Alcohol septal ablation(ASA) reduces left ventricular outflow tract(LVOT) pressure gradient in patients with hypertrophic obstructive cardiomyopathy(HOCM),which leads to left ventricular remodeling. We sought to descr...Alcohol septal ablation(ASA) reduces left ventricular outflow tract(LVOT) pressure gradient in patients with hypertrophic obstructive cardiomyopathy(HOCM),which leads to left ventricular remodeling. We sought to describe the early to midterm changes and modulating factors of the remodeling process using cardiac MRI(CMR). Methods and Results-CMR was performed at baseline and 1 and 6 months after ASA in 29 patients with HOCM(age 52± 16 years). Contrast enhanced CMR showed no infarct-related hyperenhancement outside the target septal area. Septal mass decreased from 75± 23 g at baseline to 68± 22 and 58± 19 g(P< 0.001) at 1-and 6-month follow-up, respectively. Remote, nonseptal mass decreased from 141± 41 to 132± 40 and 111± 27 g(P< 0.001), respectively. Analysis of temporal trends revealed that septal mass reduction was positively associated with contrast-enhanced infarct size and transmural or left-sided septal infarct location at both 1 and 6 months. Remote mass reduction was associated with infarct location at 6 months but not with contrast-enhanced infarct size. By linear regression analysis, percentage remote mass reduction correlated significantly with LVOT gradient reduction at 6-month follow-up(P=0.03). Conclusions-Left ventricular remodeling after ASA occurs early and progresses on midterm follow-up, modulated by CMR infarct size and location. Remote mass reduction is associated with infarct location and correlates with reduction of the LVOT pressure gradient. Thus, myocardial hypertrophy in HOCM is, at least in part, afterload dependent and reversible and is not exclusively caused by the genetic disorder.展开更多
文摘Alcohol septal ablation(ASA) reduces left ventricular outflow tract(LVOT) pressure gradient in patients with hypertrophic obstructive cardiomyopathy(HOCM),which leads to left ventricular remodeling. We sought to describe the early to midterm changes and modulating factors of the remodeling process using cardiac MRI(CMR). Methods and Results-CMR was performed at baseline and 1 and 6 months after ASA in 29 patients with HOCM(age 52± 16 years). Contrast enhanced CMR showed no infarct-related hyperenhancement outside the target septal area. Septal mass decreased from 75± 23 g at baseline to 68± 22 and 58± 19 g(P< 0.001) at 1-and 6-month follow-up, respectively. Remote, nonseptal mass decreased from 141± 41 to 132± 40 and 111± 27 g(P< 0.001), respectively. Analysis of temporal trends revealed that septal mass reduction was positively associated with contrast-enhanced infarct size and transmural or left-sided septal infarct location at both 1 and 6 months. Remote mass reduction was associated with infarct location at 6 months but not with contrast-enhanced infarct size. By linear regression analysis, percentage remote mass reduction correlated significantly with LVOT gradient reduction at 6-month follow-up(P=0.03). Conclusions-Left ventricular remodeling after ASA occurs early and progresses on midterm follow-up, modulated by CMR infarct size and location. Remote mass reduction is associated with infarct location and correlates with reduction of the LVOT pressure gradient. Thus, myocardial hypertrophy in HOCM is, at least in part, afterload dependent and reversible and is not exclusively caused by the genetic disorder.
