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Is endothelial microvascular function equally impaired among patients with chronic Chagas and ischemic
Juliana Pereira Borges1, Fernanda de Souza Nogueira Sardinha Mendes2, Gabriella de Oliveira Lopes3
1Laboratory of Physical Activity and Health Promotion, State University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Insights
Microvascular endothelial function is similarly impaired in patients with Chronic Chagas cardiomyopathy (CCC) and ischemic cardiomyopathy. This study compared skin microvascular blood flow in these patients and healthy controls.
Area of Science:
- Cardiology
- Vascular Biology
- Tropical Medicine
Background:
- Pathophysiological pathways in Chronic Chagas cardiomyopathy (CCC) and other cardiomyopathies are not fully understood.
- Systemic microvascular abnormalities are implicated in ischemic heart disease pathogenesis.
- Microvascular endothelial function in CCC requires further investigation.
Purpose of the Study:
- To compare microvascular endothelial function in patients with CCC versus those with ischemic cardiomyopathy.
- To elucidate the role of microvascular abnormalities in CCC pathogenesis.
Main Methods:
- Assessed microvascular reactivity in 21 CCC patients, 21 ischemic cardiomyopathy patients, and 21 healthy controls.
- Measured forearm skin microvascular blood flow using laser speckle contrast imaging.
- Utilized acetylcholine (ACh) iontophoresis to assess endothelial-dependent vasodilation.
Main Results:
- Healthy controls exhibited significantly greater ACh-induced forearm blood flow increase compared to both patient groups (p < 0.0001).
- Patients with CCC and ischemic cardiomyopathy showed comparable impairments in ACh-induced skin blood flow changes (p = 0.55).
Conclusions:
- Endothelial microvascular function is equally impaired in patients with CCC and ischemic cardiomyopathy.
- Shared microvascular dysfunction may contribute to the pathophysiology of both conditions.
Background:
Chronic Chagas cardiomyopathy (CCC) and cardiomyopathies due to other etiologies involve differences in pathophysiological pathways that are still unclear. Systemic microvascular abnormalities are associated with the pathogenesis of ischemic heart disease. However, systemic microvascular endothelial function in CCC remains to be elucidated. Thus, we compared the microvascular endothelial function of patients presenting with CCC to those with ischemic cardiomyopathy disease.
Methods:
Microvascular reactivity was assessed in 21 patients with cardiomyopathy secondary to Chagas disease, 21 patients with cardiomyopathy secondary to ischemic disease and 21 healthy controls. Microvascular blood flow was assessed in the skin of the forearm using laser speckle contrast imaging coupled with iontophoresis of acetylcholine (ACh).
Results:
Peak increase in forearm blood flow with ACh iontophoresis in relation to baseline was greater in healthy controls than in patients with heart disease (controls: 162.7 ± 58.4% vs. ischemic heart disease: 74.1 ± 48.3% and Chagas: 85.1 ± 68.1%; p < 0.0001). Patients with Chagas and ischemic cardiomyopathy presented similar ACh-induced changes from baseline in skin blood flow (p = 0.55).
Conclusion:
Endothelial microvascular function was equally impaired among patients with CCC and ischemic cardiomyopathy.
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