Effect of Tofogliflozin on Systolic and Diastolic Cardiac Function in Type 2 Diabetic Patients.

PURPOSE: Recent studies have shown that sodium glucose cotransporter 2 (SGLT2) inhibitors have a favorable effect on cardiovascular events in diabetic patients. However, the underlying mechanism associated with a favorable outcome has not been clearly identified. The purpose of this study was to investigate the effect of tofogliflozin, SGLT2 inhibitor, on systolic and diastolic cardiac function in patients with type 2 diabetes mellitus (T2DM). METHODS: We enrolled 26 consecutive T2DM out-patients on glucose-lowering drugs who initiated tofogliflozin and underwent echocardiography before and ≥ 6 months after tofogliflozin administration. During this period, we also enrolled 162 T2DM out-patients taking other glucose-lowering drugs as a control group. Propensity score analysis was performed to match the patient characteristics. As a result, 42 patients (tofogliflozin group 21 patients and control group 21 patients) were finally used for analysis. Left ventricular systolic function was assessed by measuring 2D-echocardiographic left ventricular ejection fraction (LVEF) and diastolic cardiac function by pulsed wave Doppler-derived early diastolic velocity (E/e'). RESULTS: There were no significant differences in patient characteristics and echocardiographic parameters at baseline. The change in LVEF from baseline to follow-up was 5.0 ± 6.9% in the tofogliflozin group and - 0.6 ± 5.5% in the control group; difference significant, p = 0.006. The change in E/e' was - 1.7 ± 3.4 in the tofogliflozin group and 0.7 ± 4.1 in the control group; difference significant, p = 0.024. CONCLUSIONS: In addition to conventional oral glucose-lowering drugs, additional tofogliflozin administration had a favorable effect on left ventricular systolic and diastolic function in patients with T2DM.

Cardiac Rupture Due to Reinfarction in the Early Phase of Apical Myocardial Infarction.

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.

Renoprotective effect of tolvaptan in patients with new-onset acute heart failure.

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.

Clinical Implication of Coronary Artery Calcium Score in Survivors of Out-of-Hospital Cardiac Arrest.

Background: The aim of this study was to evaluate the clinical ability of coronary artery calcium (CAC) score to identify acute myocardial infarction (AMI) in survivors of out-of-hospital cardiac arrest (OHCA). Methods and Results: We studied 180 consecutive survivors of OHCA who underwent immediate non-contrast computed tomography (CT) and coronary angiography. Seventy-one patients had ST elevation or left bundle branch block (LBBB; group 1) and 109 patients did not have ST elevation or LBBB (group 2) on post-resuscitation electrocardiogram (ECG). CAC score was significantly higher in AMI compared with non-AMI in groups 1 and 2. The optimal cut-off of CAC score to identify AMI was 11.5 (sensitivity, 80%; specificity, 71%) in group 1, and 27.4 (sensitivity, 80%; specificity, 76%) in group 2. On multivariate analysis, CAC score was the strongest predictive marker of AMI (OR, 10.91; 95% CI: 6.00-25.97). In addition, CAC score was an independent predictor of 30-day survival (OR, 0.38; 95% CI: 0.15-0.95). Conclusions: Evaluation of CAC is a useful method to identify AMI in survivors of OHCA, regardless of ST changes on post-resuscitation ECG.