Detection of experimental right ventricular infarction by isopotential body surface mapping during sinus rhythm and during ectopic ventricular pacing.
Electrocardiographic (ECG) effects of experimental, isolated right ventricular infarction were studied in 10 dogs during sinus rhythm as well as during ectopic right and left ventricular pacing. Infarction was produced by injecting latex into the right coronary artery and ECG consequences were examined by body surface isopotential mapping methods using an 84 electrode torso array. During sinus rhythm, subtraction of preinfarction from postinfarction maps demonstrated that right ventricular necrosis produced abnormal negative potentials over the right hemithorax during the early, middle and late portions of the QRS complex. These patterns corresponded to loss of R waves and deepening of preexistent or development of new Q and S waves in waveforms from this region. Patterns during ectopic ventricular stimulation were compared with mean maps derived from 13 control dogs. Both left and right ventricular pacing after right ventricular infarction resulted in a right-sided abnormal minimum, similar in location to that observed during sinus rhythm, throughout the QRS complex. Thus, right ventricular necrosis does produce QRS complex changes over the right torso that are analogous to those produced by left ventricular infarction, and the dominant pattern of an abnormal right-sided minimum was present regardless of the ventricular activation pattern. This latter finding suggests that the region of right ventricular necrosis provided a supplementary path for current to reenter the heart regardless of the current source, so that an overlying electrode would record negative voltage with all activation patterns.
D000818:Animals; D002304:Cardiac Pacing, Artificial; D004285:Dogs; D004452:Echocardiography / Q000379:methods*; D004562:Electrocardiography; D006352:Heart Ventricles; D009203:Myocardial Infarction / Q000175:diagnosis* / Q000503:physiopathology; D012849:Sinoatrial Node / Q000502:physiology*