Difference between revisions of "Dilated Cardiomyopathy"

Revision as of 15:04, 15 October 2013

Also know as: DCM — Congestive Cardiomyopathy

Introduction

This disease is common in dogs and is rare in cats (with adequate taurine supplementation).

Dilated cardiomyopathy (DCM) occurs when there is a progressive reduction in systolic myocardial contractility. Decreased myocardial contractility affects the removal of blood from the ventricle at systole. A larger volume of blood increases the end diastolic pressures causing dilation of the ventricle and the development of eccentric hypertrophy.

Signalment

In the dog, giant and large breeds (e.g. Dobermann Pinscher, Boxer, Great Dane) are most at risk. Male > Females and risk increases with age.

In the cat the most commonly effected breeds are the Siamese, Burmese, Abyssinian. Again Male > Female and middle age & old age cats are most at risk.

Clinical Signs

Can be asymptomatic (Occult) DCM: Seen in predisposed breeds (e.g. Doberman Pinschers).

Clinical signs include syncope, weight loss, dyspnoea, lethargy, weakness and hindlimb paresis (cats with saddle thrombi).

Diagnosis

History and clinical signs suggest heart failure.

Physical examination will show presence of a systolic murmur, a gallop rhythm, S3 heart sound, arrhythmias, pulse deficits and pulmonary crackles.

Blood tests will show azotemia, elevated liver enzymes (+ liver congestion), signs of congestive heart failure, signs of thromboembolism (cats) and plasma taurine reduction (cats).

Radiography will show left ventricular hypertrophy (seen in Dobermans & Boxers), left atrial enlargement (seen in Dobermans & Boxers), generalised cardiomegaly (seen in giant breeds), left sided congestive heart failure signs e.g. pulmonary congestion & edema and right sided congestive heart failure signs e.g. pleural effusion and ascites.

Electrocardiography (ECG) will show rhythm disturbances e.g. atrial fibrillation (giant breeds), ventricular arrhythmias (Doberman Pinchers, Boxers), conduction disturbances and characteristic signs of hypertrophy.

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.

Treatment and Control

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).

Prognosis

Dogs:

Poor: Most breeds survive 6-12 months and in Dobermans and Boxers the prognosis is grave.

Cats:

Good: When cardiomyopathy results from taurine deficiency, but grave in other causes of cardiomyopathy.

Dilated Cardiomyopathy Learning Resources
Flashcards Test your knowledge using flashcard type questions	Myocardial Pathology Flashcards

References

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

Ettinger, S.J, Feldman, E.C. (2005) Textbook of Veterinary Internal Medicine (6th edition, volume 2) W.B. Saunders Company

