Relationship Between Impaired Microvascular Function in the Non-Infarct-Related Area and Left Ventricular Remodeling in Patients With Myocardial Infarction

Background. Myocardial flow reserve (MFR) in the non-infarct-related area (NIRA) has been reported to be impaired after the onset of myocardial infarction (MI). The aim of this study was to determine whether microvascular dysfunction in the NIRA is related to left-ventricular remodeling after MI. Methods. We prospectively studied 17 patients who suffered their first single-vessel MI, and who underwent successful revascularization. The MFR in the NIRA was assessed quantitatively using ^13N-ammonia positron emission tomography within 2 weeks after the onset. Peak creatinine kinase and the defect score on ^<99m>Tc-tetrofosmin myocardial perfusion imaging were used as an index of the severity of MI. The left-ventricular end-diastolic volume index (LVEDVI) was calculated using left ventriculography at 1 month and 6 months after the onset. Results. Patients with severely impaired MFR (< 2.09) had higher peak creatinine kinase values (6,000 ± 5,485 IU/L vs. 2,250 ± 1,950 IU/L, p = 0.0081), defect scores (16.3 ± 5.9 vs. 7.9 ± 6.5, p = 0.0404), and LVEDVI at 1 month (125.6 ± 34.4 mL/m^2 vs. 82.8 ± 17.7 mL/m^2, p = 0.0036) than those with mildly impaired MFR (≥ 2.09). Moreover, the differences of LVEDVI between the 2 groups persisted over 6 months (133.3 ± 43.6 mL/m^2 vs. 89.5 ± 17.3 mL/m^2, p = 0.0078). The MFR in the NIRA correlated inversely with the LVEDVI at 1 month and 6 months (r = -0.590, p = 0.0127 and r = -0.729, p = 0.0031, respectively). Conclusions. These data indicate that microvascular impairment in the NIRA might have contributed to left-ventricular remodeling after MI

A comprehensive validation of very early rule-out strategies for non-ST-segment elevation myocardial infarction in emergency departments:protocol for a multicentre prospective cohort study

Introduction: Recent advances in troponin sensitivity enabled early and accurate judgement of ruling-out myocardial infarction, especially non-ST elevation myocardial infarction (NSTEMI) in emergency departments (EDs) with development of various prediction-rules and high-sensitive-troponin-based strategies (hs-troponin). Reliance on clinical impression, however, is still common, and it remains unknown which of these strategies is superior. Therefore, our objective in this prospective cohort study is to comprehensively validate the diagnostic accuracy of clinical impression-based strategies, prediction-rules and hs-troponin-based strategies for ruling-out NSTEMIs. Methods and analysis: In total, 1500 consecutive adult patients with symptoms suggestive of acute coronary syndrome will be prospectively recruited from five EDs in two tertiary-level, two secondary-level community hospitals and one university hospital in Japan. The study has begun in July 2018, and recruitment period will be about 1 year. A board-certified emergency physician will complete standardised case report forms, and independently perform a clinical impression-based risk estimation of NSTEMI. Index strategies to be compared will include the clinical impression-based strategy; prediction rules and hs-troponin-based strategies for the following types of troponin (Roche Elecsys hs-troponin T; Abbott ARCHITECT hs-troponin I; Siemens ADVIA Centaur hs-troponin I; Siemens ADVIA Centaur sensitive-troponin I). The reference standard will be the composite of type 1 MI and cardiac death within 30 days after admission to the ED. Outcome measures will be negative predictive value, sensitivity and effectiveness, defined as the proportion of patients categorised as low risk for NSTEMI. We will also evaluate inter-rater reliability of the clinical impression-based risk estimation. Ethics and dissemination: The study is approved by the Ethics Committees of the Kyoto University Graduate School and Faculty of Medicine and of the five hospitals where we will recruit patients. We will disseminate the study results through conference presentations and peer-reviewed journals

Effects of door‐to‐tolvaptan time on short‐term clinical outcome in patients with acute heart failure

Abstract Aims We investigated the effects of door‐to‐tolvaptan (D2T) time on short‐term urine volume and in‐hospital clinical outcomes in patients with acute heart failure (AHF). Methods and results Patients with AHF, treated with tolvaptan at two hospitals, were enrolled in this retrospective observational study. The D2T time was defined as the time elapsed from the arrival of a patient at a participating hospital to the first administration of tolvaptan. The group with the D2T time within 6 h was defined as the ‘early group’. The primary outcome was 48‐h urine volume. The secondary outcomes were in‐hospital death, length of hospital stay, and worsening renal function (WRF) incidence. A restricted cubic spline model was used to evaluate the presence of a nonlinear association between the D2T time and 48‐h urine volume and the odds ratio of WRF incidence. Our study included a total of 138 patients with AHF who were started on tolvaptan after hospitalization. The median D2T time was 5.3 h (interquartile range: 3.0–31.9 h). Seventy‐four patients (53.6%) were classified to be in the early group. Baseline characteristics were similar in the two groups: mean age (85.4 ± 9.6 years vs. 84.5 ± 9.5 years; P = 0.59) and male sex (n = 22 [33.3%] vs. n = 29 [46%]; P = 0.16), except that patients in the early group had higher systolic blood pressure than those in the delayed group (138.2 ± 22.9 vs. 125.7 ± 21.7; P = 0.001). The initial tolvaptan dose in the delayed group was much lower than that in the early group (7.5 [7.5, 7.5] vs. 7.5 [5.6, 7.5] mg; P = 0.01). Total urine volume in 48 h did not differ in the early and delayed groups (4113 ± 1758 mL vs. 4201 ± 1893 mL; P = 0.80). The relationship between D2T time and total urine volume within 48 h increased slightly, with a peak at a D2T time of 15 h, and gradually decreased, thereafter. In‐hospital death and the length of hospital stay did not differ significantly between the two groups (n = 1, 1.3% vs. n = 4, 6.3%; P = 0.18, and 5.0 [12.0, 30.0] vs. 22.0 [14.5, 30.0] days; P = 0.17, respectively). Notably, the restricted cubic spline model for the odds ratio of WRF incidence increased as the D2T time was delayed (P for effect<0.01). Conclusions The shorter D2T time did not affect the short‐term urine volume and in‐hospital outcomes but reduced the risk of WRF incidence in patients with AHF