TY - JOUR
T1 - Prognostic impacts of dynamic cardiac structural changes in heart failure patients with preserved left ventricular ejection fraction
AU - CHART-2 investigators
AU - Yamanaka, Shinsuke
AU - Sakata, Yasuhiko
AU - Nochioka, Kotaro
AU - Miura, Masanobu
AU - Kasahara, Shintaro
AU - Sato, Masayuki
AU - Aoyanagi, Hajime
AU - Fujihashi, Takahide
AU - Hayashi, Hideka
AU - Shiroto, Takashi
AU - Sugimura, Koichiro
AU - Takahashi, Jun
AU - Miyata, Satoshi
AU - Shimokawa, Hiroaki
N1 - Funding Information:
This study was supported in part by the Grants‐in Aid from the Ministry of Health, Labour, and Welfare, the Ministry of Education, Culture, Sports, Science, and Technology, and the Agency for Medical Research and Development, Tokyo, Japan.
Funding Information:
This study was supported in part by the Grants-in Aid from the Ministry of Health, Labour, and Welfare, the Ministry of Education, Culture, Sports, Science, and Technology, and the Agency for Medical Research and Development, Tokyo, Japan. The Department of Evidence-based Cardiovascular Medicine, Tohoku University Graduate School of Medicine, is supported in part by unrestricted research grants from Daiichi Sankyo (Tokyo, Japan), Bayer Yakuhin (Osaka, Japan), Kyowa Hakko Kirin (Tokyo, Japan), Novartis Pharma (Tokyo, Japan), Dainippon Sumitomo Pharma (Osaka, Japan), Astellas Pharma (Tokyo, Japan), AstraZeneca (Osaka, Japan), Chugai Pharmaceutical (Tokyo, Japan), GlaxoSmithKline (Tokyo, Japan), Kowa Pharmaceutical (Tokyo, Japan), Mitsubishi Tanabe Pharma (Osaka, Japan), Mochida Pharmaceutical (Tokyo, Japan), MSD (Tokyo, Japan), Nippon Boehringer Ingelheim (Tokyo, Japan), Otsuka Pharmaceutical (Tokyo, Japan), Shionogi (Osaka, Japan) and Takeda Pharmaceutical (Osaka, Japan). Conflict of interest: H.S. has received lecture fees from Bayer Yakuhin (Osaka, Japan) and Daiichi Sankyo (Tokyo, Japan). All other authors have nothing to disclose. We thank all the members of the Tohoku Heart Failure Association and the staff of the Departments of Cardiovascular Medicine and Evidence-based Cardiovascular Medicine, Tohoku University Graduate School of Medicine for their contributions. This study was supported in part by the Grants-in Aid from the Ministry of Health, Labour, and Welfare, the Ministry of Education, Culture, Sports, Science, and Technology, and the Agency for Medical Research and Development, Tokyo, Japan. The Department of Evidence-based Cardiovascular Medicine, Tohoku University Graduate School of Medicine, is supported in part by unrestricted research grants from Daiichi Sankyo (Tokyo, Japan), Bayer Yakuhin (Osaka, Japan), Kyowa Hakko Kirin (Tokyo, Japan), Novartis Pharma (Tokyo, Japan), Dainippon Sumitomo Pharma (Osaka, Japan), Astellas Pharma (Tokyo, Japan), AstraZeneca (Osaka, Japan), Chugai Pharmaceutical (Tokyo, Japan), GlaxoSmithKline (Tokyo, Japan), Kowa Pharmaceutical (Tokyo, Japan), Mitsubishi Tanabe Pharma (Osaka, Japan), Mochida Pharmaceutical (Tokyo, Japan), MSD (Tokyo, Japan), Nippon Boehringer Ingelheim (Tokyo, Japan), Otsuka Pharmaceutical (Tokyo, Japan), Shionogi (Osaka, Japan) and Takeda Pharmaceutical (Osaka, Japan). Conflict of interest: H.S. has received lecture fees from Bayer Yakuhin (Osaka, Japan) and Daiichi Sankyo (Tokyo, Japan). All other authors have nothing to disclose.
Funding Information:
The Department of Evidence‐based Cardiovascular Medicine, Tohoku University Graduate School of Medicine, is supported in part by unrestricted research grants from Daiichi Sankyo (Tokyo, Japan), Bayer Yakuhin (Osaka, Japan), Kyowa Hakko Kirin (Tokyo, Japan), Novartis Pharma (Tokyo, Japan), Dainippon Sumitomo Pharma (Osaka, Japan), Astellas Pharma (Tokyo, Japan), AstraZeneca (Osaka, Japan), Chugai Pharmaceutical (Tokyo, Japan), GlaxoSmithKline (Tokyo, Japan), Kowa Pharmaceutical (Tokyo, Japan), Mitsubishi Tanabe Pharma (Osaka, Japan), Mochida Pharmaceutical (Tokyo, Japan), MSD (Tokyo, Japan), Nippon Boehringer Ingelheim (Tokyo, Japan), Otsuka Pharmaceutical (Tokyo, Japan), Shionogi (Osaka, Japan) and Takeda Pharmaceutical (Osaka, Japan).