Fossum, T. W. et. al. (2007) Small Animal Surgery (Third Edition) Mosby Elsevier

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@@ Line 3: / Line 3: @@
 == Introduction  ==
+This disease is '''common in dogs''' and is rare in cats (with adequate taurine supplementation).
-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.
+Dilated cardiomyopathy (DCM) occurs when there is a progressive reduction in systolic myocardial contractility. Decreased myocardial contractility affects the removal of blood from the ventricle at systole. A larger volume of blood increases the end diastolic pressures causing dilation of the ventricle and the development of '''eccentric hypertrophy'''.
 ==Signalment==
+In the dog, giant and large breeds (e.g. Dobermann Pinscher, Boxer, Great Dane) are most at risk. Male > Females and risk increases with age.
-'''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.
+In the cat the most commonly effected breeds are the Siamese, Burmese, Abyssinian. Again Male > Female and middle age & old age cats are most at risk.
-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.
 == Clinical Signs ==
-The natural history of the disease is described in two phases.
+Can be asymptomatic (Occult) DCM: Seen in predisposed breeds (e.g. Doberman Pinschers).
-The '''asymptomatic (occult) phase''' is when no clinical signs are apparent, but there may be structural, functional or electrical abnormalities. These include increased left ventricular and left atrial internal diameter, reduced myocardial contractility and ventricular premature contractions. The duration of this occult phase is variable and can last from months to years.
+Clinical signs include syncope, weight loss, dyspnoea, lethargy, weakness and hindlimb paresis (cats with saddle thrombi).
-The '''overt clinical phase''' is when clinical signs, such as congestive heart failure (CHF), syncope and exercise intolerance, develop. Arrhythmias are common in this stage.
+<br>
 == Diagnosis ==
-===History and Physical Examination===
-Asymptomatic (occult) phase
-* Physical examination may be unremarkable
-* Soft, systolic heart murmur
-* Arrhythmia with pulse deficits
-Overt clinical phase
-* History may include: exercise intolerance, lethargy, anorexia, muscle wasting (cardiac cachexia), syncope, abdominal distension (ascites)
-* Systolic heart murmur
-* Arrhythmia with pulse deficits
-* Increased respiratory rate and effort, increased bronchovesicular sounds, pulmonary crackles (left-sided congestive heart failure)
-* Weakness
-* Jugular venous distension and/or jugular pulsation, hepatomegaly, ascites (right-sided congestive heart failure)
-===Thoracic Radiographs===
-Radiographs are performed in the clinical phase to diagnose congestive heart failure and monitor response to treatment.
-===Electrocardiography (ECG)===
+History and clinical signs suggest [[:Category:Heart Failure|heart failure]].
-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:
-* One or more VPC in an at-risk breed
-* Atrial fibrillation appears to be an early sign of disease in Irish Wolfhounds, whereas other breeds develop atrial fibrillation in advanced disease.
-* 24 hour Holter ECG recording:
-** Greater than 100 VPCs is suggestive of DCM or ARVC
-** Between 50 and 100 VPCs in an at-risk breed is suspicious. Holter recording should be repeated in 3-6 months.
-During the clinical phase, the following may be detected:
+Physical examination will show presence of a systolic murmur, a gallop rhythm, S3 heart sound, arrhythmias, pulse deficits and pulmonary crackles.
-* Occasional VPCs or superventricular premature complexes (SVPCs)
-* Ventricular tachycardia
-* Atrial fibrillation
-* Left bundle branch block morphology
-===Echocardiography===
+Blood tests will show [[azotemia]], elevated liver enzymes (+ liver congestion), signs of congestive heart failure, signs of [[thromboembolism]] (cats) and plasma taurine reduction (cats).
-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.
-===Blood Tests===
+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.
-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.
-'''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).
+Electrocardiography (ECG) will show rhythm disturbances e.g. [[Atrila Fibrillation|atrial fibrillation]] (giant breeds), ventricular arrhythmias (Doberman Pinchers, Boxers), conduction disturbances and characteristic signs of hypertrophy.
-'''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.
+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.
 <br>
 == Treatment and Control ==
-===Asymptomatic (Ocult) phase===
-'''Pimobendan''' has recently been demonstrated to prolong the time to onset of clinical signs and extend survival in Dobermans with asymptomatic (occult) DCM.
-===Clinical phase===
+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).
-In the clinical phase, treatment involves the use of diuretics, ACE inhibitors and positive inotropes. Antiarrhythmic drugs may also be necessary.
 <br>
@@ Line 78: / Line 44: @@
 == Prognosis ==
-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%).
+'''Dogs: '''
+Poor: Most breeds survive 6-12 months and in Dobermans and Boxers the prognosis is grave.
+'''Cats: '''
+Good: When cardiomyopathy results from taurine deficiency, but grave in other causes of cardiomyopathy.
 <br>
 {{Learning
-|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis00923.asp, Dilated cardiomyopathy]<br>[https://www.vetstream.com/canis/Content/Illustration/ill33682.asp, DCM - long axis ultrasound]
 |flashcards = [[Myocardial Pathology Flashcards]]
 }}
 == References==
-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''
-{{citation
-|initiallast = Summerfield
-|initialfirst = N.J.
-|initiallast = Boswood
-|initialfirst = A.
-|initiallast = O'Grady
-|initialfirst = M.R.
-|initiallast = Gordon
-|initialfirst = S.G.
-|initiallast = Dukes-McEwan
-|initialfirst = J.
-|initiallast = Oyama
-|initialfirst = M.A.
-|initiallast = Smith
-|initialfirst = S.
-|initiallast = Patteson
-|initialfirst = M.
-|initiallast = French
-|initialfirst = A.T.
-|initiallast = Culshaw
-|initialfirst = G.J.
-|initiallast = Braz-Ruivo
-|initialfirst = L.
-|initiallast = Estrada
-|initialfirst = A.
-|initiallast = O'Sullivan
-|initialfirst = M.L.
-|initiallast = Loureiro
-|initialfirst = J.
-|initiallast = Willis
-|initialfirst = R.
-|initiallast = Watson
-|initialfirst = P.
-|year = 2012
-|jtitle = Efficacy of Pimobendan in the Prevention of Congestive Heart Failure or Sudden Death in Doberman Pinschers with Preclinical Dilated Cardiomyopathy (The PROTECT Study)
-|jor = Journal of Veterinary Internal Medicine
-|vol = 26(6)
-|Range = 1337–1349
-}}
+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''
+Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine '''(6th edition, volume 2) ''W.B. Saunders Company''
+Fossum, T. W. et. al. (2007) '''Small Animal Surgery''' (Third Edition) ''Mosby Elsevier ''