RESUMO
CONTEXT: Vascular changes can be a risk factor for recurrent and new events of stroke. However, few information is known regarding the variables related to aortic pulse wave morphology in stroke individuals. OBJECTIVE: To analyze aortic pulse wave morphology (arterial stiffness indices, hemodynamics and vascular variables) and to compare the paretic and non-paretic sides in individuals after chronic stroke. DESIGN: In this cross-sectional study stroke individuals had arterial stiffness indices, hemodynamics and vascular variables assessed with brachial artery oscillometry. T-test (CI95%) was used in order to compare the variables between the paretic and non-paretic sides. RESULTS: Twenty individuals were included, 65% men (60.3 SD 16.7 years). The following variables: (mean difference [CI95%]): coefficient of reflection (-2.33 [-4.60 to -0.07]), peak of ejection wave, P1 (5.32 [2.75 to 7.90] and peak of ejection wave, P2 (6.17 [2.55 to 9.78]), central diastolic blood pressure (mean difference [IC95%]): (-3.75 [-6.09 to -1.40]), central systolic blood pressure (-6.17 [-9.74 to -2.59]), mean arterial pressure (-4.46 [-7.08 to -1.84]), peripheral diastolic blood pressure (-3.48 [-5.94 to -1.02]) and peripheral systolic blood pressure (-5.53 [-9.54 to -1.52]) were higher in paretic than non-paretic side. Hemodynamics parameters were similar in both sides. CONCLUSIONS: In this study we demonstrated, for the first time, that many parameters from aortic pulse wave were higher in paretic compared with non-paretic side in individuals after chronic stroke, suggesting that peripheral vascular changes affect heart-vascular coupling in these individuals.
RESUMO
Vascular disorders have a direct link to mortality in the acute phase of Trypanosoma cruzi infection. However, the underlying mechanisms of vascular dysfunction in this phase are largely unknown. We hypothesize that T. cruzi invades endothelial cells causing dysfunction in contractility and relaxation of the mouse aorta. Immunodetection of T. cruzi antigen TcRBP28 was observed in endothelial cells. There was a decreased endothelial nitric oxide synthase (eNOS)-derived NO-dependent vascular relaxation, and increased vascular contractility accompanied by augmented superoxide anions production. Endothelial removal, inhibition of cyclooxygenase 2 (COX-2), blockade of thromboxane A2 (TXA2) TP receptors, and scavenger of superoxide normalized the contractile response. COX-2, thromboxane synthase, inducible nitric oxide synthase (iNOS), p65 NFκB subunit and p22(phox) of NAD(P)H oxidase (NOX) subunit expressions were increased in vessels of chagasic animals. Serum TNF-α was augmented. Basal NO production, and nitrotyrosine residue expression were increased. It is concluded that T. cruzi invades mice aorta endothelial cells and increases TXA2/TP receptor/NOX-derived superoxide formation. Alongside, T. cruzi promotes systemic TNF-α increase, which stimulates iNOS expression in vessels and nitrosative stress. In light of the heart failure that develops in the chronic phase of the disease, to understand the mechanism involved in the increased contractility of the aorta is crucial.
