TY - JOUR
T1 - Quantification of myocardial iron deficiency in nonischemic heart failure by cardiac T2* magnetic resonance imaging
AU - Nagao, Michinobu
AU - Matsuo, Yoshio
AU - Kamitani, Takeshi
AU - Yonezawa, Masato
AU - Yamasaki, Yuzo
AU - Kawanami, Satoshi
AU - Abe, Kohtaro
AU - Mukai, Yasushi
AU - Higo, Taiki
AU - Yabuuchi, Hidetake
AU - Takemura, Atsushi
AU - Yoshiura, Takashi
AU - Sunagawa, Kenji
AU - Honda, Hiroshi
N1 - Funding Information:
Drs. Nagao and Kawanami received research grants from Bayer HealthCare Japan (Tokyo, Japan) and Philips Electronics Japan . Mr. Takemura is an employee of Philips Electronics Japan (Tokyo, Japan). The other authors have no conflicts of interest to disclose.
PY - 2014/3/15
Y1 - 2014/3/15
N2 - The aim of this study was to use T2* cardiac magnetic resonance (CMR) imaging to quantify myocardial iron content in patients with heart failure (HF) and to investigate the relation between iron content, cardiac function, and the cause of HF. CMR data were analyzed from 167 patients with nonischemic and 31 with ischemic HF and 50 patients with normal ventricular function. Short-axis T2* imaging was accomplished using 3-T scanner and multiecho gradient-echo sequence. Myocardial T2* value (M-T2*) was calculated by fitting the signal intensity data for the mid-left ventricular (LV) septum to a decay curve. Patients with nonischemic HF were categorized into patients with LV ejection fraction (LVEF) <35% or ≥35%. The relation between nonischemic HF with LVEF <35% and the risk for major adverse cardiac events was analyzed by multivariate logistic regression analysis using M-T2* and HF biomarkers. M-T2* was significantly greater for patients with nonischemic HF (LVEF <35%: 29 ± 7 ms, LVEF ≥35%: 26 ± 5 ms) than for patients with normal LV function (22 ± 3 ms, p <0.0001) or ischemic HF (22 ± 4 ms, p <0.001). The odds ratio was 1.21 for M-T2* (p <0.0001) and 1.0015 for brain natriuretic peptide (p <0.0001) in relation to nonischemic HF with LVEF <35%. Furthermore, this value was 0.96 for systolic blood pressure (p = 0.012) and 1.02 for M-T2* (p = 0.03) in relation to the risk for major adverse cardiac events in patients with nonischemic HF. In conclusion, T2* CMR demonstrated the robust relation between myocardial iron deficiency and nonischemic HF. M-T2* is a biomarker that can predict adverse cardiac function in patients with nonischemic HF.
AB - The aim of this study was to use T2* cardiac magnetic resonance (CMR) imaging to quantify myocardial iron content in patients with heart failure (HF) and to investigate the relation between iron content, cardiac function, and the cause of HF. CMR data were analyzed from 167 patients with nonischemic and 31 with ischemic HF and 50 patients with normal ventricular function. Short-axis T2* imaging was accomplished using 3-T scanner and multiecho gradient-echo sequence. Myocardial T2* value (M-T2*) was calculated by fitting the signal intensity data for the mid-left ventricular (LV) septum to a decay curve. Patients with nonischemic HF were categorized into patients with LV ejection fraction (LVEF) <35% or ≥35%. The relation between nonischemic HF with LVEF <35% and the risk for major adverse cardiac events was analyzed by multivariate logistic regression analysis using M-T2* and HF biomarkers. M-T2* was significantly greater for patients with nonischemic HF (LVEF <35%: 29 ± 7 ms, LVEF ≥35%: 26 ± 5 ms) than for patients with normal LV function (22 ± 3 ms, p <0.0001) or ischemic HF (22 ± 4 ms, p <0.001). The odds ratio was 1.21 for M-T2* (p <0.0001) and 1.0015 for brain natriuretic peptide (p <0.0001) in relation to nonischemic HF with LVEF <35%. Furthermore, this value was 0.96 for systolic blood pressure (p = 0.012) and 1.02 for M-T2* (p = 0.03) in relation to the risk for major adverse cardiac events in patients with nonischemic HF. In conclusion, T2* CMR demonstrated the robust relation between myocardial iron deficiency and nonischemic HF. M-T2* is a biomarker that can predict adverse cardiac function in patients with nonischemic HF.
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U2 - 10.1016/j.amjcard.2013.11.061
DO - 10.1016/j.amjcard.2013.11.061
M3 - Article
C2 - 24461766
AN - SCOPUS:84896714751
SN - 0002-9149
VL - 113
SP - 1024
EP - 1030
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 6
ER -