title: Predictors of systolic augmentation from left ventricular preexcitation in patients with dilated cardiomyopathy and intraventricular conduction delay.
abstract: BACKGROUND
  VDD pacing can enhance systolic function in patients with dilated cardiomyopathy and discoordinate contraction; however, identification of patients likely to benefit is unclear. We tested predictors of systolic responsiveness on the basis of global parameters as well as directly assessed mechanical dyssynchrony.
  
  
  RESULTS
  Twenty-two DCM patients with conduction delay were studied by cardiac catheterization with a dual-sensor micromanometer to measure LV and aortic pressures during sinus rhythm and LV free-wall pacing. Pacing enhanced isovolumetric (dP/dt(max)) and ejection-phase (pulse pressure, PP) systolic function by 35+/-21% and 16.4+/-11%, respectively, and these changes correlated directly (r=0.7, P=0.001). %DeltadP/dt(max) was weakly predicted by baseline QRS (r=0.6, P<0.02), more strongly by baseline dP/dt(max) (r=0.7, P=0.001), and best by bidiscriminate analysis combining baseline dP/dt(max) < or =700 mm Hg/s and QRS > or =155 ms to predict %DeltadP/dt(max) > or =25% and %DeltaPP > or =10% (P<0.0005, chi(2)), with no false-positives. Benefit could not be predicted by %DeltaQRS. To test whether basal mechanical dyssynchrony predicted responsiveness to LV pacing, circumferential strains were determined at approximately 80 sites throughout the LV by tagged MRI in 8 DCM patients and 7 additional control subjects. Strain variance at time of maximal shortening indexed dyssynchrony, averaging 28.0+/-7.1% in normal subjects versus 201.4+/-84.3% in DCM patients (P=0.001). Mechanical dyssynchrony also correlated directly with %DeltadP/dt(max) (r=0.85, P=0.008). Conclusions-These results show that although mechanical dyssynchrony is a key predictor for pacing efficacy in DCM patients with conduction delay, combining information about QRS and basal dP/dt(max) provides an excellent tool to identify maximal responders.
authors.affiliation: Division of Cardiology, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
authors.forename: G S
authors.initials: GS
authors.lastname: Nelson
authors.forename: C W
authors.initials: CW
authors.lastname: Curry
authors.forename: B T
authors.initials: BT
authors.lastname: Wyman
authors.forename: A
authors.initials: A
authors.lastname: Kramer
authors.forename: J
authors.initials: J
authors.lastname: Declerck
authors.forename: M
authors.initials: M
authors.lastname: Talbot
authors.forename: M R
authors.initials: MR
authors.lastname: Douglas
authors.forename: R D
authors.initials: RD
authors.lastname: Berger
authors.forename: E R
authors.initials: ER
authors.lastname: McVeigh
authors.forename: D A
authors.initials: DA
authors.lastname: Kass
mesh_terms: D000328:Adult; D000368:Aged; D001794:Blood Pressure; D002037:Bundle-Branch Block / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D002311:Cardiomyopathy, Dilated / Q000150:complications / Q000503:physiopathology*; D004562:Electrocardiography; D006339:Heart Rate; D006801:Humans; D008279:Magnetic Resonance Imaging; D008875:Middle Aged; D010138:Pacemaker, Artificial; D011237:Predictive Value of Tests; D013599:Systole / Q000502:physiology*; D016277:Ventricular Function, Left / Q000502:physiology*