Effects of in-hospital diuretic therapy on electrolytes concentration, renal function and survival in 85 dogs with acute congestive heart failure

Critically hill patients with acute congestive heart failure (CHF) may often show haemoconcentration, dysnatremia, dyskalemia and increased azotemia, due to aggressive diuretic therapy. Haemocon-centration is associated with lower risk of mortality, while dysnatremia and dyskalemia are associated with higher mortality in human medicine. The aim of this study was to retrospectively evaluate the impact of in-hospital diuretic therapy for CHF on selected laboratory parameters and long-term mortality. Dogs with clinical and radiological evidence of CHF confirmed by echocardiography were included. Blood samples collected through out the hospitalization at presentation (T0) and discharge (T1) were: venous blood gas analysis (VBGA), serum creatinine (sCr), blood ureanitrogen (BUN), microhematocrit (Htc) and total proteins (TP). Length of hospital stay, ACVIM class and other clinical indices were recorded. Haemoconcentration was defined as a simultaneous increase in Htc and total protein. A total of 85 dogs (45 male and 40 female; mean age 11.07 \ue003 2.54 years; mean weight 8.86 \ue003 6.92 kg) were included. Thirty-six dogshad previous episodes of CHF. Mean length of in-hospital stay was 31.15 \ue003 17.35 hours. Treatment protocol included a single furosemide endovenous bolus at 2 mg/kg followed by multiple 1 mg/kg bolus/hour until respiratory rate reach 40 respiratory rate. Each dog received 8.6 \ue003 2.8 mg/kg and 11.1 \ue003 2.9 mg/kg furosemide in 24 and 48 hours respectively. Ten dogs received higher furosemide doses or torasemide bolus. Haemoconcentration was reached in the 33% of dogs. Considering the VBGA and biochemistry results, the number of dogs showing extra-range values (T0-T1) were respectively: hyponatremia (10-23), hypernatremia (13-17), hypokalemia (18-30), hyperkalemia (10-10), hypocloremia (46-61), increased BUN (26-34), increased sCr (3-8). Fourty-one dogs experienced cardiac death, 12 during hospitalization, the remaining dogs between 3 and 721 days after admission. Stepwise backward regression demonstrated haemoconcentration (HR 0.33) and disnatremia (HR 2.85) influence over outcome. Statisti-cally significant correlation (Pearson) was seen between furosemide dose and kalemia (r = 120.32, P = 0.014) and between BUN and sCr (r = 0.27, P = 0.021). No correlation was seen between furosemide dose and the variables sCr, BUN, Htc and between sCr and Htc. In conclusion, haemoconcentration and disnatremia affected the out-come in dogs with CHF. Haemoconcentration was associated withlower risk of mortality and had to be considered a target in CHF therapy. In-hospital diuretic therapy increased electrolyte disorder due to loop diuretics inhibition of the renal Na, K, Cl cotransporter in the Henle's loop and disnatremia was a risk factor for adverse outcome. Diuretics doses and haemoconcentration didn't play a direct role in inducing renal disfunction

Pulmonary ballon valvuloplasty in 95 dogs: effect of valve morphology on immediate and late outcome

Pulmonic stenosis (PS) is one of the most common congenital heart defects in dogs. Pulmonary balloon valvuloplasty (PBV) is now the treatment of choice for PS in humans as in dogs. In human PBV has gained acceptance as the first option in the management of PS in any age group (newborn, children, adult) and any valve morphology (typical or dysplastic). Valve morphology, hinge point diameter and immediate higher residual gradient are identified as the most significant independent predictors of long term results. Concerning dogs, only few studies analyzed the importance of valve morphology as selection criteria for PBV. The first purpose of this retrospective study is evaluating if valve morphology is an important factor for successful PBV as it has been confirmed for human. PBV was performed in 95 dogs (75 type A PS, 16 a type B and 4 intermediate type). The mean peak Doppler gradient before PBV was 124 mmHg (\ub140) in dogs with type A (range 45-227 mmHg) and 133 mmHg (\ub130) in dogs with type B (range 65-182 mmHg). The mean peak Doppler gradient after the PBV (24h) was for the type A 49 mmHg (\ub121) (range 15-104 mmHg) and for the type B 68 mmHg (\ub124) (range 35-109 mmHg), documenting a significant reduction of gradient in both groups (P<0,0001). The mean peak Doppler gradient at 1 year was 55 mmHg (\ub120) in dogs with type A (range 15-110 mmHg) and 73 mmHg (\ub131) in dogs with type B (range 25-119 mmHg), confirming a persistent gradient reduction in both groups (P<0,0001). The mean pressure gradient after the procedure at 24h (P<0,001) and at 1 year (P<0,05) between group A and B resulted to be lower in type A, suggesting better results. The PBV was considered successful (more than 50% reduction in pressure gradient from baseline) in 65 dog with type A (90%) and in 7 dogs with PS type B (54%). The PBV was performed without significant complications in 93% of dogs (88 dogs: 71 with type A, 13 with type B and 4 with intermediate type). Our study allows the following conclusions: PBV is effective in type A and B PS, furthermore PBV is more effective in type A. In human literature similar results are reported. The PBV of patient with dysplastic valve was less effective (61,11%) when compared with those with typical PS (80,59%). Despite the success rate was lower in the dysplastic group, PBV is still considered the first treatment option in both types of PS. Finally PBV in type B (or dysplastic) may avoided or delayed the need of surgery and provided a good long outcome in dogs as it occurs in humans

The predictive value of clinical, radiographic, echocardiographic variables and cardiac biomarkers for assessing risk of the onset of heart failure or cardiac death in dogs with preclinical myxomatous mitral valve disease enrolled in the DELAY study

