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A 1.5-year-old, female-spayed mix breed dog was presented with recurrent episodes of shaking and excessive panting attributed to drug-refractory ventricular arrhythmia (VA) characterized predominantly by incessant periods of ventricular bigeminy. The VA had a narrow QRS morphology, suggestive of an origin near the His-bundle or fascicular system. Diagnostic evaluation found no structural heart disease or underlying etiology. Three-dimensional electroanatomic mapping and radiofrequency catheter ablation were pursued. Voltage mapping demonstrated normal bi-ventricular voltage (≥1.5 mV) without any fractionated or multi-component electrograms, indicating absence of ventricular myocardial scar. Pace mapping identified an endocardial origin of the VA at the basal anterior-septum of the left ventricle, distal to the His-bundle and near the left bundle branch. Two ablation lesions were delivered to this site, and a left bundle branch block was temporarily induced. The dog recovered uneventfully. One month later, the owners reported a remarkable improvement in clinical signs and follow up 48-hour Holter monitor found complete resolution of VA.

Background The pathophysiology of heart failure involves maladaptive angiotensin peptides (APs) and enzymes, including angiotensin 2 (AT2) and angiotensin converting enzyme (ACE), as well as recently described alternative components, such as angiotensin 1-7 (Ang1-7) and angiotensin converting enzyme 2 (ACE2). The relative effects of different neurohormonal-targeting drugs on balance of APs in dogs with heart disease are unknown. Hypothesis/objectives Plasma AP concentrations differ in dogs receiving angiotensin converting enzyme inhibitors (ACEIs) vs angiotensin receptor blockers (ARBs) and recombinant human ACE2 (rhACE2) will further increase these differences. Animals Eight dogs with degenerative mitral valve disease (DMVD). Methods Prospective open-label trial. Equilibrium concentrations of APs from plasma during PO ACEI treatment and then after 14 days of PO ARB treatment using telmisartan were measured using liquid chromatography-tandem mass spectroscopy before and after in vitro incubation with rhACE2. Results Concentration of Ang1-7 was increased during ARB treatment (Ang1-7: 443 pg/mL; 95% confidence interval [CI] = 247-794 pg/mL) vs ACEI (Ang1-7: 182 pg/mL; 95% CI = 66.2-503 pg/mL; P = .01). Incubation with rhACE2 decreased traditional APs while increasing beneficial alternative APs, and Ang1-7 was significantly higher in the ARB + rhACE2 (880 pg/mL; 95% CI = 560-1383 pg/mL) vs ACEI + rhACE2 (455 pg/mL; 95% CI = 188-1104 pg/mL; P = .03) group. The most favorable theoretical AP profile was achieved in the ARB + rhACE2 group. Conclusions and clinical importance The AP profile during telmisartan treatment is associated with higher plasma Ang1-7 as compared with during ACEI. This favorable shift is potentiated in vitro by combination of ARB + rhACE2. These data support potential AP-targeting strategies and drugs in dogs with DMVD.

Background In human patients, cumulative urine volume (uVol) and urine sodium (uNa) can be predicted using spot urine samples and these quantitative measures help detect low diuretic responsiveness (LDR). Hypothesis/objectives Formulas using spot urine samples predict cumulative uVol and uNa output after oral administration of furosemide to dogs. Animals Eight healthy dogs, 6 dogs with congestive heart failure (CHF). Methods Prospective interventional study. Spot urine samples at 180 and 270 minutes after furosemide (3 mg/kg PO) were used to predict cumulative uVol and uNa output over 7 hours. Differentiation of dogs fulfilling predefined criteria for LDR was examined using receiver operating characteristic (ROC) curves. Results Predicted uNa output at 180 minutes (r s = 0.763, [95% confidence interval [CI], 0.375‐0.923], P = .002) and 270 minutes (r = 0.816, [95% CI, 0.503‐0.940], P

Background The pathophysiology of heart failure involves maladaptive angiotensin peptides (APs) and enzymes, including angiotensin 2 (AT2) and angiotensin converting enzyme (ACE), as well as recently described alternative components, such as angiotensin 1‐7 (Ang1‐7) and angiotensin converting enzyme 2 (ACE2). The relative effects of different neurohormonal‐targeting drugs on balance of APs in dogs with heart disease are unknown. Hypothesis/Objectives Plasma AP concentrations differ in dogs receiving angiotensin converting enzyme inhibitors (ACEIs) vs angiotensin receptor blockers (ARBs) and recombinant human ACE2 (rhACE2) will further increase these differences. Animals Eight dogs with degenerative mitral valve disease (DMVD). Methods Prospective open‐label trial. Equilibrium concentrations of APs from plasma during PO ACEI treatment and then after 14 days of PO ARB treatment using telmisartan were measured using liquid chromatography‐tandem mass spectroscopy before and after in vitro incubation with rhACE2. Results Concentration of Ang1‐7 was increased during ARB treatment (Ang1‐7: 443 pg/mL; 95% confidence interval [CI] = 247‐794 pg/mL) vs ACEI (Ang1‐7: 182 pg/mL; 95% CI = 66.2‐503 pg/mL; P = .01). Incubation with rhACE2 decreased traditional APs while increasing beneficial alternative APs, and Ang1‐7 was significantly higher in the ARB + rhACE2 (880 pg/mL; 95% CI = 560‐1383 pg/mL) vs ACEI + rhACE2 (455 pg/mL; 95% CI = 188‐1104 pg/mL; P = .03) group. The most favorable theoretical AP profile was achieved in the ARB + rhACE2 group. Conclusions and Clinical Importance The AP profile during telmisartan treatment is associated with higher plasma Ang1‐7 as compared with during ACEI. This favorable shift is potentiated in vitro by combination of ARB + rhACE2. These data support potential AP‐targeting strategies and drugs in dogs with DMVD.