Echocardiography-guided ethanol septal reduction for hypertrophic obstructive cardiomyopathy. Academic Article uri icon

Overview

abstract

  • BACKGROUND: Left ventricular outflow tract (LVOT) obstruction is frequently responsible for symptoms in hypertrophic obstructive cardiomyopathy (HOCM). Medical therapy is often not sufficient to control these symptoms, and surgical myotomy-myomectomy is required. METHODS AND RESULTS: We enrolled 33 symptomatic patients with HOCM and obstruction (>/=40 mm Hg gradient at rest or >/=60 mm Hg dobutamine-provoked). By contrast echocardiography, the bulging septum was localized and infarcted by injection of 2 to 5 mL of absolute ethanol into the septal artery(ies) supplying the hypertrophied area. Baseline echocardiograms with Doppler, myocardial perfusion tomograms, and treadmill exercise or pharmacological testing were compared with those at 6 weeks and 6 months. The mean rise in creatine kinase was 1964+/-796 U. All patients experienced symptomatic relief; NYHA class decreased from 3. 0+/-0.5 to 0.9+/-0.6 (P<0.001). Exercise time increased from 286+/-193 to 421+/-181 seconds (P=0.03). The resting and dobutamine-provoked gradient decreased from 49+/-33 and 96+/-34 mm Hg to 9+/-19 (P<0.001) and 24+/-31 mm Hg (P<0.001), respectively. Echocardiograms repeated at 6 weeks after the procedure showed a 28% reduction in septal thickness and 17% reduction in left ventricular mass. Myocardial perfusion imaging showed a "septal amputation pattern," with scarring in the upper and middle septal areas. Complete heart block developed in 11 patients, who then required permanent pacemaker implantation. CONCLUSIONS: Echocardiography-guided ethanol septal reduction in patients with HOCM is a safe, minimally invasive procedure that provides symptomatic relief with improved hemodynamic and left ventricular parameters.

publication date

  • October 27, 1998

Research

keywords

  • Cardiomyopathy, Restrictive
  • Ethanol
  • Heart Septum
  • Ventricular Outflow Obstruction

Identity

Scopus Document Identifier

  • 0032573118

Digital Object Identifier (DOI)

  • 10.1161/01.cir.98.17.1750

PubMed ID

  • 9788829

Additional Document Info

volume

  • 98

issue

  • 17