| Literature DB >> 26589516 |
Takashi Nakamura1, Yoshitaka Iwanaga2, Masakazu Yasuda1, Takayuki Kawamura1, Yuki Miyaji1, Hanako Morooka1, Shunichi Miyazaki1.
Abstract
Myocardial fibrosis is frequently observed and may be associated with the prognosis in patients with hypertrophic cardiomyopathy (HCM); however, the clinical pathophysiological features, particularly in terms of fibrosis, of hypertrophic obstructive cardiomyopathy (HOCM) remain unclear. This study aimed to determine a role of local fibrosis in HOCM using cardiac magnetic resonance (CMR). 108 consecutive HCM patients underwent CMR. HOCM was defined as a left ventricular outflow tract (LVOT) pressure gradient ≥30 mmHg at rest. Myocardial mass and fibrosis mass by late gadolinium-enhancement CMR (LGE-CMR) were calculated and the distribution/pattern was analyzed using the AHA 17-segment model. LV ejection fraction (LVEF) was significantly higher in patients with HOCM (n = 19) than in those with nonobstructive HCM (n = 89) (P < 0.05). Both total myocardial and fibrosis masses in LV were similar in the two groups (P = 0.385 and P = 0.859, respectively). However, fibrosis in the basal septum was significantly less frequent in the HOCM group than in the nonobstructive HCM group (P < 0.01). The LVOT pressure gradient was significantly higher in the basal-septal non-fibrosis group than in the fibrosis group (23.6 ± 37.3 vs. 4.8 ± 11.4 mmHg, P < 0.01). Multivariate analysis revealed that basal-septal fibrosis was an independent negative predictor of LVOT obstruction in addition to the local wall thickness and LVEF as positive predictors in HCM patients. In conclusion, a significant association was observed between LVOT obstruction and basal septal fibrosis by LGE-CMR in HCM patients. In addition to negative impact of basal-septal fibrosis, basal-septal hypertrophy and preserved global LV contractility may be associated with the pathophysiological features of LVOT obstruction.Entities:
Keywords: Hypertrophic obstructive cardiomyopathy; Magnetic resonance imaging; Myocardial fibrosis
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Year: 2015 PMID: 26589516 DOI: 10.1007/s10554-015-0806-8
Source DB: PubMed Journal: Int J Cardiovasc Imaging ISSN: 1569-5794 Impact factor: 2.357