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

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Abstract

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.

Introduction

Chagas' disease is a major public health problem in several Central and South American countries [1]. Chronic Chagas' heart disease is its most important clinical presentation [2], and sudden death and congestive heart failure are the leading causes of death [3]. Current evidence suggests that sustained monomorphic ventricular tachycardia (VT) degenerating into ventricular fibrillation is the major mechanism of sudden death in this setting [3]; however, hemodynamically stable sustained VT also occurs in a subset of chagasic patients [3], [4]. Although the ultimate factors leading to sustained, monomorphic VT in chagasic patients are not fully understood, nonhomogeneous conduction in a scarred ventricular area is believed to be the most important causative factor [4], [5], [6], [7]. Patients with nonsustained VT are also at risk, especially when ventricular dysfunction is present [3].

Despite angiographically normal coronary epicardial arteries, Chagas' patients typically mimic post-myocardial infarction patients, in showing segmental ventricular dysynergies which appear during the early stages of the chronic phase of disease [8], [9], [10], [11], [12]. Another peculiar finding in the natural history of Chagas' heart disease is the early and prominent right ventricular (RV) involvement that explains why chagasic patients with heart failure usually have predominant systemic congestion [9], [10]. Even though the apical aneurysm has been recognized as the most typical and prevalent left ventricular (LV) regional wall motion abnormality in Chagas' disease [8], [9], [10], [11], [12], previous attempts to manage patients with recurrent sustained VT through surgical apical aneurysmectomy have been unsuccessful [5]. Also, preliminary reports suggest that the substrate for VT in most chagasic patients could be related to scars within the LV inferolateral wall [5], [6], [7].

It is not known whether the location of wall motion abnormalities within the left and right ventricles could differentiate between chagasic patients with sustained versus nonsustained VT. While several mechanisms have been proposed for the genesis of segmental wall motion abnormalities in this setting [13], [14], [15], [16], [17], [18], [19], [20], [21], there is persuasive evidence that myocardial ischemia at the microvascular level may play a relevant role in the formation of the chronic myocardial lesions [17], [18], [19], [20], [21]. However, no studies have correlated the presence of perfusion and/or wall motion impairment with the development of either sustained or nonsustained VT in chagasic patients.

The present study was designed to compare the clinical, electrocardiographic, angiographic, electrophysiologic, biventricular wall motion, and myocardial perfusion characteristics of chagasic patients with sustained versus nonsustained VT.

Section snippets

Study population

The subjects of this study were 56 consecutive patients with Chagas' heart disease who were referred from the general outpatient clinic of this Institution to the Arrhythmia Outpatient Unit of the Division of Cardiology, Hospital das Clínicas of the Medical School of Ribeirão Preto for evaluation and therapy of either sustained or nonsustained ventricular tachycardia between May 1996 and August 1999. Twenty-eight patients had spontaneous sustained VT (S-VT group) and the remaining 28 patients

Patient characteristics

The clinical, electrocardiographic, electrophysiologic, and radionuclide angiography findings for the two groups are shown in Table 1. There were no significant differences between groups with respect to age and gender. Syncope episodes were significantly more frequent in S-VT group compared to NS-VT (43% versus 11%, p=0.007). The mean left and right ventricular ejection fractions, as assessed by radionuclide angiography, were also comparable in the two groups. No significant difference was

Location of sustained VT-related reentrant circuit sites

Forty-two sustained monomorphic VTs were induced during programmed ventricular stimulation in 25 S-VT group patients, and endocardial mapping for attempted radiofrequency ablation was accomplished in 33 VTs in 24 patients. The mean cycle length of mapped VTs was 387±79 ms (range 280 to 570 ms). Twenty-seven VTs had a right bundle-branch block configuration, and six had a left bundle branch-block configuration. In 10 of the 33 VTs, a critical site of the VT-reentry circuit was identified, and

Discussion

This is the first study correlating clinical, electrophysiological, and wall motion/myocardial perfusion disturbances in chagasic patients with either nonsustained or sustained VT. As expected, syncopal episodes were more common in patients with S-VT, but no other clinical and Holter characteristics could distinguish between the two groups of chagasic patients. Also, sustained VT was induced by programmed ventricular stimulation in a much higher proportion of S-VT group patients compared to

Limitations of the study

The present study population represents a small subset of chagasic patients with relatively preserved LV ejection fraction. Therefore, the findings of this study may not apply to patients with different clinical characteristics. Also, the implications of these observations for long-term prognosis and clinical management of these patients have not been addressed in this study, and remain to be established. It is important to note that no patient in this series was refractory to amiodarone. This

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