Yasumori Sujino

Impact of hypoalbuminemia, frailty, and body mass index on early prognosis in older patients (≥85 years) with ST-elevation myocardial infarction

BACKGROUND The optimal treatment strategies for acute ST-elevation myocardial infarction (STEMI) in older patients are unclear because of the high risk of mortality in this population. Hypoalbuminemia, frailty, and body mass index (BMI) have been reported to worsen the prognosis of some older patients with cardiovascular disease, but the specific impact of these factors on the prognosis after STEMI is poorly understood. The aim of this study was to investigate the impact of these factors on early outcomes in patients aged ≥85 years with acute STEMI. METHODS Sixty-two consecutive eligible patients aged ≥85 years (mean age, 88.1±2.5 years; age range, 85-94 years; female, 41.9%; primary percutaneous coronary intervention, 67.7%) who were admitted to our hospital with STEMI were retrospectively reviewed. Baseline patient characteristics, echocardiographic, electrocardiographic, and laboratory findings, and the Canadian Study of Health and Aging Clinical Frailty Scale (CSHA-CFS) score were assessed. The primary endpoint was in-hospital mortality and the secondary endpoint was failure of discharge to home. Independent baseline variables with a p-value of <0.15 in the univariate analyses were included in the multivariate analyses. RESULTS Multivariate analysis identified a higher baseline serum troponin I level [p=0.046; odds ratio (OR): 1.02], lower baseline albumin level (p=0.035, OR: 0.16), and CSHA-CFS score ≥6 (p=0.028, OR: 6.38) as independent predictors of in-hospital mortality. Lower BMI (p<0.001, OR: 0.49) and CSHA-CFS frailty score ≥6 (p=0.002, OR: 16.69) were identified as independent predictors of failure of discharge to home. CONCLUSIONS These findings indicate that the serum albumin level, CSHA-CFS score, and BMI, in addition to serum troponin I level, have an impact on the early prognosis of older patients with STEMI.

Cardiac Magnetic Resonance Imaging in Giant Cell Myocarditis Intriguing Associations With Clinical and Pathological Features

Giant cell myocarditis (GCM) is rare and often fatal. Proper diagnosis is crucial, because immunosuppressive therapy has been reported to increase the median transplant-free survival time from 3.0 to 12.3 months.1 Although endomyocardial biopsy plays an essential role in early diagnosis, it may yield false-negative results. Imaging examinations including cardiac magnetic resonance (CMR) may facilitate the diagnosis, but the associations between specific CMR findings and the clinical features and pathological findings remain unclear. We present a patient with characteristic CMR findings, with intriguing associations with the clinical features and pathological findings of the biopsy and autopsy. A 73-year-old woman presented with acute chest pain and dyspnea that had continued for 7 hours. Her medical history was unremarkable, with the exception of uveitis and dyslipidemia. Initial examination showed resting blood pressure 132/83 mm Hg, heart rate 103 bpm, and respiratory rate 17 breaths/min. She required 5 L/min of oxygen via facemask to maintain Spo2>98%. Coarse crackles were heard over both lung fields. X-ray demonstrated mild cardiomegaly with bilateral pulmonary congestion (Figure 1). Electrocardiography, which had been within normal limits 2 years previously, showed changes resembling acute myocardial infarction (Figure I in the online-only Data Supplement). Echocardiography showed global hypokinesis in the left ventricular (LV) wall, and regional akinesis in the septum and inferoseptal wall. Coronary artery angiography revealed no significant stenosis or intracoronary plaque rupture. Her serum creatinine kinase level was high at 2558 IU/L. CMR was performed on day 7. Cine-CMR showed global hypokinesis in …

Validation and Recalibration of Seattle Heart Failure Model in Japanese Acute Heart Failure Patients

BACKGROUND Precise risk stratification in heart failure (HF) patients enables clinicians to tailor the intensity of their management. The Seattle Heart Failure Model (SHFM), which uses conventional clinical variables for its prediction, is widely used. We aimed to externally validate SHFM in Japanese HF patients with a recent episode of acute decompensation requiring hospital admission. METHODS AND RESULTS SHFM was applied to 2470 HF patients registered in the West Tokyo Heart Failure and National Cerebral And Cardiovascular Center Acute Decompensated Heart Failure databases from 2006 to 2016. Discrimination and calibration were assessed with the use of the c-statistic and calibration plots, respectively, in HF patients with reduced ejection fraction (HFrEF; <40%) and preserved ejection fraction (HFpEF; ≥40%). In a perfectly calibrated model, the slope and intercept would be 1.0 and 0.0, respectively. The method of intercept recalibration was used to update the model. The registered patients (mean age 74 ± 13 y) were predominantly men (62%). Overall, 572 patients (23.2%) died during a mean follow-up of 2.1years. Among HFrEF patients, SHFM showed good discrimination (c-statistic = 0.75) but miscalibration, tending to overestimate 1-year survival (slope = 0.78; intercept = -0.22). Among HFpEF patients, SHFM showed modest discrimination (c-statistic = 0.69) and calibration, tending to underestimate 1-year survival (slope = 1.18; intercept = 0.16). Intercept recalibration (replacing the baseline survival function) successfully updated the model for HFrEF (slope = 1.03; intercept = -0.04) but not for HFpEF patients. CONCLUSIONS In Japanese acute HF patients, SHFM showed adequate performance after recalibration among HFrEF patients. Using prediction models to tailor the care for HF patients may improve the allocation of medical resources.