ADVANCES IN MITRAL VALVE DISEASE

Transcription

1 Vet Times The website for the veterinary profession ADVANCES IN MITRAL VALVE DISEASE Author : Gemma Hopkins Categories : Vets Date : June 1, 2009 Gemma Hopkins relates an informative meeting where common beliefs on mitral valve disease were challenged Is coughing a sign of heart failure? Does mitral valve disease (MVD) only occur in smallbreed dogs? These and other questions relating to the management of canine MVD were discussed in a seminar at the Potters Herron Hotel, Romsey. It was presented by European specialist in veterinary cardiology Luca Ferasin, and sponsored by CEVA Animal Health. MVD, also known as endocardiosis, myxomatous valvular insufficiency and chronic valvular insufficiency, accounts for 75 per cent of acquired heart failure cases and is one of the most common causes of death in adult dogs. The disease is associated with the development of thickened, nodular, misshapen valve leaflets and thickening and lengthening of the chordae tendinae, which results in valvular incompetence and subsequent mitral regurgitation. Why does MVD occur? Dr Ferasin described a number of theories, but explained that causes of MVD were still not completely understood. Many breeders believe it develops due to endocarditis, secondary to dental disease, with bacteraemia originating from the oral cavity. Another suggestion is that MVD may be a side effect of routine vaccination. It has also been postulated that wear and tear from the repeated opening and closing of the valve may be to blame. However, as not all adult dogs are affected by MVD, other predisposing factors must be necessary. These may include collagen 1 / 6

2 abnormalities and/or damage to the outer endothelial lining of the mitral valve. Traditionally, MVD was considered to only affect smallbreed dogs, but Dr Ferasin explained that the disease was also observed clinically in larger breeds, such as German shepherd dogs. In these breeds the degree of valve thickening and prolapse is usually less pronounced than in small-breed dogs. MVD is typically a disorder of middle-aged and older dogs; it is rarely seen in dogs less than five years old. However, mitral regurgitation may be present in some cavalier King Charles spaniels less than 12 months of age. In this breed the disease is thought to be inherited as a polygenic trait. Pathophysiological mechanisms associated with this disease were clearly illustrated, including valvular regurgitation, jet lesions, chamber dilation, renin-angiotensin-aldosterone system (RAAS) activation, endpoint of chamber compliance, venous congestion, pulmonary oedema, pulmonary hypertension, arrhythmias and myocardial infarction and fibrosis. The fall in cardiac output leads to the activation of several neurohormonal compensatory mechanisms aimed at improving the heart s mechanical environment. Sympathetic nervous system activation, for example, attempts to maintain cardiac output with an increase in heart rate, increased myocardial contractility and peripheral vasoconstriction (increased catecholamines). RAAS activation also results in vasoconstriction (angiotensin and an increase in blood volume, with retention of salt and water (aldosterone). Concentrations of vasopressin and natriuretic peptides also increase. Furthermore, there may be progressive cardiac dilatation or alterations in cardiac structure (remodelling). Myocardial fibrosis is thought to be an important complication of cardiac remodelling, which leads to impaired contractility and arrhythmogenesis. Although cardiac remodelling is a complex, multifactorial phenomenon, angiotensin II, noradrenaline and aldosterone seem to play a pivotal role. Therefore, pharmacological interventions aimed at blocking these mechanisms may have some theoretical justification. Clinical examination On clinical examination, dogs with MVD typically have a left apical systolic murmur. However, there is a wide variation in how rapidly the disease progresses, and some dogs can remain asymptomatic for years. Dr Ferasin explained that, at present, there was no convincing evidence that asymptomatic dogs might benefit from early therapeutic intervention either with ACE inhibitors or pimobendan. Furthermore, the use of furosemide in patients that are not in heart failure must be avoided, due to the risk of dehydration, electrolyte imbalance (especially magnesium and potassium), renal hypoperfusion and stimulation of the RAAS. Rather than treating these patients, Dr Ferasin recommends close monitoring and instructs owners how to monitor their dog s respiratory rate at rest. Clinical signs of congestive heart failure include tachypnoea/ dyspnoea, lethargy and exercise 2 / 6

