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Background: Acute cardiorenal syndrome type 1 (CRS-1) is defined by a rapid cardiac dysfunction leading to acute kidney injury (AKI). Neutrophil gelatinase-associated lipocalin (NGAL) is expressed on the surface of human neutrophils and epithelial cells, such as renal tubule cells, and its serum (sNGAL) and urinary have been used to predict AKI in different clinical settings., Aim: To characterize CRS-1 in a cohort of patients with acute heart diseases, evaluating the potentiality of sNGAL as an early marker of CRS-1., Methods: We performed a retrospective cohort, multi-centre study. From January 2010 to December 2011, we recruited 202 adult patients admitted to the coronary intensive care unit (CICU) with a diagnosis of acute heart failure or acute coronary syndrome. We monitored the renal function to evaluate CRS-1 development and measured sNGAL levels within 24 h and after 72 h of CICU admission., Results: Overall, enrolled patients were hemodynamically stable with a mean arterial pressure of 92 (82-107) mmHg, 55/202 (27.2%) of the patients developed CRS-1, but none of them required dialysis. Neither the NGAL delta value (AUC 0.40, 95%CI: 0.25-0.55) nor the NGAL peak (AUC 0.45, 95%CI: 0.36-0.54) or NGAL cut-off (≥ 140 ng/mL) values were statistically significant between the two groups (CRS-1 vs no-CRS1 patients). The area under the ROC curve for the prediction of CRS-1 was 0.40 (95%CI: 0.25-0.55) for the delta NGAL value and 0.45 (95%CI: 0.36-0.54) for the NGAL peak value. Finally, in multivariate analysis, the risk of developing CRS-1 was correlated with age > 60 years, urea nitrogen at admission and 24 h-urine output (AUC 0.83, SE = 60.5% SP = 93%), while sNGAL was not significantly correlated., Conclusion: In our population, sNGAL does not predict CRS-1, probably as a consequence of the mild renal injury and the low severity of heart disease. So, these data might suggest that patient selection should be taken into account when considering the utility of NGAL measurement as a biomarker of kidney damage., Competing Interests: Conflict-of-interest statement: Ronco C is a consultant of Astute Medical, OCD, Asahi Medical, Baxter, Toray Medical. None of the other authors have any financial interest related to this study to disclose. DC received an honorarium from Inverness Medical Inc. for a speech., (©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.)

Acute decompensated heart failure and fluid overload are the most common causes of hospitalization in heart failure patients and they often contribute to disease progression. Initial treatment encompasses intravenous diuretics, although there might be a percentage of patients refractory to this pharmacologic approach. New technologies have been developed to perform extracorporeal ultrafiltration in fluid-overloaded patients. Newer simplified devices permit ultrafiltration to be performed with peripheral venous access and low blood flows, making ultrafiltration feasible at most hospitals and acute care settings. Extracorporeal ultrafiltration then is prescribed and conducted by specialized teams and fluid removal is planned to restore a status of hydration close to normal. Recent clinical trials, and European and North American practice guidelines, suggest that ultrafiltration is reasonable for patients with refractory congestion not responding to medical therapy and assigned to this recommendation a class IIa, level of evidence B. It seems that a close collaboration between nephrologists and cardiologists may be the key for a collaborative therapeutic effort in heart failure patients. Further studies suggest that wearable technologies might become available soon to treat patients in ambulatory and de-hospitalized settings. These new technologies may help to cope with the increasing demand for care of chronic heart failure patients., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Background: Reperfusion remains the definitive treatment for acute myocardial infarction (AMI), but restoring blood flow carries the potential to exacerbate the ischemia-related injury. Postconditioning might modify reperfusion-induced adverse events., Study Design: The POSTconditioning during Coronary Angioplasty in Acute Myocardial Infarction (POST-AMI) trial is a single-center, prospective, randomized study, with a planned inclusion of 78 patients with ST-elevation AMI. Patients will be randomly assigned to the postconditioning arm [primary angioplasty (PA) and stenting followed by brief episodes of ischemia-reperfusion early after recanalization] or non-postconditioning arm. All patients will be treated medically according to current international guidelines, including glycoprotein IIb/IIIa inhibitors before PA. The primary end point is to evaluate whether postconditioning, compared to plain PA, reduces infarct size estimated by cardiac magnetic resonance (CMR) at 30 +/- 10 days after the AMI. Secondary end points are microvascular obstruction observed at CMR, ST-segment resolution, angiographic myocardial blush grade <2, non-sustained/sustained ventricular tachycardia in the 48 h following PA, left ventricular remodeling and function at follow-up CMR, and the reduction of major adverse cardiac events at 30 days and 6 months., Conclusion: The POST-AMI trial will evaluate the usefulness of postconditioning in limiting infarct size during the early and late phases after AMI., (Copyright 2010 S. Karger AG, Basel.)

Purpose: To evaluate the immediate and midterm outcome and analyze the debris captured after repeat endovascular intervention for the treatment of in-stent restenosis after carotid artery stenting (CAS)., Methods: Thirty-one consecutive patients (27 men; mean age 63.7+/-13.0 years, range 53- 81) underwent repeat endovascular intervention (balloon angioplasty and provisional stenting) for the treatment of 32 in-stent restenoses following CAS., Results: Procedural success was achieved in all patients. An additional stent was implanted in 10 (31%) cases. No procedural complication was observed. Filter analysis was performed in 17 (53%) procedures; on 12 (71%), macroscopically visible material was captured. The histomorphometric analysis performed on 6 (19%) filters showed fibrin nets entrapping erythrocytes, leucocytes, platelets, and in 2 cases, fibrous hypercellular tissue fragments. At 30 days and during follow-up (mean 17+/-5 months), no deaths, transient ischemic attacks, or strokes were observed. In 1 (3.1%) patient, asymptomatic recurrence of ISR was found on Doppler ultrasonography and successfully treated with balloon angioplasty., Conclusion: Repeat endovascular intervention using balloon angioplasty with provisional stenting and routine cerebral protection appears to be a feasible, safe, and clinically effective strategy for the treatment of in-stent restenosis after CAS.