Conduction Velocity Dispersion Predicts Postinfarct Ventricular Tachycardia Circuit Sites and Associates With Lipomatous Metaplasia

Abstract

BackgroundRegional myocardial conduction velocity (CV) dispersion has not been studied in postinfarct patients with ventricular tachycardia (VT). ObjectivesThis study sought to compare the following: 1) the association of CV dispersion vs repolarization dispersion with VT circuit sites; and 2) myocardial lipomatous metaplasia (LM) vs fibrosis as the anatomic substrate for CV dispersion. MethodsAmong 33 postinfarct patients with VT, we characterized dense and border zone infarct tissue by late gadolinium enhancement cardiac magnetic resonance, and LM by computed tomography, with both images registered with electroanatomic maps. Activation recovery interval (ARI) was the time interval from the minimum derivative within the QRS complex to the maximum derivative within the T-wave on unipolar electrograms. CV at each EAM point was the mean CV between that point and 5 adjacent points along the activation wave front. CV and ARI dispersion were the coefficient of variation (CoV) of CV and ARI per American Heart Association (AHA) segment, respectively. ResultsRegional CV dispersion exhibited a much larger range than ARI dispersion, with median 0.65 vs 0.24; P < 0.001. CV dispersion was a more robust predictor of the number of critical VT sites per AHA segment than ARI dispersion. Regional LM area was more strongly associated with CV dispersion than fibrosis area. LM area was larger (median 0.44 vs 0.20 cm2; P < 0.001) in AHA segments with mean CV <36 cm/s and CoV_CV >0.65 than those with mean CV <36 cm/s and CoV_CV <0.65. ConclusionsRegional CV dispersion more strongly predicts VT circuit sites than repolarization dispersion, and LM is a critical substrate for CV dispersion.