderoğlu K, Gümüşdağ A, Aruğaslan E, Keskin M, Eren M. Neutrophil-to-Lymphocyte Ratio Predicts Contrast-Induced Acute Kidney Injury in Patients with ST-Elevation Myocardial Infarction Treated with Primary Percutaneous Coronary Intervention.  J Teh Univ Heart Ctr 2019;14(2):59-66.

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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.