Azotemia and glomerular filtration rate in dogs with chronic valvular disease.

BACKGROUND: Little information is available about the prevalence of renal dysfunction in dogs with chronic valvular heart disease (CVD). HYPOTHESIS: Azotemia and a decrease in glomerular filtration rate (GFR) are more severe with increased severity of CVD. ANIMALS: 124 (study No. 1) and 24 (study No. 2) client-owned dogs with CVD. METHODS: A retrospective study (study No. 1) was performed to assess the prevalence of azotemia in the New York Heart Association (NYHA) classes of heart failure in dogs with CVD. A prospective study (study No. 2) was then designed to determine GFR in dogs with different degrees of CVD severity. Complete physical examination, electrocardiography, blood pressure measurement, thoracic radiographs, echocardiography, and plasma and urine analyses were also performed. RESULTS: In study No. 1, 50% of the dogs were azotemic and the percentage of azotemic dogs increased with functional class (up to 70% in NYHA class IV patients). In study No. 2, 8/24 dogs were azotemic. Plasma urea and creatinine were higher in NYHA class III-IV dogs compared with class I-II dogs. The GFR was lower (P < .001) in NYHA class III-IV dogs (1.7 +/- 0.7 mL/min/kg) than in class I to II dogs (3.1 +/- 0.8 mL/min/kg). Only 1 dog in class I-II had a GFR below 2 mL/min/kg and only 2/9 class III-IV dogs had a GFR above 2 mL/min/kg. CONCLUSION AND CLINICAL RELEVANCE: Azotemia and renal impairment increase with the severity of congestive heart failure and are frequent findings in dogs with CVD. It remains to be shown if deterioration of renal function is a direct result of progression of the heart disease.

Severe pulmonary arterial hypertension due to Angiostrongylosus vasorum in a dog.

A dog was presented with a history of dyspnea, coughing, and ascites. Angiostrongylosis and severe pulmonary arterial hypertension (PAH) were found, as well as a marked discordance between the electrical and mechanical events of the heart. Pulmonary arterial hypertension related to Angiostrongylus vasorum has rarely been reported.

Isoflurane inhaled at the onset of reperfusion potentiates the cardioprotective effect of ischemic postconditioning through a NO-dependent mechanism.

Postconditioning (PCD) is known to reduce infarct size (IS). Here, we investigated whether isoflurane, which is known to potentiate preconditioning, also potentiates PCD and whether NO is involved. Accordingly, open-chest rabbits underwent 30-minute coronary artery occlusion (CAO) followed by 3-hour coronary artery reperfusion (CAR). In control and postconditioned (4 cycles of 30s-CAR/30s-CAO after the 30-min CAO), rabbits were anesthetized with pentobarbital alone or in combination with isoflurane inhaled (i) throughout the experiment or (ii) only during CAR. With pentobarbital alone, PCD significantly reduced IS versus control (39 +/- 7% vs. 55 +/- 4% of the risk zone, respectively, P < 0.05). Isoflurane--0.5% throughout the experiment did not alter IS in both control and PCD groups. Isoflurane--2% throughout the experiment reduced IS in control (37 +/- 8%, P < 0.05 vs. pentobarbital alone) and enhanced the protective effect of PCD (IS = 21 +/- 3%, P < 0.05 vs. both control and PCD under pentobarbital alone). When isoflurane--2% was administered only during reperfusion, IS was not changed in control (53 +/- 3%) but combination with PCD reduced IS to 23 +/- 4% (P < 0.05 vs. both control and PCD under pentobarbital alone). L-arginine analog N-nitro-L-arginine methyl ester administered before reperfusion did not properly alter IS (53 +/- 6%) but abolished the effect of PCD alone (IS = 47 +/- 7%) or in combination with isoflurane--2% during reperfusion (55 +/- 3%). Thus, isoflurane potentiates PCD at reperfusion through a NO-dependent mechanism.

Diagnostic potential of natriuretic peptides in the occult phase of golden retriever muscular dystrophy cardiomyopathy.

The objective of the study was to determine whether the plasma concentrations of atrial and brain natriuretic peptides (ANP and BNP, respectively) could be reliable markers of cardiac alterations during occult cardiomyopathy in Golden Retriever Muscular Dystrophy (GRMD). Fifty Golden Retrievers without any clinical or radiographic sign of heart disease were included in this study (21 GRMD dogs and 29 controls). Controls and GRMD dogs were divided into 2 subgroups according to age (< and > or =12 months old, respectively). All dogs underwent echocardiography and determination of BNP and ANP plasma concentrations by radioimmunoassay. No ventricular dilatation or dysfunction was observed in either control or GRMD dogs. ANP plasma concentration did not differ significantly between controls and GRMD dogs (mean +/- SD = 72 +/- 49 versus 58 +/- 23 pg/mL, respectively, P = .21). This finding was confirmed in both subgroups of dogs (ie, those < and > or =12 months old). In contrast, BNP plasma concentrations were significantly higher in GRMD dogs than in controls (mean +/- SD = 117 +/- 92 versus 46 +/- 22 pg/mL, respectively, P < .05). In dogs > or =12 months old, sensitivity and specificity of BNP for identifying GRMD with a cutoff of 65 pg/mL were 78 and 86%, respectively. For the same cutoff value, sensitivity dropped to 42%, whereas specificity reached 100% in dogs <12 months old. In conclusion, BNP may be a useful biochemical marker of asymptomatic cardiomyopathy. However, this peptide does not allow very early detection because its optimal discriminatory power was observed in adult dogs (ie, > or =12 months of age).