ual-chamber pacing (DDD) is a therapeutic alternative to surgical septal myotomy -myectomy for patients with hypertrophic obstructive cardiomyopathy (HOCM). A reduction in the left ventricular (LV) outflow obstruction by DDD has been demonstrated in previous studies, 1-8 and although pacing-induced paradoxical septal motion is the most conceivable mechanism, 1,2,7,8 there are no data regarding the effects of DDD on regional wall deformation, particularly of the ventricular septum.Myocardial deformation can be quantified by echocardiographic strain and strain rate (SR) imaging, 9-12 techniques based on processing the velocity data from tissue velocity imaging. These methods are able to identify regional changes associated with a range of pathologies, 13,14 and in particular, those associated with pacing. 15,16 Recently, Breithardt et al reported that in heart failure patients, the peak strain and SR in the ventricular septum was decreased by cardiac resynchronization therapy, indicating that there was more ejection force during systole. 15 Given that DDD decreases global LV contractility in HOCM patients, 17,18 the opposite phenomenon might occur during DDD and could be the underlying mechanism of the responsiveness to DDD. Strain and SR imaging are a noninvasive approach to determining such changes in regional wall deformation,
Circulation Journal Vol.70, January 2006which was the aim of the present study.
Methods
PatientsBetween December 1994 and April 2001, 18 patients with HOCM underwent pacemaker implantation (DDD) at Osaka Medical College for persistently high LV pressure gradient (LVPG). Of these, 2 patients died from sudden cardiac death during follow-up and of the remaining 16 patients, 14 accepted the study protocol and were enrolled. Each patient had been stable in clinical condition (functional class I or II) on the basis of long-term DDD. Exclusion criteria included chronic atrial fibrillation, dilated phase of disease process, and prior septal myotomy -myectomy operation. Atrioventricular delay was optimized in individual patients to achieve the lowest LVPG at their last visit to the outpatient department. Each patient gave informed consent before the echocardiographic examination.
Two-Dimensional and Doppler EchocardiographyAll patients underwent 2-dimensional Doppler, and tissue velocity imaging during DDD and immediately after the DDD was turned off. We used a commercially available echocardiographic apparatus (Vivid 7 echocardiographic (GE-Vingmed Ultrasound, Horten, Norway)) with a 2.5-MHz transducer. Changes in LV volume were assessed by modified Simpson's rule using the apical 4-chamber view. Parameters of LV diastolic function were also assessed by pulsed Doppler echocardiography: early and atrial filling velocity at the mitral valve and their ratio, and the decelera-