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== Introduction  ==
 
== Introduction  ==
This disease is the most '''common''' form of cardiomyopathy in dogs.
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Dilated cardiomyopathy (DCM) is characterized by progressive '''systolic dysfunction''' (loss of myocardial contractile function) and '''ventricular dilation''' (eccentric hypertrophy).
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Dilated cardiomyopathy (DCM) is characterized by progressive '''systolic dysfunction''' (loss of myocardial contractile function) and '''ventricular dilation''' (eccentric hypertrophy). This is the most common form of cardiomyopathy in dogs. There are breed predispositions and familial distributions, suggesting an underlying causal genetic mutation. An autosomal dominant inheritance pattern with incomplete and age-dependent penetrance has been reported.
    
==Signalment==
 
==Signalment==
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Giant and large breeds (e.g. Doberman Pinscher, Irish Wolfhound and Great Dane) are most at risk.  
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'''Giant and large breeds''' are most at risk. Predisposed breeds include: Irish Wolfhound, Great Dane, Newfoundland, Leonberger, St. Bernard, Dobermann Pinscher, Boxer, Dogue de Bordeaux and the Portuguese Water dog.  
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Prevalence increases with age and the typical age at diagnosis is 6-8 years.  
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Prevalence increases with age and the typical age at diagnosis is 6-8 years. A severe juvenile form is recognized in the Portuguese Water dog.  
    
Male dogs are more frequently affected than females, particularly in Doberman Pinschers.
 
Male dogs are more frequently affected than females, particularly in Doberman Pinschers.
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== Diagnosis ==
 
== Diagnosis ==
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===History and Physical Examination===
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History and clinical signs suggest [[:Category:Heart Failure|heart failure]].
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Asymptomatic (occult) phase
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* Physical examination may be unremarkable
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* Soft, systolic heart murmur
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* Arrhythmia with pulse deficits
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Physical examination will show presence of a systolic murmur, a gallop rhythm, S3 heart sound, arrhythmias, pulse deficits and pulmonary crackles.
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Overt clinical phase
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* History may include: exercise intolerance, lethargy, anorexia, muscle wasting (cardiac cachexia), syncope, abdominal distension (ascites)
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* Systolic heart murmur
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* Arrhythmia with pulse deficits
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* Increased respiratory rate and effort, increased bronchovesicular sounds, pulmonary crackles (left-sided congestive heart failure)
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* Weakness
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* Jugular venous distension and/or jugular pulsation, hepatomegaly, ascites (right-sided congestive heart failure)
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Blood tests will show [[azotemia]], elevated liver enzymes (+ liver congestion), signs of congestive heart failure, signs of [[thromboembolism]] (cats) and plasma taurine reduction (cats).
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===Thoracic Radiographs===
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Radiographs are performed in the clinical phase to diagnose congestive heart failure and monitor response to treatment.  
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Radiography will show left ventricular hypertrophy (seen in Dobermans & Boxers), left atrial enlargement (seen in Dobermans & Boxers), generalised cardiomegaly (seen in giant breeds), [[Heart Failure, Left-Sided|left sided congestive heart failure]] signs e.g. pulmonary congestion & edema and [[Heart Failure, Right-Sided|right sided congestive heart failure]] signs e.g. pleural effusion and ascites.
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===Electrocardiography (ECG)===
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A normal ECG does not rule out the presence of DCM, but is the test of choice for detecting arrhythmias. In the occult phase, arrhythmias may be the first indication of disease. The following are associated with a high index of suspicion for occult DCM:
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* One or more VPC in an at-risk breed
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* Atrial fibrillation appears to be an early sign of disease in Irish Wolfhounds, whereas other breeds develop atrial fibrillation in advanced disease.
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* 24 hour Holter ECG recording:
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** Greater than 100 VPCs is suggestive of DCM or ARVC
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** Between 50 and 100 VPCs in an at-risk breed is suspicious. Holter recording should be repeated in 3-6 months.  
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Electrocardiography (ECG) will show rhythm disturbances e.g. [[Atrial Fibrillation|atrial fibrillation]] (giant breeds), ventricular arrhythmias (Doberman Pinchers, Boxers), conduction disturbances and characteristic signs of hypertrophy.
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During the clinical phase, the following may be detected:
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* Occasional VPCs or superventricular premature complexes (SVPCs)
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* Ventricular tachycardia
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* Atrial fibrillation
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* Left bundle branch block morphology
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Echocardiography will show a hypokinetic left ventricle (i.e. reduced fractional shortening therefore reduced contractility), reduced ejection fraction (i.e. % end diastolic volume ejected at systole), decreased ventricular wall thickness, left atrial enlargement and mitral regurgitation.
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===Echocardiography===
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Echocardiographic changes may include left ventricular dilation (increased  left ventricular end-diastolic diameter), systolic dysfunction (reduced myocardial contractility), mitral regurgitation secondary to dilation of the mitral annulus and atrial enlargement.
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===Blood Tests===
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Changes on serum biochemistry analysis may include [[azotemia]], this is common in dogs receiving diuretic therapy and is usually pre-renal in nature. Electrolyte abnormalities, such as mild hyponatraemia and hypokalaemia, are also common in dogs with congestive heart failure.
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'''Cardiac biomarkers''', NT-proBNP and cardiac troponin I (cTnI), may be helpful in detecting DCM. Troponin I may be elevated in cardiac disease and will also be elevated as a consequence of haemodynamically significant arrhythmias. Plasma concentrations of NT-proBNP may be elevated in pre-clinical disease and increase with severity. It is important to note that neither biomarker is specific to DCM and merely indicates the heart is under stress/stretch (NT-proBNP) or that there is damage to cardiomyocytes (cTnI).
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'''Taurine''' deficiency may contribute to a DCM phenotype in the American Cocker Spaniel, Dalmatian, Labrador Retriever and Golden Retriever. Most dogs with taurine-deficient DCM will have plasma taurine levels <25nmol/L. This is important to recognize, as in these cases cardiac function and prognosis can be substantially improved by taurine supplementation.  
    
