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Degenerative Mitral Valve Disease (view source)

Revision as of 14:44, 29 June 2016

180 bytes removed ,  14:44, 29 June 2016
→‎Treatment
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== Treatment ==
 
== Treatment ==
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===Stage B===
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There is no evidence that any therapy slows the progression of asymptomatic disease.
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===Stage C===
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Medical management is intended to alleviate clinical signs and prolong life.
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If animal is presented in left or right sided heart failure treatment is given at the onset of clinical signs. Such treatments include ACE inhibitors and diuretics.
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'''Furosemide''' is a potent first-line diuretic that can be administered orally or parenterally, depending on the clinical status of the patient. Most patients with congestive heart failure secondary to DMVD require lifelong diuretic therapy.  
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If the disease is detected but the animal is not yet in heart failure then no treatment is required. Exercise must also be restricted and special formulated sodium reduced  cardiac diets recommended.  
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The addition of an '''ACE inhibitor''' is considered standard therapy.  The benefits of ACE inhibitors are related to their vasodilator action and also protecting the heart from the detrimental effects of RAAS activation.  
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Symptomatic treatments are also given if clinical signs persist while the animal is on heart failure medications.  
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'''Pimobendan''' is phosphodiesterase inhibitor that is both a ''positive inotrope'' and ''vasodilator'' (inodilator). A randomized clinical trial (QUEST) demonstrated a survival benefit associated with Pimobendan administration, relative to Benazepril. Use of triple therapy with furosemide, an ACE inhibitor and Pimobendan is recommended. When financial or compliance concerns limit the therapeutic choices, evidence suggests that Pimobendan is superior to an ACE inhibitor.  
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No treatment is recommended prior to the onset of heart failure. Once there is evidence of congestive heart failure, treatment is aimed at its management through a combination of drugs.  
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Aldosterone may contribute to the development of myocardial fibrosis. Complete suppression of RAAS is generally not achieved by ACE inhibition alone. Therefore the addition of '''Spironolactone''' may be beneficial.
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The aims of treatment are to:
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1. '''Reduce Preload'''
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::Diuretics to reduce circulating fluid volume (Frusemide, Benzofluazide, Spironolactone, Amiloride)
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::Vasodilators to reduce venous return (Nitrates, ACE inhibitors, Alpha antagonists)
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2. '''Reduce Afterload
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::Vasodilators to decrease systemic vascular resistance
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:::ACE inhibitors e.g. Enalapril, Benzapril, Imidopril 
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:::Pimobendan
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:::Calcium channel blockers e.g. Amlodipine
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:::Nitrates e.g. Nitroprusside
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3. '''Enhance Systolic function
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::Positive inotropes to increase cardiac contractility and increase cardiac output (Pimobendan, Digoxin, Dobutamine, Xanthines)
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4. '''Improve Diastolic function
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::Negative chronotropes to increase the length of diastole (Digoxin, Atenolol)
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::Calcium channel blockers to improve relaxation (Amlodipine)
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5. '''Control cardiac arrhythmias using anti-arrhythmic drugs
      
== Prognosis ==
 
== Prognosis ==
Lwilkie
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