Doença da valva mitral em cães: repercussões cardiovascular e renal.

Abstract

This thesis consists of three chapters that address the mitral valve disease (MVD) in dogs under the aspects of cardiac function, renal and its therapy. Two of the chapters are presented as scientific article and as a case report. In the first chapter aimed to correlate the concentrations of cardiac biomarker N-terminal prohormone of B-type natriuretic peptide (NT-proBNP) and hormone aldosterone in dogs with mitral valve disease (MVD) to the findings of echodopplercardiograms, x-rays and serum biochemical tests. It also estimated the components of biological variability of NTproBNP. There was a reduction in mean aldosterone and a small positive correlation with aldosterone serum Na+ in GMVDA and negative correlation of NT-proBNP with Na+ serum in GMVDT. Serum average concentrations of NT-proBNP of MVD groups were above the average of the GC, but there was no significant difference; the amounts resulting from r-IoI was 2.66 and RCV 47.3%. The ratio of left atrial diameter - aorta (LA/Ao) showed up increased comparing T0 the GMVDA to GMVDT; the DC of GMVDT had significant difference when compared to the CG; animals Class B2 and C, when spread over the treatment time, had the shortening fraction values (FS) and ejection fraction (EF) of T0-GMVDA and GMVDT above the GC. These findings demonstrated that treatment employed in dogs with MVD this study stabilized NTproBNP values even after one year of treatment and the use of ACE inhibitors determined reduction in aldosterone concentrations and consequent reduction in blood pressure and congestive heart failure. The second chapter proposed to evaluate the glomerular filtration rate (GFR), fractional excretion of electrolytes and Cystatin C in dogs with MVD before and during treatment with ACE inhibitors (enalapril and benazepril) associated with furosemide. There was a significant reduction of serum aldosterone between the times of GMVD and groups; P/U C, creatinine, urea, Cystatin C were normal before and no change after treatment; GFR remained normal, but with reduction throughout treatment. There was an increase of mean EF Na+, K+ and Cl- both in relation to the reference value on the GC indicating tubular injury. However, EF Ca+2i and EF P been increased, indicating a reduction in tubular reabsorption both before and during treatment. Given the results can be concluded that the MVD caused reduction in GFR and tubular damage, but the diuretic action of furosemide in tubular reabsorption did not compromise the homeostasis of electrolytes. The third chapter described the renal repercussion on a dog with MVD treated with furosemide, pimobendan and benazepril and concluded that the MVD caused tubular injury and proteinuria persisted and worsened after the initiation of treatment with furosemide and benazepril. Thus, it was verified the presence of cardiorenal syndrome that should be monitored in order to adapt the treatment to minimize early renal lesions.