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BACKGROUND Vascular healing response associated with adjunctive n‐3 polyunsaturated fatty acid therapy therapy in patients receiving strong statin therapy remains unclear. The aim of this study was to evaluate the effect of polyunsaturated fatty acid therapy with eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) in addition to strong statin therapy on coronary atherosclerotic plaques using optical coherence tomography. METHODS AND RESULTS This prospective multicenter randomized controlled trial included 130 patients with acute coronary syndrome treated with strong statins. They were assigned to either statin only (control group, n=42), statin+high‐dose EPA (1800 mg/day) (EPA group, n=40), statin+EPA (930 mg/day)+DHA (750 mg/day) (EPA+DHA group, n=48). Optical coherence tomography was performed at baseline and at the 8‐month follow‐up. The target for optical coherence tomography analysis was a nonculprit lesion with a lipid plaque. Between baseline and the 8‐month follow‐up, fibrous cap thickness (FCT) significantly increased in all 3 groups. There were no significant differences in the percent change for minimum FCT between the EPA or EPA+DHA group and the control group. In patients with FCT

BackgroundUrinary neutrophil gelatinase‐associated lipocalin (U‐NGAL) is an early predictor of acute kidney injury and adverse events in various diseases; however, in acute decompensated heart failure patients, its significance remains poorly understood. This study aimed to investigate the prognostic value of U‐NGAL on the first day of admission for the occurrence of acute kidney injury and long‐term outcomes in acute decompensated heart failure patients. Methods and ResultsWe studied 260 acute decompensated heart failure patients admitted to our department between 2011 and 2014 by measuring U‐NGAL in 24‐hour urine samples collected on the first day of admission. Primary end points were all‐cause death, cardiovascular death, and heart failure admission. Patients were divided into 2 groups according to their median U‐NGAL levels (32.5 μg/gCr). The high‐U‐NGAL group had a significantly higher occurrence of acute kidney injury during hospitalization than the low‐U‐NGAL group (P=0.0012). Kaplan‐Meier analysis revealed that the high‐U‐NGAL group exhibited a worse prognosis than the low‐U‐NGAL group in all‐cause death (hazard ratio 2.07; 95%CI 1.38‐3.12, P=0.0004), cardiovascular death (hazard ratio 2.29; 95%CI 1.28‐4.24, P=0.0052), and heart failure admission (hazard ratio 1.77; 95%CI 1.13‐2.77, P=0.0119). The addition of U‐NGAL to the estimated glomerular filtration rate significantly improved the predictive accuracy of all‐cause mortality (P=0.0083). ConclusionsIn acute decompensated heart failure patients, an elevated U‐NGAL level on the first day of admission was related to the development of clinical acute kidney injury and independently associated with poor prognosis.

In May 2005 a 68-year-old woman received a VDD pacemaker implantation in the right pectoral region at our hospital for the treatment of complete atrioventricular block. In July 2008, she was diagnosed with dilated cardiomyopathy based on histological testing. In November 2008, she developed syncope due to ventricular tachycardia while at another hospital. She underwent external electrical cardioversion with an anterior-lateral paddle position using a single shock of 100 J. This shock led to severe bradycardia resulting in a transfer to our hospital. The physician who provided the shock could not have been aware that the patient had an implanted pacemaker. The skin above the pulse generator was burned. The electrocardiogram showed no pacing spikes or ventricular escape rhythm. Investigation of the pacemaker 3 hours after cardioversion revealed reprogramming of the device and a marked rise in the lead impedance (>3,000 ohm). Removal of the generator and implantation of a biventricular cardioverter defibrillator were required. The emergency situation, the small size of the generator, the small incision made using the buried suture method, and the patient's obesity all probably contributed to the physician's not noticing the implanted pacemaker. It is important to increase awareness of the severe consequences that may follow if the physician administering external defibrillation does not know about the patient's implanted pacemaker.