Abstract 11006: Pathological Mechanism of LV Out-flow Obstruction in Hypertrophic Cardiomyopathy: Insights From Cardiac Magnetic Resonance Analysis
Background: Myocardial fibrosis is frequently observed and may be associated with the prognosis in patients with hypertrophic cardiomyopathy (HCM). However, with regard to pathologic basis, the difference between HCM patients with and without LV outflow-tract (LVOT) obstruction remains unclear. Therefore, we sought to determine the different characteristics between hypertrophic obstructive cardiomyopathy (HOCM) and hypertrophic nonobstructive cardiomyopathy (HNCM) using delayed-enhancement cardiac magnetic resonance (DE-CMR).
Methods: Fifty-three HCM patients receiving regular outpatient treatment underwent CMR (cine and DE imaging). HOCM was defined as LVOT pressure gradient>30 mmHg at rest. LV mass and fibrosis mass was calculated and the distribution/pattern was analyzed using 17 segment model.
Results: In total patients, mean maximal wall thickness was 20.3 ± 3.2mm and any DE was observed in 45 (85%) patients. There were no significant differences in clinical characteristics including clinical cardiac events between HOCM (n=13) and HNCM (n=40) patients. Plasma BNP level was only significantly higher in patients with HOCM compared to HNCM (p<0.01). In total myocardial segments, both LV myocardial mass and fibrosis mass were similar in two groups (p=0.301 and p=0.485, respectively). However, in basal septum (segment 2 and 3), HOCM group showed significantly less fibrosis compared to HNCM group (p<0.01). LVOT pressure gradient was significantly higher in non-fibrosis group in basal septum than that in fibrosis group (p < 0.01). In multivariate analysis, the existence of fibrosis (DE) and wall thickness in basal septum were independent determinants of LVOT obstruction in HCM (p<0.01).
Conclusions: In HCM patients, a significant inverse association was observed between LVOT obstruction and myocardial fibrosis in basal septum by DE-CMR. Local hypertrophy without fibrosis in LVOT may explain the pathological mechanism of LVOT obstruction.
- © 2013 by American Heart Association, Inc.