title: Conduction system abnormalities in patients with obstructive hypertrophic cardiomyopathy following septal reduction interventions.
abstract: We observed the impact of percutaneous transluminal septal myocardial ablation (PTSMA) and myectomy on the conduction system in patients with obstructive hypertrophic cardiomyopathy (HC). Septal reduction intervention is capable of eliminating the left ventricular outflow tract obstruction in patients with obstructive HC; however, conduction system abnormalities are frequent consequences of these procedures. A standard 12-lead electrocardiogram and Doppler echocardiogram were obtained in 204 patients who underwent PTSMA (n = 70) or myectomy (n = 134) before and at average of 3 months after intervention. Of 146 patients who had normal conduction systems before intervention, the duration of the QRS complex was significantly prolonged from 98 +/- 15 to 130 +/- 25 ms (p <0.0001), with right bundle branch block (RBBB) developing in 62% patients after PTSMA, and from 100 +/- 13 to 154 +/- 20 ms (p <0.0001), with left bundle branch block (LBBB) developing in 93% patients after myectomy. No significant difference in the QRS duration was found in the remaining 58 patients who had preexisting conduction abnormalities after intervention. In 174 patients without a preexisting permanent pacemaker, a pacemaker was implanted in 22% versus 13% of patients who underwent PTSMA (overall and without preexisting conduction block, respectively) and 10% versus 2% of patients with myectomy. The duration of baseline QRS was an independent predictor for the requirement of a permanent pacemaker (p <0.0001). Thus, RBBB often develops after PTSMA and LBBB is very frequently produced by myectomy. A possible requirement of a permanent pacemaker should always be considered before intervention when patients have preexisting RBBB or LBBB.
authors.affiliation: Department of Cardiovascular Medicine, Cleveland, Ohio 44195, USA.
authors.forename: Jian Xin
authors.initials: JX
authors.lastname: Qin
authors.forename: Takahiro
authors.initials: T
authors.lastname: Shiota
authors.forename: Harry M
authors.initials: HM
authors.lastname: Lever
authors.forename: Craig R
authors.initials: CR
authors.lastname: Asher
authors.forename: Zoran B
authors.initials: ZB
authors.lastname: Popović
authors.forename: Neil L
authors.initials: NL
authors.lastname: Greenberg
authors.forename: Deborah A
authors.initials: DA
authors.lastname: Agler
authors.forename: Jeanne K
authors.initials: JK
authors.lastname: Drinko
authors.forename: Nicholas G
authors.initials: NG
authors.lastname: Smedira
authors.forename: E Murat
authors.initials: EM
authors.lastname: Tuzcu
authors.forename: Bruce W
authors.initials: BW
authors.lastname: Lytle
authors.forename: James D
authors.initials: JD
authors.lastname: Thomas
mesh_terms: D002037:Bundle-Branch Block / Q000209:etiology / Q000503:physiopathology; D002312:Cardiomyopathy, Hypertrophic / Q000503:physiopathology / Q000601:surgery* / Q000628:therapy; D016022:Case-Control Studies; D015331:Cohort Studies; D015150:Echocardiography, Doppler; D004562:Electrocardiography; D005260:Female; D006327:Heart Block / Q000209:etiology / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology*; D006346:Heart Septum / Q000601:surgery*; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D010138:Pacemaker, Artificial; D011183:Postoperative Complications / Q000209:etiology / Q000503:physiopathology; D014694:Ventricular Outflow Obstruction / Q000503:physiopathology / Q000601:surgery