Background: The risk of contrast-induced acute kidney injury (CI-AKI) following coronary intervention is particularly high among patients with chronic kidney disease (CKD). Among these patients, baseline neutrophil gelatinase-associated lipocalin (NGAL), a marker of tubular damage, reflects the severity of renal impairment. We evaluated whether the baseline serum NGAL level may be a marker for the development of CI-AKI following percutaneous coronary intervention (PCI). Methods: Eighty-eight CKD patients treated with PCI were included. Serum NGAL levels were drawn upon hospital admission. Receiver operator characteristic (ROC) methods were used to identify the optimal sensitivity and specificity for the observed NGAL level compared with the estimated glomerular filtration rate (eGFR) calculated for patients with CI-AKI. Results: Overall CI-AKI incidence was 43%. Baseline serum NGAL levels were significantly higher in patients with CI-AKI than in patients without CI-AKI (150 vs. 103 ng/mL, p < 0.001). According to the ROC curve, baseline NGAL levels performed better than eGFR to predict CI-AKI (AUC 0.753 vs. 0.604), with the optimal cutoff value for baseline NGAL to predict CI-AKI being 127 ng/mL (sensitivity of 68% and specificity of 68%, p < 0.001). In a multivariate logistic regression model, the NGAL level >127 ng/mL ng/mL was independently associated with CI-AKI (HR 9.84, 95% CI: 1.96–40.3; p = 0.01). Conclusion: Baseline serum NGAL levels in CKD patients may identify a high-risk population for CI-AKI following PCI. Further studies on larger populations are required to validate the potential utility of NGAL measurements in monitoring specific CKD-associated conditions.

Physicians use Holter electrocardiography (ECG) monitoring to evaluate some patients with syncope in the internal medicine department. We questioned whether Holter ECG should be used in the presented setting. Included were all consecutive patients admitted with syncope to one of our nine internal medicine departments who had completed a 24 h Holter ECG between 2018 and 2021. A diagnostic Holter was defined as one which altered the patient’s treatment and met ESC/ACC/AHA diagnostic criteria. A total of 478 Holter tests were performed for syncope evaluation during admission to an internal medicine department in the study period. Of them, 25 patients (5.2%) had a diagnostic Holter finding. Sinus node dysfunction was the most frequent diagnostic recording (13 patients, 52%). In multivariant analysis, predictors for diagnostic Holter were older age (OR 1.35, 95% CI 1.08–1.68), heart failure with preserved ejection fraction (OR 4.1, 95% CI 1.43–11.72), and shorter duration to Holter initiation (OR 0.73, 95% CI 0.56–0.96). There was a positive correlation between time from admission to Holter and hospital stay, r(479) = 0.342, p < 0.001. Our results suggest that completing a 24 h Holter monitoring during admission to the internal medicine department should be restricted to patients with a high pre-test probability to avoid overuse and possible harm.

Recent practice guidelines recommended the use of new stress, functional, and damage biomarkers in clinical practice to prevent and manage acute kidney injury (AKI). Biomarkers are one of the tools used to define various AKI phenotypes and provide prognostic information regardless of an acute decline in renal function. We investigated the incidence and possible implications of AKI phenotypes among ST elevation myocardial infarction patient treated with primary coronary intervention. We included 281 patients with STEMI treated with PCI. Neutrophil gelatinase associated lipocalin (NGAL) was utilized to determine structural renal damage and functional AKI was determined using the KDIGO criteria. Patients were stratified into four AKI phenotypes: no AKI, subclinical AKI, hemodynamic AKI, and severe AKI. Patients were assessed for in-hospital adverse events (MACE). A total of 46 patients (44%) had subclinical AKI, 17 (16%) had hemodynamic AKI, and 42 (40%) had severe AKI. We observed a gradual and significant increase in the occurrence of MACE between the groups being highest among patients with severe AKI (10% vs. 19% vs. 29% vs. 43%; p < 0.001). In a multivariable regression model, any AKI phenotype was independently associated with MACE with an odds ratio of 4.15 (95% CI 2.1–8.3, p < 0.001,) for subclinical AKI, 4.51 (95% CI 1.61–12.69; p = 0.004) for hemodynamic AKI, and 12.9 (95% CI 5.59–30.1, p < 0.001) for severe AKI. In conclusion, among STEMI patients, AKI is a heterogeneous condition consisting of distinct phenotypes, addition of novel biomarkers may overcome the limitations of sCr-based AKI definitions to improve AKI phenotyping and direct potential therapies.

Coronary microvascular dysfunction (CMD) is increasingly recognized as a cause of angina in patientswith or without epicardial coronary artery disease. Emerging evidence suggests a pathophysiologic relationship between CMD and atrial fibrillation (AF), but few studies have evaluated this association using invasive microvascular assessment. We performed a single-center, retrospective analysis of prospectively collected data of consecutive patients undergoing clinically indicated invasive assessment of coronary microvascular function between November 2019 and January 2025. All patients underwent invasive coronary angiography with physiological assessment in the left anterior descending artery, including fractional flow reserve (FFR), coronary flow reserve (CFR), index of microvascular resistance (IMR), and resistive reserve ratio (RRR). CMD was defined by the presence of at least one abnormal parameter: CFR 25, or RRR <3.5. AF was defined as a documented history of atrial fibrillation in medical records prior to the procedure, classified as paroxysmal, persistent, or permanent. CMD was present in 219/422 patients (52%; median age 69 years; 55% female). AF was more prevalent in CMD vs. non-CMD patients (13% vs. 6%, p = 0.019). Among the 42 patients with AF, 30 (71%) had paroxysmal, 5 (12%) persistent, and 7 (17%) permanent AF; persistent or permanent AF was more common in CMD patients with AF (38% vs. 8%). In multivariable analysis, AF was independently associated with CMD (adjusted OR 2.19, 95% CI 1.07-4.63, p = 0.031), along with older age and ischemic heart disease. CMD patients with AF had higher LV filling pressures, reduced RV systolic function, and larger left atrial volume index. AF is independently associated with CMD, with a higher prevalence of persistent/permanent AF among CMD patients. These findings suggest a bidirectional relationship warranting further investigation in larger prospective cohorts.