Relation of regional sympathetic denervation and myocardial perfusion disturbance to wall motion impairment in Chagas’ cardiomyopathy

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Abstract

Impairment of sinus node autonomic control and myocardial perfusion disturbances have been described in patients with chronic Chagas’ cardiomyopathy. However, it is not clear how these conditions contribute to myocardial damage. In this investigation, iodine-123 (I-123) meta-iodobenzylguanidine (MIBG) and thallium-201 myocardium segmental uptake were studied in correlation with the severity of left ventricular (LV) dysfunction detected in various phases of Chagas’ heart disease. Group I consisted of 12 subjects (43 ± 4 years, 7 men) with no symptoms and no cardiac involvement on electrocardiogram (ECG) or echocardiography; group II consisted of 13 patients (48 ± 3 years, 9 men) with abnormal resting ECG and/or echocardiographic segmental abnormalities, and LV ejection fraction of ≥0.5; group III was comprised of 12 patients (59 ± 3 years, 10 men) with more severe heart disease, LV dilation, and LV ejection fraction of <0.5. Eighteen control volunteers (38 ± 3 years, 9 men) were also included in the study. I-123 MIBG single-photon emission computed tomographic (SPECT) segmental uptake defects were observed in group I (33%), group II (77%), and group III (92%). Quantitative analysis showed mean areas of reduced LV I-123-MIBG uptake: group I was 3.7 ± 2.1%; group II was 8.3 ± 2.3%; and group III was 19.0 ± 3.3%. The differences between group I and both groups II and III were statistically significant (p <0.001, analysis of variance test). Myocardial perfusion defects (reversible, fixed, and paradox) were observed in group I (83%), group II (69%), and group III (83%). A marked topographic association between perfusion, innervation, and wall motion abnormalities (assessed by gated-SPECT perfusion studies) was observed in all the groups. Defects predominated in the inferior, posterior lateral, and apical LV regions. Thus, extensive impairment of cardiac sympathetic function at the ventricular level occured early in the course of Chagas’ cardiomyopathy and was related to regional myocardial perfusion disturbances, before wall motion abnormalities. Both conditions are associated with progression of ventricular dysfunction.

Section snippets

Study population

The study population consisted of 37 subjects from endemic regions who had positive standard serologic tests (immunofluorescence reaction) for Chagas’ disease. They were divided into 3 groups according to the severity of myocardial dysfunction as characterized by recent clinical and/or pathophysiologic classifications.16, 17

Group I was comprised of 12 asymptomatic subjects (43 ± 4 years [mean ± SEM], 7 men) with no cardiac involvement as evaluated by chest x-rays, 12-lead electrocardiogram

Global left ventricular function (planar gated blood pool studies)

As expected by group characteristics, mean LV ejection fraction values for each group showed extremely significant differences (p <0.0001), whereas the Tukey-Kramer multiple comparison test indicated that group I results were not significantly different from controls (p = 0.099) (Table 1).

Segmental wall motion analysis (gated blood pool SPECT studies)

In group II, 85% of patients had wall motion abnormalities. A total of 21% of segments were involved: 14 segments had mild, 13 segments had moderate, and 8 segments had severe hypokinesia, and 10 segments had

Discussion

In this study, regional MIBG uptake abnormalities were detected in patients with Chagas’ heart disease in which concomitant causes of autonomic disturbances were ruled out, except for coronary artery disease, which was only excluded in group II and III patients with reversible defects, but could not be definitely excluded, by angiography, in all subjects. The regional MIBG uptake abnormalities found in chagasic patients clearly indicated the presence of anatomic and/or functional disturbances

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