Publisher Copyright:
© 2020 The Authors. European Journal of Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.
PY - 2020/12
Y1 - 2020/12
N2 - Aims: We aimed to examine temporal changes in left ventricular (LV) structures and their prognostic impacts in patients with heart failure (HF) and preserved ejection fraction (HFpEF). Methods and results: In the Chronic Heart Failure Analysis and Registry in the Tohoku District-2 (CHART-2) study (n = 10 219), we divided 2698 consecutive HFpEF patients (68.9 ± 12.2 years, 32.1% female) into three groups by LV hypertrophy (LVH) and enlargement (LVE) at baseline: (−)LVH/(−)LVE (n = 989), (+)LVH/(−)LVE (n = 1448), and (+)LVH/(+)LVE (n = 261). We examined temporal changes in LV structures and their prognostic impacts during a median 8.7-year follow-up. From (−)LVH/(−)LVE, (+)LVH/(−)LVE to (+)LVH/(+)LVE at baseline, the incidence of the primary outcome, a composite of cardiovascular death or HF admission, significantly increased. Among 1808 patients who underwent echocardiography at both baseline and 1 year, we noted substantial group transitions from baseline to 1 year; the transition rates from (−)LVH/(−)LVE to (+)LVH/(−)LVE, from (+)LVH/(−)LVE to (−)LVH/(−)LVE, from (+)LVH/(−)LVE to (+)LVH/(+)LVE, and from (+)LVH/(+)LVE to (+)LVH/(−)LVE were 27% (182/671), 22% (213/967), 6% (59/967), and 26% (44/170), respectively. In the univariable Cox proportional hazard model, patients who transitioned from (+)LVH/(−)LVE to (+)LVH/(+)LVE or remained in (+)LVH/(+)LVE had the worst subsequent prognosis [hazard ratio (HR) 4.65, 95% confidence interval (CI) 3.09–6.99, P < 0.001; HR 4.01, 95% CI 2.85–5.65, P < 0.001, respectively], as compared with those who remained in (−)LVH/(−)LVE. These results were unchanged after adjustment for the covariates including baseline LV ejection fraction (LVEF) and 1-year LVEF change. Conclusion: In HFpEF patients, LV structures dynamically change over time with significant prognostic impacts, where patients who develop LVE with LVH have the worst prognosis.
AB - Aims: We aimed to examine temporal changes in left ventricular (LV) structures and their prognostic impacts in patients with heart failure (HF) and preserved ejection fraction (HFpEF). Methods and results: In the Chronic Heart Failure Analysis and Registry in the Tohoku District-2 (CHART-2) study (n = 10 219), we divided 2698 consecutive HFpEF patients (68.9 ± 12.2 years, 32.1% female) into three groups by LV hypertrophy (LVH) and enlargement (LVE) at baseline: (−)LVH/(−)LVE (n = 989), (+)LVH/(−)LVE (n = 1448), and (+)LVH/(+)LVE (n = 261). We examined temporal changes in LV structures and their prognostic impacts during a median 8.7-year follow-up. From (−)LVH/(−)LVE, (+)LVH/(−)LVE to (+)LVH/(+)LVE at baseline, the incidence of the primary outcome, a composite of cardiovascular death or HF admission, significantly increased. Among 1808 patients who underwent echocardiography at both baseline and 1 year, we noted substantial group transitions from baseline to 1 year; the transition rates from (−)LVH/(−)LVE to (+)LVH/(−)LVE, from (+)LVH/(−)LVE to (−)LVH/(−)LVE, from (+)LVH/(−)LVE to (+)LVH/(+)LVE, and from (+)LVH/(+)LVE to (+)LVH/(−)LVE were 27% (182/671), 22% (213/967), 6% (59/967), and 26% (44/170), respectively. In the univariable Cox proportional hazard model, patients who transitioned from (+)LVH/(−)LVE to (+)LVH/(+)LVE or remained in (+)LVH/(+)LVE had the worst subsequent prognosis [hazard ratio (HR) 4.65, 95% confidence interval (CI) 3.09–6.99, P < 0.001; HR 4.01, 95% CI 2.85–5.65, P < 0.001, respectively], as compared with those who remained in (−)LVH/(−)LVE. These results were unchanged after adjustment for the covariates including baseline LV ejection fraction (LVEF) and 1-year LVEF change. Conclusion: In HFpEF patients, LV structures dynamically change over time with significant prognostic impacts, where patients who develop LVE with LVH have the worst prognosis.
KW - Cardiac structures
KW - Heart failure with preserved ejection fraction
KW - Prognosis
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U2 - 10.1002/ejhf.1945
DO - 10.1002/ejhf.1945
M3 - Article
C2 - 32592517
AN - SCOPUS:85089137019
VL - 22
SP - 2258
EP - 2268
JO - European Journal of Heart Failure
JF - European Journal of Heart Failure
SN - 1388-9842
IS - 12
ER -