Cardiovascular changes in renal failure.
ABSTRACT In patients with renal failure cardiovascular complications are an important clinical problem and cardiac death is the main cause of death in these patients. It is well documented that cardiac risk is increased by a factor of 20 in uremic patients compared with age- and sex-matched segments of the general population. This finding in patients with renal failure can be at least partially explained by the well-described structural and metabolic abnormalities of the myocardium. The present article focuses on the structural changes in the heart and the vasculature and their potential repercussions for cardiovascular function, in particular their contribution to the high cardiovascular morbidity and mortality in patients with renal failure.
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ABSTRACT: Although renal dysfunction is a known risk factor for cardiovascular disease (CVD), there are few experimental studies investigating the cardiovascular consequences of this condition. To analyze the impact of the induction of renal dysfunction on biomarkers of cardiovascular risk and on the histology of subepicardial vessels. This experimental study involved thirty Wistar male rats, which were divided into two groups. One (chronic kidney disease - CKD group) underwent renal ablation, and the other (SHAM group) was submitted to kidney manipulation only. Both groups were followed up for eight weeks. During follow-up, serum levels of urea, phosphorus and TNF-α were measured. Heart tissue was processed for histological analysis. The CKD group had increased levels of urea and phosphorus, in comparison with the SHAM group. The levels of TNF-α were increased in the CKD group and undetectable in the SHAM group (p < 0.05). Thickness of the middle layer of the subepicardial vessels of the CKD group was significantly higher than that of the SHAM group (p = 0.011). Induction of renal dysfunction in rats increased the biomarkers of cardiovascular risk and led to a thickening of the subepicardial vessels when compared with normal controls.Jornal Brasileiro de Nefrologia 12/2011; 33(4):408-12.
Conference Paper: Pole assignment and a theorem from exterior algebra[Show abstract] [Hide abstract]
ABSTRACT: This paper presents an extension of a basic decomposition result from the exterior algebra of F-vector spaces to that of free F[s]-modules and explains its relevance to certain pole assignment problems associated with minimal design.Decision and Control including the 16th Symposium on Adaptive Processes and A Special Symposium on Fuzzy Set Theory and Applications, 1977 IEEE Conference on; 01/1978
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ABSTRACT: BACKGROUND: Left ventricle (LV) structural change in chronic kidney disease (CKD) patients is due principally to a chronic increase in volume and pressure overload. LV torsion has been shown to be a key factor of evaluating LV function, but has rarely been assessed in CKD by three-dimensional speckle tracking imaging (3D STI). The purpose of this study is to evaluate LV torsion in CKD patients receiving hemodialysis compared with normal healthy subjects. METHODS: Twenty-seven CKD patients on hemodialysis and 27 healthy volunteers were recruited. 3D STI was performed immediately before hemodialysis in the dialysis room. The rotation, twist, and torsion of the LV were automatically calculated by commercialized software for each segment of the LV. RESULTS: Body weight (P < 0.01), both systolic and diastolic blood pressure (P < 0.01), end diastolic and end systolic volume (P < 0.05), and ejection fractions (P < 0.01) showed statistically significant differences between the two groups. There were also significant differences in global value of rotation (3.0 ± 2.0 vs. 2.5 ± 1.9 deg P < 0.05), twist (4.6 ± 3.3 vs. 2.7 ± 1.9 deg P < 0.05), basal torsion (1.6 ± 1.1 vs. 0.9 ± 0.6 deg/cm P < 0.05) and regional torsion (1.6 ± 1.2 vs. 0.9 ± 0.8 deg/cm P < 0.05) between healthy volunteers and CKD patients. CONCLUSION: Assessment of LV torsion by newly developed 3D STI is less laborious and time-consuming. Decrease of LV torsion in CKD patients might be due to the marked disarray of myocardial fibers in a uremic heart that affects LV structure, resulting in non-uniform LV torsion.