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Diagnosis and treatment of congestive heart failure in canines.


Cardiac diseases are common causes of mortality in canines and is a significant problem in geriatric animals (Guglielmini, 2003). Evaluation of heart function is usually accomplished by radiography, electrocardiography and if possible by echocardiography (Reynolds and Oyama, 2008). The main stay of therapy for CHF has been diuretics and angiotensin converting enzyme (ACE) inhibitors with or without Digoxin. Despite improvements in pharmacological treatment and prevention, heart failure remains a serious problem with a poor prognosis. Pimobendan, an inodilator has been found to reduce morbidity in CHF (Fuentes, 2004). So the following study was undertaken to evaluate the efficacy of Pimobendan in the management of CHF in dogs.

Materials and Methods

Dogs presented during 2014 were the study population. Cases with signs referable to cardiac diseases were subjected to thorough physical examination, blood work electrocardiography and echocardiography to confirm the diagnosis of CHF. Among the CHF dogs, 12 dogs were randomly allotted to two treatment groups viz. I and II. Group I received conventional treatment of Frusemide (Lasix (a) 40 mg tabs) @ 2-4 mg/kg b. wt. and Spironolactone (Lasilactone (a) 50) @ 1-2 mg/ kg b. wt. two or three times a day, Enalapril (Envas (b) 2.5, 5, 10, 20 mg tabs) @ 0.5 mg/kg b. wt. twice daily and Digoxin (Lanoxin (c) 0.25 mg tabs) if needed @ 0.01 to 0.005 mg/kg b. wt. twice daily. Group II dogs along with the conventional treatment received Pimodendan (5 mg tab, Vetmedin (d) or Safeheart (e)) @ 0.25 mg/kg b. wt. twice daily. The cases were followed up once a month for two months. To evaluate the efficacy of therapy, 6 clinical variables were selected. For each variable other than survival, a score of 0 was given if there was complete resolution of clinical signs, 1 if there was improvement but without complete resolution, 2 if there was no improvement and 3 if the condition worsened during therapy. For survival, a score of 0 was given if the dog was alive at the end of study period and 3 if it died during the study period. The mean of the scores for each variable was used for grading response to therapy and for comparison between groups.

Results and Discussion

The clinical signs of CHF observed in the 12 dogs were coughing (5), dyspnea (4), ascites (4), anorexia (5), hemoptysis (2), tachypnea (2) and exercise intolerance (2). Clinical signs seen in CHF are as a result of congestion and forward failure (Knight, 1994). Hematology and biochemical parameters were within normal values except for 2 dogs which had mild leukocytosis. The reason for this could be stress leukogram and activation of neurohormonal system as indicated by Ristic (2004). One dog at the beginning of treatment period developed elevated creatinine (from 1.4 mg/dL to 1.7 mg/ dL). Azotemia is a common complication of advanced CHF or even well managed cases of CHF (Kittleson, 2000).





Electrocardiographic findings included sinus tachycardia, atrial fibrillation (Fig. 1) tall R waves and sinus tachycardia with tall R waves (Fig. 2). In the present study, 3 dogs did not have ECG abnormalities. This finding is similar to Cote (2010) who has observed that ECG is not always an absolute indicator of normalcy or disease.

Echocardiographic findings included enlarged left atrium (Fig. 3) mitral regurgitation and mitral leaflet thickening in 3 cases and were diagnosed as degenerative mitral valve disease, and decreased fractional shortening (Fig. 4), ejection fraction and increased E point to septal separation in 9 cases which were diagnosed as dilated cardiomyopathy. Echocardiography is a non-invasive method to diagnose the etiology of CHF as reported by Tidholm et al., 2001.

