Objective: Contrast-induced nephropathy (CIN) is associated with significantly increased morbidity and mortality after percutaneous coronary intervention (PCI). Patients with acute coronary syndrome (ACS) are at higher risk of CIN. The platelet-to-lymphocyte ratio (PLR) is closely linked to inflammatory conditions. We hypothesized that PLR levels on admission can predict the development of CIN after PCI for ACS. Subjects and Methods: A total of 426 patients (mean age 63.17 ± 13.01 years, 61.2% males) with ACS undergoing PCI were enrolled in this study. Admission PLR levels were measured before PCI. Serum creatinine values were measured before and within 72 h after the administration of contrast agents. Patients were divided into 2 groups: the CIN group and the no-CIN group. CIN was defined as an increase in serum creatinine level of ≥0.5 mg/dl or 25% above baseline within 72 h after contrast administration. Results: CIN developed in 53 patients (15.9%). Baseline PLR was significantly higher in patients who developed CIN compared to those who did not (160.8 ± 29.7 and 135.1 ± 26.1, respectively; p < 0.001). Multivariate analyses found that PLR [odds ratio (OR) 3.453, 95% confidence interval (CI) 1.453-8.543; p = 0.004] and admission creatinine (OR 6.511, 95% CI 1.759-11.095; p = 0.002) were independent predictors of CIN. Conclusions: The admission PLR level is an independent predictor of the development of CIN after PCI in ACS.

Turkeye relationship between lipoprotein(a) and coronary artery disease, as well as its variable nature following myocardial infarction AbstractPurpose: e present study aimed to investigate the relationship between the severity of coronary artery disease (CAD) and level of Lipoprotein (LP)(a).Methods: e study included 52 CAD patients and a control group consisting of 38 individuals. e patients were classi ed into three groups based on the clinical form of CAD (stable angina pectoris, SAP, unstable angina pectoris,UAP, and myocardial infarction,MI), and were further divided into three groups based on CAD severity (1-, 2-and 3-vessel). Serum Lp(a) levels were monitored 4, 8, and 24 h, 10 and 30 days following acute MI in 18 patients.Results: Based on regression analysis, Lp(a) was not correlated with other lipoproteins or with risk factors of CAD, such as body mass index, smoking, family history, diabetes, age, gender, and hypertension (r = 0.08-0.22). 72% of the patients in the CAD group and 24% of the control group had an Lp(a) level >30 mg dL -1 (P = 0.004), and Lp(a) levels were higher in 3-vessel patients than in 2-vessel and 1-vessel CAD patients (86% vs. 68%, P = 0.02 and 86% vs. 62%, P=0.01, respectively). Serum Lp(a) levels were higher in the UAP and MI groups than in the SAP group (48 ± 44.7 mg dL -1 , 49 ± 36.1 mg dL -1 and 31.2 ± 22.3 mg dL -1 , respectively,P=0.02). Lp(a) levels increased a er acute MI, and reached peak levels 10 days post-MI (41% increase, P=0.001) and remained considerably elevated (18%) 30 days post-MI (P=0.01).Conclusion: Serum Lp(a) was higher in the UAP and MI patients in comparison with the SAP patients, and was higher in 3-vessel CAD in comparison with 1-and 2-vessel CAD patients.

No abstract