Acute effects of alcohol septal ablation on systolic and diastolic left ventricular function in patients with hypertrophic obstructive cardiomyopathy

¹ Leiden University Medical Center, Netherlands
² Thoraxcenter, Erasmus Medical Center, Netherlands

^* To whom correspondence should be addressed. E-mail: p.steendijk{at}lumc.nl.

Accepted 11 March 2008

	Abstract

Objective Hypertrophic obstructive cardiomyopathy (HOCM) often leads to heart failure, severe symptoms, and death. PTSMA by alcohol injection efficiently reduces LV outflow tract pressure gradient and improves symptoms. We determined acute changes in hemodynamics and systolic and diastolic left ventricular (LV) function after percutaneous transluminal septal myocardial ablation (PTSMA).

Methods In 17 consecutive patients with symptomatic HOCM referred for PTSMA, the target vessel was determined by myocardial contrast trans-thoracic echocardiography. An over-the-wire balloon was inflated in the target vessel and multiple 0.5mL alcohol injections were performed. LV systolic and diastolic function was assessed by online pressure-volume loops obtained by conductance catheter at baseline and acutely after the procedure.

Results In all patients except two, a single septal branch was treated using a total of 2.0±0.5mL ethanol per patient. The rest and post extra-systolic gradient were significantly decreased after PTSMA (79±38 to 14±16mmHg and 130±50 to 34±33mmHg respectively, both p<0.001). Ejection fraction decreased (78±9 to 67±13%, p<0.001). Cardiac output, heart rate, and stroke work were unchanged, but systolic and diastolic volume increased. End-systolic and end-diastolic pressure significantly decreased (166±27 to 129±26mmHg, p<0.001 and 25±6 to 21±7mmHg, p=0.049, respectively). Significant rightward shift (p<0.001) and decreased slope (p=0.041) of the end-systolic pressure-volume relation indicated reduced contractility, whereas diastolic stiffness, -dP/dtMIN, and Tau were significantly improved after the procedure.

Conclusions PTSMA acutely reduced systolic function but promptly improved diastolic function with maintained cardiac output and stroke work. Improved diastolic function and increased end-diastolic volume compensated for the systolic loss and resulted in maintained hemodynamics.