Ventricular tachycardia in Chagas' disease: a comparison of clinical, angiographic, electrophysiologic and myocardial perfusion disturbances between patients presenting with either sustained or nonsustained forms

Ventricular tachycardia (VT) is common among patients with Chagas' heart disease but the ultimate mechanisms responsible for its sustained and nonsustained forms are not understood. This study aimed at determining which factors differentiate between patients with sustained (S-VT) and nonsustained VT (NS-VT). Fifty-six consecutive chagasic patients with VT were prospectively selected: 28 patients with spontaneous S-VT and 28 patients with NS-VT. The patients underwent clinical, angiographic, electrophysiologic and myocardial perfusion examination. Syncope episodes (S-VT: 43% versus NS-VT: 11%, p=0.007) and induction of S-VT by programmed ventricular stimulation (S-VT: 89% versus NS-VT: 7%, p=0.001) were significantly more frequent in S-VT patients. Evidence of a scar-related reentry was observed in all 24 S-VT patients who underwent endocardial mapping for attempted radiofrequency ablation of 33 VTs. Overall, 29 VTs arose from the LV (88%) and 4 VTs arose from the RV (12%). Among these, 27 VTs (82%) were related to LV inferolateral scar, 2 VTs (6%) were related to LV apical scar, and 4 VTs (12%) were related to RV scars. A significantly higher prevalence of wall motion abnormalities (S-VT: 82% versus NS-VT: 46%, p=0.005) and myocardial perfusion defects (basal segments, S-VT: 95.5% versus NS-VT: 44%, p=0.001) was documented within the LV inferior and/or posterolateral regions in S-VT patients compared to NS-VT. In conclusion: (a) VT may arise from various regions in both ventricles, but LV inferolateral scar is the main source of S-VT reentrant circuits; (b) there is good topographic correlation between myocardial perfusion, wall motion abnormalities and areas that originate S-VT; (c) although to a lesser extent, wall motion and perfusion defects also occur in a relevant proportion of chagasics with NS-VT.