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Aims Although tolvaptan has been reported to prevent worsening renal function (WRF) in patients with advanced acute heart failure (AHF), evidence regarding the effect of tolvaptan on renal function in patients with new-onset AHF is not available. This study aimed to investigate the renoprotective effect of tolvaptan in patients hospitalized with new-onset AHF. Methods and results A total of 122 consecutive patients hospitalized with new-onset AHF between May 2015 and December 2018 were retrospectively evaluated. WRF was defined as an absolute increase in serum creatinine ≥0.3 mg/dL (≥26.4 μmol/L) within 48 h or a 1.5-fold increase in serum creatinine after hospitalization. The furosemide group (n = 75) and the tolvaptan add-on group (n = 47) were compared. The tolvaptan group consists of patients who received tolvaptan as an individual physicians' decision. The incidence of WRF was significantly lower in the tolvaptan add-on group (8.5%) than in the furosemide group (24.0%, P = 0.03). Multivariate logistic regression analysis revealed that tolvaptan treatment was an independent variable related to the prevention of WRF [odds ratio (OR), 0.20; 95% confidence interval (CI), 0.05-0.85]. Furthermore, subgroup analysis revealed a more favourable effect of tolvaptan in patients with serum creatinine ≥1.1 mg/dL on admission (OR, 0.23; 95% CI, 0.06-0.98) and an ejection fraction <50% (OR, 0.19; 95% CI, 0.04-0.90). Conclusions A lower incidence of WRF was observed in patients with new-onset AHF who were treated with the tolvaptan add-on therapy, specifically those with left ventricular systolic dysfunction and renal impairment on admission.

A 72-year-old woman with hypertension, dyslipidemia, and diabetes mellitus presented to our hospital because of the sudden onset of chest pain. Emergency coronary angiography showed acute occlusion of the distal left anterior descending artery and coronary intervention with a drug-eluting stent was performed. Sudden cardiopulmonary arrest occurred on the sixth day of hospitalization, but coronary angiography showed no remarkable progression of the coronary artery diseases, including the site of stent implantation. An autopsy revealed that the cause of the sudden death was apical free wall rupture. In addition, the different timing of acute and sub-acute infarct findings were observed in the apical wall by histology, which indicated cardiac rupture was due to reinfarction at early phase of apical acute myocardial infarction. Although the rate of mechanical complications, including cardiac rupture, is decreasing in the era of primary coronary intervention, in addition to the well-known risk factors of cardiac rupture, the reinfarction of the culprit myocardial site in the early phase of acute myocardial infarction was considered as a possible risk factor of cardiac rupture.(Int Heart J 2019; 60: 974-978)

Methods Subjects A total of 250 consecutive patients with OHCA who underwent immediate CT and CAG between January 2011 and December 2018 were enrolled. Because coronary stent and ectopic calcification interfere with precise evaluation of coronary artery calcification, patients with a prior history of coronary artery stent implantation or those on regular hemodialysis (n=64) and those who did not return to spontaneous cardiac rhythm (n=6) were excluded from this study. Informed consent was obtained by an opt-out procedure from all patients. The study protocol was approved by the ethics committee of Kansai Medical University Medical Center and Kansai Medical University. Management OHCA patients were given continuous cardiopulmonary resuscitation in accordance with the Basic/Advanced Cardiac Life Support guideline. 10-12 Patients with continuous cardiac arrest at hospital arrival received extracorporeal membrane oxygenation by the attending emergency physician.