Background The behavior of the comprehensive circulating renin‐angiotensin system (RAS) in dogs with myxomatous mitral valve disease (MMVD) before to the onset of congestive heart failure remains largely unexplored. Hypothesis/Objectives The classical and alternative RAS activity and aldosterone concentrations will be significantly higher in dogs with American College of Veterinary Internal Medicine (ACVIM) stage B2 MMVD compared to normal dogs and dogs with ACVIM stage B1 MMVD. Animals One‐hundred seventeen client‐owned dogs (normal = 60; B1 = 31; B2 = 26). Methods Prospective observational study. Angiotensin peptides (AP) and aldosterone concentrations were measured using liquid chromatography and mass spectrometry. Angiotensin converting enzymes 1 and 2 (ACE, ACE2) and renin activity surrogates were calculated from AP concentrations. Equilibrium dialysis (ED) and immediate protease inhibition (PI) methods of AP quantification were compared in 14 healthy dogs. Results Core RAS activity and aldosterone concentrations did not differ among the 3 groups. However, the balance between the alternative and classical RAS differed, with dogs with stage B2 MMVD having significantly higher ACE2 activity surrogate (ACE2surr) when compared to normal dogs (adjusted P = .02; ratio of medians for ACE2surr [B2:normal], 1.89; 95% confidence interval [CI]: 1.4‐2.6). The ED and PI methods of AP quantification were highly correlated (AngI, r = .9, P < .0001; AngII, r = .8, P = .001). Conclusions and Clinical Importance Circulating alternative RAS activity, specifically the surrogate measure of ACE2 activity, was increased in dogs with stage B2 MMVD as compared to normal dogs. Equilibrium dialysis results are analogous to immediate protease inhibition in dogs.

No abstract

Case series summary Three cats presented for clinical signs of respiratory distress and varying etiologies of anemia. Echocardiograms revealed evidence of cardiac dilation without other significant structural or functional heart disease. Thoracic imaging via point-of-care ultrasound and/or radiographs confirmed evidence of volume overload by pleural effusion. Each cat was diagnosed with presumed high-output cardiac failure secondary to anemia. Mainstays of treatment included controlling congestion and correcting the anemia with transfusions in the short-term while addressing the underlying etiology of the anemia in the long-term. Relevance and novel information Reports, treatment and management of high-output failure in the veterinary literature are limited. Extrapolating from human medicine, cats presenting with anemia and findings consistent with volume overload will benefit from treatment of their anemia to reduce neuroendocrine activation and the associated sodium and water retention. Therefore, blood transfusion should neither be avoided nor delayed in anemic cats with changes consistent with volume overload and congestive heart failure.

No abstract

A 2-month-old, 8.5 kg (18.7 lb), entire, female Chesapeake Bay Retriever presented for increased respiratory effort. Physical examination revealed a V/VI left basilar systolic heart murmur, mild dyspnoea and hepatomegaly. An echocardiogram revealed leftsided volume overload, evidence of moderate pulmonary hypertension, markedly distended hepatic veins and caudal vena cava, and increased aortic and pulmonary flow velocities in the absence of overt structural heart disease, which was suspicious for highoutput cardiac failure. Thoracic radiographs revealed pulmonary oedema. An abdominal ultrasound revealed a hepatic vascular malformation. Medical management with furosemide was elected. A computed tomography was not pursued. The dog has done well over 9-month follow-up, with only one escalation in dose. Treatment of high-output cardiac failure in a dog secondary to a hepatic vascular malformation has not been previously reported. Intervention to attenuate flow through the hepatic vascular malformation or portocaval shunt could be considered; however, short-term treatment goals are controlling congestion.