None of the dogs in the study showed any adverse reaction to any of the medications. One dog in Group I died before the end of the monitoring period. This could be due to the reason that the dog had severe to life threatening congestive heart failure at the beginning of the study. The scores for the clinical variables (except survival) were assigned based on subjective assessment of the owner and attending Veterinarian. Group II dogs had lower mean scores. Hence Pimobendan therapy was found to be beneficial in the present study. Pimobendan is a phosphodiesterase III inhibitor and calcium channel sensitizer causing a inodilating effect, at reduced myocardial oxygen consumption energy expenditure when compared to other positive inotropic agents as indicated by Fuentes, 2004 and Atkinson et al., 2009 which would explain the effect seen in the present study. One concern with the use of newer drugs like Pimobendan is the cost of medication, which can be very high indeed for large breed dogs, but given the improvement in quality of life, Veterinarians and owners may be justified in prescribing and administering them respectively.


Atkinson, K.J., Fine, D.M., Thombs, L.A., Gorelick, J.J. and Durham, H.E. (2009). Evaluation of pimobendan and N-terminal probrain natriuretic peptide in the treatment of pulmonary hypertension secondary to degenerative mitral valve disease in dogs. J. Vet. Intern. Med. 23: 1190-96.

Cote, E. (2010). Electrocardiography and cardiac arrhythmias. In Ettinger, S.E. and Feldman, F.C., (eds): Textbook of Veterinary Internal Medicine, 7th edn, W. B. Saunders Co., Philadelphia, p. 1159-87.

Fuentes, V.L. (2004). Use of pimobendan in the management of heart failure. Vet. Clin. North. Am.: Small. Anim. Pract. 34: 1145-56.

Guglielmini, L. (2003). Cardiovascular diseases in the aging dog: Diagnostic and therapeutic problems. Vet. Res. Comm. 27: 555-60.

Kittleson, M.D. (2000). Therapy of heart failure. In Ettinger, S. E. and Feldman, F. C., (eds): Textbook of Veterinary Internal Medicine, 5th edn, W. B. Saunders Co., Philadelphia, p. 713-37.

Knight, D.H. (1994). Pathophysiology of heart failure. In Ettinger, S. E. and Feldman, F. C., (eds): Textbook of Veterinary Internal Medicine, 4th edn, W. B. Saunders Co., Philadelphia, p 891-25.

Reynolds, C. and Oyama, M.A. (2008). Biomarkers in the diagnosis of canine heart disease. Vet. Focus 18: 2-6.

Ristic, J. (2004). Clinical assessment of the dog with suspected cardiac disease. In. Pract. 26: 192-99.

Tidholm, A., Haggstrom, J., Borgarelli, M. and Tarducci, A. (2001). Canine idiopathic dilated cardiomyopathy. Part I: Aetiology, clinical characteristics, epidemiology and pathology. The. Vet. J. 162: 92-107.

(a)--Brand of Hoechst Marion Roussel Ltd., Pune

(b)--Brand of Cadila Pharma, Ahmedabad

(c)--Brand of Burroughs Wellcome, Mumbai

(d)--Brand of Boehringer Ingelheim, Mumbai

(e)--Brand of Sava Vet, Mumbai

B.R. Deepti (1), S. Yathiraj (2), P.T. Ramesh, L. Ranganath (3) and H.D. Narayanaswamy (4)

Department of Veterinary Medicine Veterinary College Karnatka Veterinary, Animal and Fisheries Sciences University (KVAFSU) Hebbal Bengaluru--560024 (Karnataka)

(1.) Assistant Professor and Corresponding author. E-mail:

(2.) Dean

(3.) Department of Veterinary Surgery and Radiology

(4.) Department of Veterinary Pathology
Table 1: Mean scores for resolution
of clinical signs in CHF dogs

Group                I         II

Ascites             1.33      0.67
Dyspnoea             1         0
Anorexia            2.67      0.5
Survival             1         0
Activity             1         0
Cough               1.33      0.67
Total mean          1.34      0.31
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Title Annotation:Clinical Article
Author:Deepti, B.R.; Yathiraj, S.; Ramesh, P.T.; Ranganath, L.; Narayanaswamy, H.D.
Publication:Intas Polivet
Geographic Code:9INDI
Date:Jan 1, 2016
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