Changes in Myocardial Perfusion Correlate With Deterioration of Left Ventricular Systolic Function in Chronic Chagas' Cardiomyopathy

Hiss, Flávio Cantarelli; Lascala, Thiago Florentino; Maciel, Benedito Carlos; Marin-Neto, José Antônio; Simões, Marcus Vinı́cius

doi:10.1016/j.jcmg.2008.09.012

Cited by 75 publications

(99 citation statements)

References 22 publications

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“…The individual increase in the perfusion defect area at rest (possibly indicating the presence of fi brosis) was signifi cantly correlated with the corresponding reduction in LV ejection fraction (with a mean decrease over time in the entire group of patients from 55% ± 11% to 50% ± 13%). Hence, in this longitudinal study, the deterioration of LV systolic function over time was associated with both the presence of reversible ischemic defects at the initial assessment and an increase in the extent of irreversible perfusion defects during follow-up 50 .…”

Section: Coronary Microvascular Dysfunctionmentioning

confidence: 74%

“…This suggestion may indeed be the case based on a more recent study of 36 patients with serologically proven Chagas disease who were initially evaluated with Tc-99m-Sestamibi MPS at rest and during physical exercise and who had the nuclear examination repeated after a mean period of 5.6 years 50 . Of the 36 patients, 20 (56%) exhibited reversible ischemic myocardial perfusion defects involving an average of 10.2% ± 9.7% of the LV area, as determined by the SPECT technique.…”

Section: Coronary Microvascular Dysfunctionmentioning

confidence: 93%

See 1 more Smart Citation

Pathogenesis of chronic Chagas cardiomyopathy: the role of coronary microvascular derangements

Marin-Neto

Simões

Rassi

2013

Rev. Soc. Bras. Med. Trop.

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There is ample experimental and clinical evidence of functional and structural microvascular abnormalities occurring in patients with Chagas cardiomyopathy, possibly due to the infl ammatory process and/or autonomic disturbances caused by Trypanosoma cruzi infection. Those microvascular derangements are likely to constitute at least an ancillary factor that potentiates and amplifi es the chronic infl ammation in myocardial tissue. It is possible to devise appropriate therapeutic interventions aimed at reverting or slowing the progression of the microvascular abnormalities to positively affect the natural history of Chagas cardiomyopathy.

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Section: Coronary Microvascular Dysfunctionmentioning

confidence: 74%

Section: Coronary Microvascular Dysfunctionmentioning

confidence: 93%

Pathogenesis of chronic Chagas cardiomyopathy: the role of coronary microvascular derangements

Marin-Neto

Simões

Rassi

2013

Rev. Soc. Bras. Med. Trop.

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“…The impairment of cardiac sympathetic function at the ventricular level that occurs early in the course of Chagas cardiomyopathy is related to regional myocardial perfusion disturbances (Hiss et al, 2009). This occurs before wall motion abnormalities can be demonstrated (Hiss et al, 2009;Simoes et al, 2000). In the same way, abnormal vasodilatation and vasoconstriction at the microcirculatory level may cause myocardial damage in patients with Chagas disease.…”

Section: Microvascular Abnormalities and Ischemiamentioning

confidence: 99%

“…In the same way, abnormal vasodilatation and vasoconstriction at the microcirculatory level may cause myocardial damage in patients with Chagas disease. Both conditions are associated with the progression of ventricular dysfunction (Hiss et al, 2009;Simoes et al, 2000). Transient microvascular ischemic disturbances of low intensity and short duration have been postulated to be the causative mechanisms of Chagas cardiomyopathy.…”

Section: Microvascular Abnormalities and Ischemiamentioning

confidence: 99%

Chagas disease: Present status of pathogenic mechanisms and chemotherapy

et al. 2010

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There are approximately 7.8 million people in Latin America, including Chile, who suffer from Chagas disease and another 28 million who are at risk of contracting it. Chagas is caused by the flagellate protozoan Trypanosoma cruzi. It is a chronic disease, where 20%-30% of infected individuals develop severe cardiopathy, with heart failure and potentially fatal arrhythmias. Currently, Chagas disease treatment is more effective in the acute phase, but does not always produce complete parasite eradication during indeterminate and chronic phases. At present, only nifurtimox or benznidazole have been proven to be superior to new drugs being tested. Therefore, it is necessary to find alternative approaches to treatment of chronic Chagas. The current treatment may be rendered more effective by increasing the activity of anti-Chagasic drugs or by modifying the host's immune response. We have previously shown that glutathione synthesis inhibition increases nifurtimox and benznidazole activity. In addition, there is increasing evidence that cyclooxygenase inhibitors present an important effect on T. cruzi infection. Therefore, we found that aspirin reduced the intracellular infection in RAW 264.7 cells and, decreased myocarditis extension and mortality rates in mice. However, the long-term benefit of prostaglandin inhibition for Chagasic patients is still unknown.

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“…Many investigators have found abnormal myocardial perfusion using isonitrile-99m-technetium (Castro R., et al, 1988) and thallium-201 (Hagar & Rahimtoola, 1991, MarinNeto, et al, 1992 scintigraphy in chagasic patients with normal epicardial coronary arteries. Furthermore, the progression of left ventricular systolic dysfunction is associated with both, the presence of reversible perfusion defects and the increase in perfusion defects at rest (Hiss, et al, 2009, Schwartz & Wexler, 2009. Anatomopathological studies in humans also provided evidence of microvascular damage in CCC.…”

Section: Microvascular Damagementioning

confidence: 99%