title: Spatial heterogeneity of endocardial voltage amplitude in viable, chronically dysfunctional myocardium.
abstract: BACKGROUND
  Although electromechanical mapping has been used to assess cardiac physiology, interpretation is dependent upon the spatial variability of endocardial voltage and local shortening in normal and viable dysfunctional myocardium, which is currently unknown.
  
  
  METHODS
  NOGA mapping was performed in 13 pigs with an established model of viable dysfunctional myocardium produced by a chronic LAD stenosis, and five uninstrumented controls. Voltage maps (122 +/- 7 points each) were obtained in the closed-chest anesthetized state, and (18)F-2-deoxyglucose uptake and TTC staining confirmed viability.
  
  
  RESULTS
  There were systematic regional variations in voltage amplitude in both chronically-instrumented and control animals. Unipolar voltage was ~15% higher in LAD-supplied versus remote myocardium (10.8 +/- 0.3 vs. 8.9 +/- 0.4 mV, p < 0.001), with a similar relative difference in controls (14.0 +/- 0.5 vs. 12.0 +/- 0.4 mV, p < 0.02). In contrast, bipolar voltage was ~35% lower in the LAD territory of both groups (2.2 +/- 0.2 vs. 3.5 +/- 0.2 mV, p < 0.01 and 3.1 +/- 0.3 vs. 5.1 +/- 0.3 mV in controls, p < 0.01). The relative dispersion (SD/mean) of voltage was large, but significantly lower for unipolar versus bipolar measurements (39 +/- 1% vs. 70 +/- 2%, p < 0.001). Variability between hearts was partially related to end-systolic volume (r = 0.58, p < 0.05). Linear local shortening measurements were insensitive to detect anterior hypokinesis.
  
  
  CONCLUSIONS
  Our data demonstrates significant regional and spatial heterogeneity of endocardial voltage and NOGA-derived linear shortening in normal and viable dysfunctional myocardium, with large confidence intervals for individual measurements. Even though the absence of necrosis in this model precludes assessment of the sensitivity and specificity of NOGA mapping to identify infarction, our findings highlight important methodological limitations in using electromechanical mapping to determine viability.
authors.affiliation: VA Western New York Health Care System, University at Buffalo, Buffalo, NY 14214, USA. jaf7@buffalo.edu
authors.forename: James A
authors.initials: JA
authors.lastname: Fallavollita
authors.forename: Uma
authors.initials: U
authors.lastname: Valeti
authors.forename: Sameer
authors.initials: S
authors.lastname: Oza
authors.forename: John M
authors.initials: JM
authors.lastname: Canty
mesh_terms: D000818:Animals; D003326:Coronary Circulation / Q000502:physiology; D004195:Disease Models, Animal; D022062:Electrophysiologic Techniques, Cardiac / Q000379:methods*; D006321:Heart / Q000502:physiology*; D017682:Myocardial Stunning / Q000503:physiopathology*; D012680:Sensitivity and Specificity; D013552:Swine