Kimi Koide

Elevated troponin T on discharge predicts poor outcome of decompensated heart failure

Persistent elevation of cardiac troponin T (cTnT) predicts an adverse clinical outcome in patients with chronic heart failure (HF), but the underlying mechanisms remain to be determined. We investigated the association between predischarge cTnT elevation and coexistent pathophysiology in patients with decompensated HF. Plasma cTnT levels were determined before discharge in 170 patients with decompensated HF. We divided the patients into a group that was positive for cTnT [cTnT(+) group, n = 40] and a group that was negative for cTnT [cTnT(−) group, n = 130]. Multivariate analysis showed that use of β-blocker therapy (odds ratio [OR] = 0.236, P = 0.003), an elevated high-sensitivity C-reactive protein (hsCRP) level (OR = 3.731, P = 0.006), a high brain natriuretic peptide (BNP) level (OR = 3.570, P = 0.007), diabetes (OR = 3.090, P = 0.018), and anemia (OR = 2.330, P = 0.047) were independently associated with cTnT positivity. During a mean follow-up period of 441 days after discharge, total mortality (P < 0.001), cardiac death (P < 0.001), and exacerbation of HF requiring hospitalization (P = 0.007) were all more common in the cTnT(+) group than in the cTnT(−) group. Cox proportional hazards analysis showed that cTnT positivity was an independent predictor of total mortality (hazard ratio = 5.008, P = 0.004) in an age- and gender-matched model. Elevation of cTnT during convalescence was associated with lack of β-blocker therapy, a high hsCRP level at discharge, a high BNP level at discharge, diabetes, and anemia, and a worse clinical outcome in patients with decompensated HF.

Early vs. late reverse ventricular remodeling in patients with cardiomyopathy

BACKGROUND Predictors of left ventricular reverse remodeling (LVRR) and differences in the time taken to achieve LVRR remain unclear. METHODS We consecutively registered 129 patients with severe cardiomyopathy admitted with heart failure (HF). Patients were followed for a median of 778.0 days (IQ: 457.0, 1078.0). LVRR was defined as a decrease in indexed left ventricular systolic dimension of at least 15% additional to a 25% improvement in left ventricular ejection fraction at outpatient check-up compared with discharge. LVRR accomplishment within 400 days was defined as early-LVRR opposing the remaining late-LVRR patients. Primary endpoint was a composite of all-cause mortality and HF re-hospitalization. RESULTS LVRR was observed in 51 patients (39.5%). Baseline predictors for LVRR were age younger than 60 years (OR, 3.27; 95% CI 1.04-10.37, p=0.043), no history of previous HF hospitalization (OR, 0.32; 95% CI 0.12-0.86, p=0.025), and systolic blood pressure (sBP) >100mmHg at discharge (OR, 4.39; 95% CI 1.39-13.81, p=0.011). Overall, there were 51 endpoint events [LVRR 11 (21.6%) vs. non-LVRR 40 (49.4%), p<0.001]. LVRR was a significant predictor of favorable prognosis (HR, 3.77; 95% CI 1.68-8.47, p<0.001). Notably, 41 (80.4%) patients qualified for early-LVRR. Early-LVRR was associated with better prognosis compared with late-LVRR [early-LVRR 6 (14.6%) vs. late-LVRR 5 (50.0%), p=0.066]. Among assessed variables, sBP >100mmHg at discharge was a significant predictor of early-LVRR (OR, 10.87; 95% CI 1.19-100.0, p=0.034). CONCLUSION Prognosis was improved in patients who achieved LVRR. Early-LVRR tended to be an advantage in terms of long-term prognosis. Higher sBP was a predictor not only for all-LVRR but also early-LVRR.

Radial coronary interventions and post-procedural complication rates in the real world: A report from a Japanese multicenter percutaneous coronary intervention registry

world: A report from a Japanese multicenter percutaneous coronary intervention registry Atsushi Mizuno , Shun Kohsaka ⁎, Hiroaki Miyata , Kimi Koide , Taku Asano , Takahiro Ohki , Kouji Negishi , Keiichi Fukuda , Yutaro Nishi a a Department of Cardiology, St Lukes International Hospital, Tokyo, Japan b Department of Cardiology, Keio University School of Medicine, Tokyo, Japan c Department of Healthcare Quality Assessment, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan d Department of Cardiology, Tokyo Dental University, Ichikawa, Japan e Department of Cardiology, Yokohama Municipal Hospital, Yokohama, Japan

Reducing the dose of diuretics for heart failure patients: How low can it go?