<br>
 
<br>
    
== Treatment and Control ==
 
== Treatment and Control ==
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===Asymptomatic (Ocult) phase===
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'''Pimobendan''' has recently been demonstrated to prolong the time to onset of clinical signs and extend survival in Dobermans with asymptomatic (occult) DCM.
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Treat congestive heart failure (reduce preload & afterload; improve systolic function; control cardiac arrhythmias), therapeutic thoracocentesis (to remove pleural effusion in cats) and taurine supplementation (cats).
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===Clinical phase===
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In the clinical phase, treatment involves the use of diuretics, ACE inhibitors and positive inotropes. Antiarrhythmic drugs may also be necessary.  
    
<br>
 
<br>
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== Prognosis ==
 
== Prognosis ==
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'''Dogs: '''
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Prognosis from the onset of occult DCM is variable and can be years. Once clinical signs have developed, the prognosis is poor with a median survival time of 3-6 month depending on the breed. Death is usually due to refractory congestive heart failure or sudden death. The prevalence of sudden death is particularly high in Doberman Pinschers with DCM (30-50%).
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Poor: Most breeds survive 6-12 months and in Dobermans and Boxers the prognosis is grave.
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'''Cats: '''
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Good: When cardiomyopathy results from taurine deficiency, but grave in other causes of cardiomyopathy.
      
<br>
 
<br>
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== References==
 
== References==
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Tilley, L.P, Smith, F.W.K., Oyama, M.A, Sleeper, M.M (2008) '''Manual of Canine and Feline Cardiology''' (Fourth Edition) ''W.B. Saunders Company''
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{{citation
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|initiallast = Summerfield
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|initialfirst = N.J.
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|year = 2012
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|jtitle = Efficacy of Pimobendan in the Prevention of Congestive Heart Failure or Sudden Death in Doberman Pinschers with Preclinical Dilated Cardiomyopathy (The PROTECT Study)
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|jor = Journal of Veterinary Internal Medicine
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|vol = 26(6)
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|Range = 1337–1349
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}}
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Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat''' Volume 2 (Fifth Edition) ''W.B. Saunders Company''
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Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine '''(6th edition, volume 2) ''W.B. Saunders Company''
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Fossum, T. W. et. al. (2007) '''Small Animal Surgery''' (Third Edition) ''Mosby Elsevier ''
       
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