3 intolerance. Other signs, such as syncope, restlessness at night, inappetence and weight loss, may develop. In more severe cases, signs of right-sided congestive heart failure (such as ascites, liver congestion and jugular pulsation) may also occur. What about coughing? Dr Ferasin explained that, despite widespread belief, coughing was not a symptom associated with heart failure. Although left atrial dilation may cause tracheal elevation and compression of the left main-stem bronchi, he believes most of these patients develop coughing secondary to concurrent chronic airway disease. In the absence of congestive heart failure, treatment in these cases should be directed towards controlling the underlying airway disease. Further investigations Dr Ferasin explained that radiographic changes consistent with pulmonary oedema should be observed on both dorsoventral and lateral thoracic radiographs, as the enlarged left atrium was commonly misinterpreted as perihilar oedema in the lateral views. In addition to radiography, 2-D and M-mode echocardiography enables the evaluation of valvular structures and assessment of the degree of chamber dilation secondary to chronic volume overload. A direct evaluation of valvular incompetence can also be performed using colour and spectral Doppler, although a precise quantification of the degree of regurgitation requires sophisticated techniques, such as the proximal isovelocity surface area method. Although not currently in widespread veterinary use, natriuretic peptide assays are attracting increased interest. Currently, there are limitations, due to the sensitivity and specificity of these tests. Treatment Surgical repair or replacement of the mitral valve is the treatment of choice in human medicine. However, in dogs, open-heart surgery and valve repair is still limited by the prohibitive cost and high surgical risk. Medical therapy is, therefore, still the mainstay treatment for symptomatic heart failure patients. To control the congestive failure, treatment with furosemide was recommended, dosing to effect (radiographic resolution of pulmonary oedema and/or normalisation of the respiratory rate). To ensure the lowest possible dose is given, Dr Ferasin asks owners to regularly monitor the respiratory rate at rest and adjust the furosemide dose accordingly. Drugs that help to counteract RAAS activation were then described. ACE inhibitors have shown beneficial effects on mortality and quality of life in prospective clinical trials, and are indicated in all stages of symptomatic heart failure. The competitive aldosterone inhibitor spironolactone was also discussed. Although ACE inhibitors can reduce aldosterone production by inhibiting the conversion of angiotensin-i to 3 / 6

4 angiotensin-ii, they cannot inhibit local aldosterone production (due to chymase activity in the heart and blood vessels). In humans with heart failure, spironolactone has been shown to reduce the risk of death by 30 per cent. The clinical benefits of adding spironolactone to ACE inhibitor therapy have also been demonstrated in dogs. Dr Ferasin explained how systolic dysfunction can occur in dogs with MVD. Pimobendan, a potent inotropic and vasodilatory agent, has been shown to prolong the time before sudden death, euthanasia for cardiac reasons, or treatment failure in dogs with congestive heart failure (CHF) caused by MVD occurs (Quest study: median survival time 267 days versus 140 days for benazepril). Finally, other vasodilators (nitroglycerin, nitroprusside, amlodipine) and antiarrhythmic treatments were briefly discussed. Although medical therapy for CHF can result in clinical improvements from months to years, the disease is inevitably progressive, and the dog will eventually die or be euthanised, due to refractory heart failure. A large retrospective study (Borgarelli et al, 2008) involving more than 500 dogs belonging to 36 different breeds investigated prognostic indicators in dogs with MVD in congestive failure. A number of factors were identified to cause a higher risk of death. These included dogs more than eight years of age, a heart rate greater than 140bpm, and the presence of dyspnoea, syncope and/or arrhythmias. On echocardiographic examination, dogs at a higher risk of death also had bilateral mitral valve leaflet engorgement, an end-systolic volume index more than 30mL/ m 2, a left atrium:aortic ratio more than 1.7 and an E wave transmitral peak velocity (Emax) more than 1.2m/s. Dr Ferasin s talk was extremely enjoyable and informative, challenging many commonly held beliefs about MVD in dogs and explaining, in detail, information that is continually emerging about this fascinating and commonly diagnosed disease. 4 / 6

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