Despite substantial progress toward its control, Chagas disease continues to be a major public health problem in Latin America and has become a global health concern. The disease affects approximately 6 million people, of whom 20-40% will develop cardiomyopathy over the years after the initial Trypanosoma cruzi infection. Chagas cardiomyopathy is the most serious and frequent manifestation of Chagas disease. Clinical manifestations vary widely according to the severity of myocardial dysfunction, ranging from asymptomatic to severe forms, including dilated cardiomyopathy with heart failure, arrhythmias, thromboembolism events, and sudden death. Chagas disease is a risk factor for stroke regardless of the severity of cardiomyopathy, which is a leading cause of chronic disability. Classically, stroke etiology in patients with Chagas disease is thought to be cardioembolic and related to apical aneurysm, mural thrombus, and atrial arrhythmias. Although most strokes are thromboembolic, other etiologies have been observed. Small vessel disease, atherosclerosis, and cryptogenic diseases have been reported in patients with Chagas disease and stroke. The potential mechanisms involved in non-embolic strokes include the presence of associated risk factors, pro-inflammatory and prothrombotic disease states, and endothelial dysfunction. However, the contribution of each mechanism to stroke in Chagas disease remains unclear. The review aims to provide an overview of stroke in Chagas disease, highlighting the main pathophysiological mechanisms, clinical presentation, approaches for prevention, and unanswered questions regarding treatment strategies.
Introduction: Pathologic derangements of rheumatic mitral stenosis (MS) change valve shape which may determine the hemodynamic severity of the obstruction. This study was designed to assess the role of mitral valve shape on transvalvar pressure gradients in patients with MS. Methods: A total of 186 patients with MS, area of 1.1 ± 0.3 cm 2 , who underwent three-dimensional (3D) transesophageal echocardiographic study, were enrolled. A set of morphological variables to assess the mitral valve (MV) geometry, including diameter, area, height, volume and aortic-mitral angle was obtained using dedicated software. 3D doming index, the proposed index to differentiate between conical and dome shapes, was calculated by dividing the valvar volume (tenting volume) by the valvar height (tenting height). The resulting "average area" was divided by the minimum area of the 3D annulus (Figure 1). Determinants of mean pressure gradient were assessed using linear regression models. Results: The 3D doming index was significantly correlated with transmitral gradient in the multivariate model (p = 0.007), adjusted for age, sex, heart rate, pulmonary artery systolic pressure, net atrioventricular compliance (C n ), and left atrial volume. Specifically, the inclusion of 3D doming index in a model with other factors that influence gradients resulted in improvement in model performance evaluated by R 2 which increased from 0.57 to 0.60. In the 152 patients who underwent successful percutaneous valvuloplasty, there was a significant correlation between the percentage of increase in the valve area and 3D doming index (r = 0.2; p <0.026), after adjustment for the echo score revisited. Conclusions: In rheumatic MV stenosis, 3D geometric shape was associated with transmitral pressure gradient, independent of other parameters. 3D Doming index correlated with the percentage increase in MV area in a subgroup undergoing valvuloplasty.
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