March 20, 2001Open Access
View Full PaperRegression of Left Ventricular Hypertrophy After Nonsurgical Septal Reduction Therapy for Hypertrophic Obstructive Cardiomyopathy
Key Result
Nonsurgical septal reduction therapy significantly decreased left ventricular mass from 301 g at baseline to 190 g at 2 years (P<0.01) in patients with hypertrophic obstructive cardiomyopathy.
Study Design
Type
Cohort (n=26)
Structured PICO
Does nonsurgical septal reduction therapy with intracoronary ethanol reduce left ventricular mass and outflow tract gradient in patients with hypertrophic obstructive cardiomyopathy?
P
Population
26 patients (mean age 53 years) with hypertrophic obstructive cardiomyopathy who underwent nonsurgical septal reduction therapy, followed for 2 years.
E
Exposure
Nonsurgical septal reduction therapy (NSRT) with intracoronary ethanol
O
Outcome
Left ventricular mass and outflow tract gradient at 1 and 2 yearssurrogate
Nonsurgical septal reduction therapy with intracoronary ethanol induces favorable long-term left ventricular remodeling, significantly reducing LV mass and outflow tract gradient at 2 years.
Main Result
Absolute Event Rate: 190% vs 301%
p-value: p=<0.01
Abstract
BACKGROUND: Hypertrophic obstructive cardiomyopathy (HOCM) is characterized by left ventricular hypertrophy (LVH) in the absence of increased external load. Recently, nonsurgical septal reduction therapy (NSRT) with intracoronary ethanol has been introduced to treat severely symptomatic patients with outflow tract obstruction. Its long-term effects on LV mass, however, are unknown. METHODS AND RESULTS: The LV size, function, and outflow tract gradient of 26 HOCM patients (53+/-15 years old) who underwent NSRT were assessed by echocardiography at baseline and 1 and 2 years after the procedure. LVH was evaluated by wall thickness of individual myocardial segments, planimetered myocardial area, and mass. The outflow gradient decreased from 36+/-6 mm Hg before NSRT to 0+/-3 mm Hg at 2 years (P<0.001), with patients experiencing symptomatic improvement (P<0.05). LV end-diastolic and end-systolic dimensions increased significantly at both 1 and 2 years (P<0.001). All parameters of LVH showed evidence of regression. LV mass decreased (301+/-78 g at baseline, 223+/-5 g at 1 year, and 190+/-58 g at 2 years; P<0.01), with the 2-year reduction in mass related to infarct size and the acute reduction in outflow tract gradient (r=0.48, P<0.05 and r=0.63, P<0.01, respectively). CONCLUSIONS: NSRT results in LV remodeling that is characterized by an increase in LV size and a decrease in the extent of LVH.