We assessed the relation between platelet-to-lymphocyte ratio (PLR) on admission and contrast-induced nephropathy (CIN) in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS). A total of 488 patients with NSTE-ACS who underwent urgent coronary angiography were enrolled. Levels of PLR and creatinine were measured before angiography and at 72 hours after angiography. Patients were divided into 2 groups, namely, the CIN group, 80 patients (16.3%; age 65.3 ± 12.5years; 66.7% men) and the non-CIN group, 408 patients (83.7%; age 61.2 ± 12.3 years; 72.5% men). Patients in the CIN group had significantly higher PLR than those in the non-CIN group (152.9 ± 99.6 vs 120.4 ± 66.1, P < .001). In logistic regression analysis, PLR (odds ratio [OR] 1.004, 95% confidence interval [CI] 1.001-1.007, P = .02), diabetes mellitus (OR 1.75, 95% CI 1.02-2.98, P = .03), and ST-segment depression on admission electrocardiogram (OR 1.68, 95% CI 1.00-2.81, P = .04) were independent predictors of CIN. The PLR was an independent predictor of CIN after angiography in patients with NSTE-ACS.

Contrast-induced acute kidney injury (CI-AKI) is associated with increased mortality, morbidity, and prolonged hospitalization. Patients with acute coronary syndrome (ACS) have a 3-fold higher risk of developing CI-AKI. The aim of our study was to evaluate the predictors of CI-AKI and long-term prognosis in patients with ACS who developed CI-AKI (1083 patients were enrolled). Contrast-induced acute kidney injury was defined as an increase of ≥0.5 mg/dL and/or an increase of ≥25% of pre-percutaneous coronary intervention (PCI) to post-PCI serum creatinine levels within 48 to 72 hours after the procedure. Primary end point was defined as all-cause mortality, myocardial infarction, and cerebrovascular event at long-term follow-up (36 ± 12 months). Contrast-induced acute kidney injury occurred in 178 (16.4%) of the 1083 patients. The primary end points were significantly high in patients with ACS who developed CI-AKI (P < .001). The occurrence of CI-AKI was identified as an independent predictor of primary end point. Risk of CI-AKI development was more frequently seen in patients with ACS. Also, patients who developed CI-AKI have worse prognosis at long-term follow-up. Additional preventive treatment strategies need to be developed in this group of patients.

Background/Objectives: Inflammation contributes to atherosclerotic progression and may intensify after percutaneous coronary intervention (PCI). In stable coronary artery disease (CAD), whether post-procedural inflammation is prognostically distinct from baseline inflammatory status and post-procedural renal function remains unclear. Methods: We studied 496 consecutive patients with stable CAD undergoing elective PCI. The primary outcome was a composite of death, myocardial infarction, stroke, or repeat revascularization. Post-PCI high-sensitivity C-reactive protein (hs-CRP) and creatinine were measured 18–24 h after PCI. Multivariable Cox models used clinically prespecified covariates, with hs-CRP log-transformed (hazard ratio [HR] per doubling) and additionally adjusted for its pre-PCI level; discrimination was assessed by ROC analysis with bootstrap internal validation. Results: The endpoint occurred in 43 patients (8.7%) over a median follow-up of 10 months. Post-PCI hs-CRP was independently associated with the endpoint after adjustment for pre-PCI hs-CRP, post-PCI creatinine, and albumin (HR 1.43 per doubling, 95% CI 1.05–1.96, p = 0.025), and after further adjustment for angiographic and procedural characteristics (HR 1.54, p = 0.008); pre-PCI hs-CRP was not independent (p = 0.083). Post-PCI creatinine was independently associated in every model (HR 1.16 per 0.1 mg/dL, p = 0.001) and identified a largely non-overlapping high-risk group. Conclusions: After elective PCI in stable CAD, post-PCI hs-CRP was independently associated with adverse outcomes and provided prognostic information beyond baseline hs-CRP and procedural characteristics in the fitted models, rather than merely reflecting baseline inflammatory status. Post-PCI renal function was a complementary, largely independent risk signal.

Background: Non-dipping blood pressure pattern, characterized by a blunted nocturnal decline in blood pressure, is associated with increased cardiovascular morbidity and mortality. Restless legs syndrome (RLS) has been linked to sympathetic hyperactivity and altered circadian regulation, potentially contributing to abnormal blood pressure patterns. This study aimed to evaluate the relationship between RLS and non-dipping pattern in patients undergoing ambulatory blood pressure monitoring. Methods: In this prospective observational study, 501 eligible participants were included after excluding those with obstructive sleep apnea syndrome, type 1 diabetes, or morbid obesity. RLS was diagnosed according to National Institutes of Health consensus criteria using clinical assessment, the International RLS Study Group scale, and the Berlin Questionnaire. A non-dipping pattern was defined as <10% nocturnal reduction in mean systolic or diastolic blood pressure. Results: RLS was diagnosed in 158 patients (31.5%). Compared with controls, RLS patients were more often female and had higher rates of diabetes and hyperlipidemia. Non-dipping was significantly more prevalent in the RLS group (69.0% vs 48.7%, P < .001), accompanied by lower systolic and diastolic blood pressure variability (both P < .001). In multivariable logistic regression, independent predictors of RLS included female sex (β = 0.701, P = .049), hyperlipidemia (β = 0.850, P = .031), and non-dipping status (β = 1.057, P < .001). Receiver operating characteristic analysis demonstrated modest predictive ability (area under the curve = 0.601; 95% confidence interval 0.557–0.645). Conclusions: RLS is independently associated with a non-dipping blood pressure pattern, even after excluding major confounders. These findings suggest a shared autonomic mechanism linking RLS with impaired nocturnal blood pressure regulation and heightened cardiovascular risk.