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An Urban Experience
Early identification of congestive heart failure
MMVD is characterized by chronic progression, and
at a certain point, for some dogs, the disease may no longer be compensated for; the forward cardiac output decreases, and the pulmonary capillary pressure exceeds the threshold for pulmonary edema. Early detection of dogs developing decompensated CHF is highly desirable in order to initiate appropriate treatment strategies for dogs affected. Accordingly, there is a need for clinical variables with a prognostic value and which can aid in early identification of mild CHF.
A soft murmur in a small-breed dog with MMVD is indicative that disease severity is mild and a recent published study demonstrated that CHF is unlikely
in MMVD dogs diagnosed with soft murmur. Dogs presenting with a precordial thrill rarely have mild disease, and have been shown to have a higher risk of developing CHF and/or pulmonary hypertension.
Several other physical examination- echocardiographical- and circulating biomarker variables have also been evaluated in the above mentioned aspects. At present, echocardiographical estimated left atrial and left ventricular end-diastolic dimension, radiographical estimated vertebral heart score index (VHS), and circulating concentrations of natriuretic peptides and troponin stands out as being most reliable in predicting the onset of decompensated CHF. However, a number of these variables might have acceptable predictive value for groups, but less so for individuals. Furthermore, the performance of the test improves considerably if more than one observation point in time is available, and the closer in time to CHF the dog is.
The above-mentioned tests require imaging and laboratory equipment and expertise. However, respiratory rate in dogs has proved to be a sensitive and specific single diagnostic test for identifying CHF as a cause
of respiratory clinical signs in dogs with heart disease. Studies have recently shown that healthy dogs and
dogs with subclinical left sided heart disease had an average sleeping respiratory rates (SRR) below 25 breaths/minute and rarely above 30 breaths/minute. Another study demonstrated that resolution of the CHF resulted in a reduction in respiratory rate into pre-
CHF ranges. Frequent monitoring of SRR in the dogs home environment could allow more timely therapeutic intervention or modulation in animals with severe subclinical heart disease (e.g. those with marked left atrial enlargement) or known prior history of CHF.
No medical therapy is currently known to inhibit or prevent the valvular degeneration itself, whereas surgical repair or valve replacement has the potential to improve valvular function. Case series with comparably good outcomes have been reported for surgical mitral valve repair, but this procedure is only available at very few sites in the world, and, therefore, not technically, economically, or ethically possible for most canine
and feline patients. The management of MMVD is therefore mainly concerned with improving quality of
life by prolonging the preclinical (asymptomatic) phase, ameliorating the clinical signs and improving survival. Much work has been performed in order to investigate if certain drugs could change the progression of disease in asymptomatic MMVD dogs, as this group of dogs is very large. The recently published EPIC trial demonstrated
a favorable outcome for pre-clinical MMVD dogs with cardiomegaly treated with pimobendan, compared to placebo-treated dogs, in regard to delaying onset of CHF and extending the overall survival.
Treatment of decompensated CHF is tailored for
the individual patient, and often involves concurrent treatment with two or more drugs once signs of CHF are evident. The improved survival is likely to be caused by an alleviation of the heart and the circulation, not by a fundamental change in the pathophysiology of valve degeneration.
Suggested reading
1. Madsen MB, Olsen LH, Haggstrom J, Hoglund K, Ljungvall I, Falk T, et al. Identification of 2 loci associated with development of myxomatous mitral valve disease in Cavalier King Charles Spaniels. J Hered. 2011;102 Suppl 1:S62-7.
2. Ljungvall I, Hoglund K, Lilliehook I, Oyama MA, Tidholm A, Tvedten H, et al. Serum serotonin concentration is associated with severity of myxomatous mitral valve disease in dogs. J Vet Intern Med. 2013;27(5):1105-12.
3. Schober KE, Hart TM, Stern JA, Li X, Samii VF, Zekas LJ, et al. Effects of treatment on respiratory rate, serum natriuretic peptide concentration, and Doppler echocardiographic indices of left ventricular filling pressure in dogs with congestive heart failure secondary to degenerative mitral valve disease and dilated cardiomyopathy. J Am Vet Med Assoc. 2011;239(4):468-79.
4. Porciello F, Rishniw M, Ljungvall I, Ferasin L, Haggstrom J, Ohad DG. Sleeping and resting respiratory rates in dogs and cats with medically- controlled left-sided congestive heart failure. Vet J. 2016;207:164-8.
5. Uechi M. Mitral valve repair in dogs. J Vet Cardiol. 2012;14(1):185-92.
6. Boswood A, Haggstrom J, Gordon SG, Wess G, Stepien RL, Oyama MA, et al. Effect of Pimobendan in Dogs with Preclinical Myxomatous Mitral Valve Disease and Cardiomegaly: The EPIC Study-A Randomized Clinical Trial. J Vet Intern Med. 2016;30(6):1765-79.

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