episode of acute decompensation, 111 patients (69%) were discharged on low-dose or no diuretics ( ! 40 mg furosemide equivalent; substandard dose group). Compared to those who were discharged on the standard dose of diuretics (n = 50, standard dose group), these patients were similar in age (64.4 8 16.8 vs. 68.7 8 14.8 years; p = 0.37), plasma concentration of BNP on admission (599.9 8 615.5 vs. 826.8 8 670.4 pg/ml; p = 0.07), prevalence of diabetes mellitus (28.0 vs. 27.8%; p = 1.00) and renal failure (56.0 vs. 66.7%; p = 0.39), and use of HF medications [renin-angiotensin system inhibitors (76.6 vs. 63.9%; p = 0.19) or -blockers (72.1 vs. 83.3%; p = 0.19)]. The 1-year event rate (death or HF admission) was also similar in both groups (log-rank test p = 0.12). After adjustment for known Peacock et al. [1] showed that the use of high-dose diuretics was associated with a higher rate of adverse outcomes (e.g., inhospital mortality, prolonged hospitalization or adverse renal effects) compared to decompensated heart failure (HF) patients who were on low-dose diuretics. However, in their analysis, the preset cutoff dose was equivalent to 160 mg lasix. Although diuretics improve the symptoms of HF, these agents also have adverse effects on the patient’s prognosis; therefore, they should be used in the lowest effective doses when clinically indicated [1] . Traditionally, in the Japanese HF population, much lower doses of diuretics have been employed, and even 80 mg of lasix is considered a high dose. In our analysis of 161 advanced HF patients recently discharged after an Received: February 10, 2009 Accepted: February 13, 2009 Published online: May 7, 2009

Significance of AT1 Receptor Independent Activation of Mineralocorticoid Receptor in Murine Diabetic Cardiomyopathy

Background Diabetes mellitus (DM) has deleterious influence on cardiac performance independent of coronary artery disease and hypertension. The objective of the present study was to investigate the role of the renin-angiotensin-aldosterone system, especially angiotensin II type 1a receptor (AT1aR) and mineralocorticoid receptor (MR) signaling, in left ventricular (LV) dysfunction induced by diabetes mellitus (DM). Methods and Results DM was induced by intraperitoneal injection of streptozotocin (200 mg/kg BW) in wild-type (WT) or AT1aR knockout (KO) male mice, and they were bred during 6 or 12 weeks. Some KO mice were administered the MR antagonist eplerenone (100 mg/kg body weight). At 6 weeks, LV diastolic function was impaired in WT-DM, but preserved in KO-DM. At that time point MR mRNA expression was upregulated, NADPH oxidase subunit (p47phox) and glutathione peroxidase (GPx1) mRNA expression were upregulated, the staining intensities of LV tissue for 4-hydroxy-2-nonenal was stronger in immunohistochemistry, the number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) positive cells was increased, Bcl-2 protein expression was significantly downregulated, and the expression of SERCA2a and phosphorylated phospholamban was depressed in WT-DM, while these changes were not seen in KO-DM. At 12 weeks, however, these changes were also noted in KO-DM. Eplerenone arrested those changes. The plasma aldosterone concentration was elevated in WT-DM but not in KO-DM at 6 weeks. It showed 3.7-fold elevation at 12 weeks even in KO-DM, which suggests “aldosterone breakthrough” phenomenon. However, the aldosterone content in LV tissue was unchanged in KO-DM. Conclusions DM induced diastolic dysfunction was observed even in KO at 12 weeks, which was ameliorated by minelarocorticoid receptor antagonist, eplerenone. AT1-independent MR activation in the LV might be responsible for the pathogenesis of diabetic cardiomyopathy.

Steady-state levels of troponin and brain natriuretic peptide for prediction of long-term outcome after acute heart failure with or without stage 3 to 4 chronic kidney disease.

Aim: To determine whether assessment of a combination of steady-state discharge levels of biomarkers improves risk stratification after acute decompensate HF. Study Design: Retrospective cohort study. Place and Duration of Study: Keio University Hospital, between January 2006 and September 2011. We analyzed 244 patients with acute HF due to ischemic or dilated cardiomyopathy who Research Article British Journal of Medicine & Medical Research, 2(4): 490-500, 2012 491 were enrolled in a prospective, single institution-based registry between January 2006 and September 2011. Patients were stratified by discharge values of BNP and/or TnT. The primary endpoint was a composite of HF readmission or death during the 2-year period after discharge. Results: The population was predominantly male (69.3%), and the mean age was 66.6±15.3 years. Patients with higher BNP levels or detectable TnT had a worse prognosis (BNP45.0% vs. 18.8%, p<0.001; TnT 43.8% vs. 25.1%, p=0.002, respectively). The primary event rate was additively worse among patients with both increased BNP levels and detectable TnT compared to those with increased levels of BNP or detectable TnT alone (log-rank p<0.001). A similar trend was observed in the subgroup of patients with CKD stage III–V (n=172). Conclusion: Assessment of both BNP and TnT values may have a significant predictive value for HF prognosis, even among patients with CKD, a condition affecting biomarker levels.