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Regional Wall Motion During Pacing for Hypertrophic Obstructive Cardiomyopathy
Author(s) -
JEANRENAUD XAVIER,
KAPPENBERGER LUKAS
Publication year - 1997
Publication title -
pacing and clinical electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 101
eISSN - 1540-8159
pISSN - 0147-8389
DOI - 10.1111/j.1540-8159.1997.tb03538.x
Subject(s) - medicine , ventricle , cardiology , obstructive cardiomyopathy , hypertrophic cardiomyopathy , cardiomyopathy , apex (geometry) , ejection fraction , hemodynamics , ventricular outflow tract , anatomy , heart failure
In order to assess the influence of right ventricular stimulation on LV contraction sequence in hypertrophic obstructive cardiomyopathy (HOCM), we performed a regional wall‐motion analysis of the left ventricle by comparing normal His‐Purkinje activation to pacing from the right ventricular apex. In 9 patients (5 males and 4 females, mean age 61 ± 9 years) assessed after a mean pacing period of 12 weeks (range 7–24 weeks), AV sequential pacing induced a 52% reduction in maximal pressure gradient from 76 ± 36 to 40 ± 28 mmHg (P < 0.01) as determined by Doppler examination. Regional wall‐motion analysis of the left ventricle was computed from digitized two‐dimensional echocardiographic images by means of the area shrinking method. Pacing induced a significant reduction of total septal area shrinking from 25%± 17% to 12%± 17% (P < 0.005). A tendency toward paradoxical septal motion was observed in one patient only. The apex showed no significant variation. A 6% increase in area shrinking was observed at the posterior wall and lateral free wall, from 38%± 13% to 43%± 10% (P < 0.05). Pacing did not significantly alter the global ejection fraction. A direct correlation between the magnitude of subaortic pressure gradient reduction and that of septal motion changes was found in a majority of patients. In conclusion, dual chamber pacing reduces septal wall motion in patients with HOCM obstructive cardiomyopathy. Tins might be one of the mechanisms involved in the reduction of LV outflow tract obstruction.