Objectives: To identify the predictive value on time to onset of heart failure (HF) or cardiac death of clinical, radiographic, and echocardiographic variables, as well as cardiac biomarkers N-terminal pro brain natriuretic peptide (NT-proBNP) and cardiac troponin I in dogs with preclinical myxomatous mitral valve disease (MMVD). Animals: One hundred sixty-eight dogs with preclinical MMVD and left atrium to aortic root ratio ≥1.6 (LA:Ao) and normalized left ventricular end-diastolic diameter ≥1.7 were included. Methods: Prospective, randomized, multicenter, single-blinded, placebo-controlled study. Clinical, radiographic, echocardiographic variables and plasma cardiac biomarkers concentrations were compared at different time points. Using receiving operating curves analysis, best cutoff for selected variables was identified and the risk to develop the study endpoint at six-month intervals was calculated. Results: Left atrial to aortic root ratio >2.1 (hazard ratio [HR] 3.2, 95% confidence interval [95% CI] 1.9-5.6), normalized left ventricular end-diastolic diameter > 1.9 (HR: 6.3; 95% CI: 3.3-11.8), early transmitral peak velocity (E peak) > 1 m/sec (HR: 3.9; 95% CI: 2.3-6.7), and NT-proBNP > 1500 ρmol/L (HR: 5.7; 95% CI: 3.3-9.5) were associated with increased risk of HF or cardiac death. The best fit model to predict the risk to reach the endpoint was represented by the plasma NT-proBNP concentrations adjusted for LA:Ao and E peak. Conclusions: Logistic and survival models including echocardiographic variables and NT-proBNP can be used to identify dogs with preclinical MMVD at higher risk to develop HF or cardiac death

The predictive value of clinical, radiographic, echocardiographic variables and cardiac biomarkers for assessing risk of the onset of heart failure or cardiac death in dogs with preclinical myxomatous mitral valve disease enrolled in the DELAY study

Objectives: To identify the predictive value on time to onset of heart failure (HF) or cardiac death of clinical, radiographic, and echocardiographic variables, as well as cardiac biomarkers N-terminal pro brain natriuretic peptide (NT-proBNP) and cardiac troponin I in dogs with preclinical myxomatous mitral valve disease (MMVD). Animals: One hundred sixty-eight dogs with preclinical MMVD and left atrium to aortic root ratio ≥1.6 (LA:Ao) and normalized left ventricular end-diastolic diameter ≥1.7 were included. Methods: Prospective, randomized, multicenter, single-blinded, placebo-controlled study. Clinical, radiographic, echocardiographic variables and plasma cardiac biomarkers concentrations were compared at different time points. Using receiving operating curves analysis, best cutoff for selected variables was identified and the risk to develop the study endpoint at six-month intervals was calculated. Results: Left atrial to aortic root ratio &gt;2.1 (hazard ratio [HR] 3.2, 95% confidence interval [95% CI] 1.9–5.6), normalized left ventricular end-diastolic diameter &gt; 1.9 (HR: 6.3; 95% CI: 3.3–11.8), early transmitral peak velocity (E peak) &gt; 1 m/sec (HR: 3.9; 95% CI: 2.3–6.7), and NT-proBNP &gt; 1500 ρmol/L (HR: 5.7; 95% CI: 3.3–9.5) were associated with increased risk of HF or cardiac death. The best fit model to predict the risk to reach the endpoint was represented by the plasma NT-proBNP concentrations adjusted for LA:Ao and E peak. Conclusions: Logistic and survival models including echocardiographic variables and NT-proBNP can be used to identify dogs with preclinical MMVD at higher risk to develop HF or cardiac death

DELay of Appearance of sYmptoms of Canine Degenerative Mitral Valve Disease Treated with Spironolactone and Benazepril: the DELAY Study

Introduction: Efficacy of renin-angiotensin-aldosterone system (RAAS) blockade using angiotensin-converting enzyme inhibitors (ACEi) in dogs with preclinical myxomatous mitral valve disease (MMVD) is controversial. Hypothesis: Administration of spironolactone (2\u20134 mg q 24 h) and benazepril (0.25\u20130.5 mg q 24 h) in dogs with preclinical MMVD, not receiving any other cardiac medications, delays the onset of heart failure (HF) and cardiac-related death. Moreover, it reduces the progression of the disease as indicated by echocardiographic parameters and level of cardiac biomarkers N-terminal pro brain natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI). Animals: 184 dogs with pre-clinical MMVD and left atrium-to-aortic root ratio (LA:Ao) 651.6 and normalized left ventricular end-diastolic diameter (LVEDDn) 651.7. Methods: This is a prospective, randomized, multicenter, single-blinded, placebo-controlled study. Primary outcome variable was time-to-onset of first occurrence of HF or cardiac death. Secondary end points included effect of treatment on progression of the disease based on echocardiographic and radiographic parameters, as well as variations of NT-proBNP and cTnI concentrations. Results: The median time to primary end point was 902 days (95% confidence interval (CI) 682-not available) for the treatment group and 1139 days (95% CI 732-NA) for the control group (p = 0.45). Vertebral heart score (p = 0.05), LA:Ao (p < 0.001), LVEDDn (p < 0.001), trans-mitral E peak velocity (p = 0.011), and NT-proBNP (p = 0.037) were lower at the end of study in the treatment group. Conclusions: This study failed in demonstrating that combined administration of spironolactone and benazepril delays onset of HF in dogs with preclinical MMVD. However, such treatment induces beneficial effects on cardiac remodeling and these results could be of clinical relevance