Canis ISSN: 2398-2942

Heart: occult dilated cardiomyopathy

Synonym(s): Pre-clinical DCM, concealed DCM

Contributor(s): Jordi Lopez-Alvarez, Liz Bode

Introduction

  • Second most common acquired cardiac disease in dogs, affecting especially large and giant breeds.
  • Cause: cardiomyocyte damage or death causing reduced systolic function (reduced contractility), arrhythmias or both.
  • Signs: in the occult phase, generally no overt signs of cardiac disease are noticed by owners or clinicians, but echocardiographic changes or electrocardiographic changes are already present. Biomarkers (NT-proBNP) may also be elevated.
  • Diagnosis: NT-proBNP, echocardiography and Holter monitor (24-hours ambulatory ECG).
  • Treatment: support of systolic function with pimobendan has been proven beneficial in Dobermans in the occult phase (PROTECT study). Control arrhythmias if criteria of malignancy are present (ie R-on-T phenomenon, fast ventricular rhythms, multiform ventricular rhythms).
  • Prognosis: the prognosis in the occult phase is variable depending on the rate of progression towards the clinical phase, but it should be considered guarded once clinical signs develop.
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Pathogenesis

Etiology

  • Primary dilated cardiomyopathy Heart: dilated cardiomyopathy (DCM) is thought to be a genetic disease, probably with incomplete penetrance and influenced by environmental modifying factors (diet, exercise, stress levels, etc), but with a strong familial transmission, at least within some affected lines.
  • The mode of inheritance may be autosomal dominant in most affected breeds (Doberman, Great Dane, Newfoundland and Boxers).
  • Primary dilated cardiomyopathy is a diagnosis made by exclusion: nutritional, metabolic, endocrine, tachycardia-induced, toxic and infectious causes may lead to secondary dilated cardiomyopathy.

Predisposing factors

General

  • Genetic background (breed and family).
  • Presence of modifying factors (eg: diet, stress, exertion).

Pathophysiology

  • DCM is characterized by:
    • Decreased contractile function (systolic dysfunction): the affected myocardium is unable to generate the pressure required to maintain cardiac output, leading to volume overload changes (ventricular dilation). Eventually, increased left ventricular filling pressures may lead to atrial dilation and development of congestive heart failure.
    • Arrhythmia formation: several theories explain the development of supraventricular and ventricular arrhythmias:
      • Cardiomyocyte death and replacement fibrosis leads to an “irritable focus” easily triggered to cause arrhythmias.
      • Myocardial stretch induces high catecholamine levels causing an arrhythmic substrate.
      • Atrial myocardial stretch induces the formation of micro re-entrant pathways leading to atrial fibrillation.
      • Dysfunction of the ion channels responsible for electrical conduction across the heart; this may be due to disruption of the sarcolemma-sarcomere link, channel protein gene’s mutation or others.
  • Patients with occult DCM have decreased systolic function alone, arrhythmias alone, or a combination of both, but these are not severe enough to cause overt clinical signs.

Timecourse

  • The length of the transition from occult DCM to overt DCM is variable and depends on the breed.
  • Some Cocker spaniels may remain in the occult phase and not develop clinical signs.
  • On average, Doberman pinschers have a protracted occult phase (>2-3 years), although some Dobermans may hardly have an occult phase and develop clinical signs early in the disease process.

Epidemiology

  • The prevalence of the disease is not well studied for the majority of breeds.
  • The prevalence of DCM in Doberman pinscher may be as high as 58% in some areas. 

Diagnosis

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Treatment

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Prevention

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Holler P J, Wess G (2014) Sphericity index and E-point-to-septal-separation (EPSS) to diagnose dilated cardiomyopathy in Doberman Pinschers. J Vet Intern Med 28 (1), 123-129 PubMed.
  • Summerfield N, Boswood A, O’Grady M, Gordon S, Dukes-McEwan J, Oyama M, Smith S, Patteson M, French A, Culshaw G, Braz-Ruivo L, Estrada A, O’Sullivan M, Loureiro J, Willis R and Watson P (2012) Efficacy of Pimobendan in the Prevention of Congestive Heart Failure or Sudden Death in Doberman Pinschers with Preclinical Dilated Cardiomyopathy (The PROTECT Study). J Vet Intern Med 26, 1337-1349 PubMed.
  • Wess G, Butz V, Mahling M, Hartmann K (2011) Evaluation of N-terminal pro-B-type natriuretic peptide as a diagnostic marker of various stages of cardiomyopathy in Doberman Pinschers. Am J Vet Research 72, 642-649 PubMed.
  • Stern J, Meurs K, Spier A, Koplitz S, Baumwart R (2010) Ambulatory electrocardiographic evaluation of clinically normal adult Boxers J Am Vet Med Assoc 236, 430-433 PubMed.
  • Wess G, Simak J, Mahling M, Hartmann K (2010) Cardiac troponin I in Doberman Pinschers with cardiomyopathy. J Vet Intern Med 24(4), 843-849 PubMed.
  • Wess G, Schulze A, Geraghty N & Hartmann K (2010) Ability of a 5-minute electrocardiography (ECG) for predicting arrhythmias in Doberman pinschers with cardiomyopathy in comparison with a 24-hours Ambulatory ECG. J Vet Intern Med 24, 367-37 PubMed.
  • Wess G, Schulze A, Butz V, Simak J, Killich M, Keller LJ, Maeurer J, Hartmann K (2010) Prevalence of dilated cardiomyopathy in Doberman Pinschers in various age groups. J Vet Intern Med 24 (3), 533-538 PubMed.
  • Martin M, Stafford M, Celona B (2009) Canine dilated cardiomyopathy: a retrospective study of signalment, presentation and clinical findings in 369 cases. J Small Anim Pract 50, 23-29 PubMed.
  • Sanderson S L (2006) Tarine and carnitine in canine cardiomyopathy. Vet Clin North Am Small Anim Pract 36 (6), 1325-1343, vii-viii PubMed.
  • Tidholm A, Jonsson L (2005) Histologic characterization of canine dilated cardiomyopathy. Vet Pathol 42 (1), 1-8 PubMed.
  • O'Grady M R & O'Sullivan (2004) Dilated cardiomyopathy: an update. Vet Clin North Am Small Anim Pract 34 (5), 1187-1207 PubMed.
  • Meurs K, Spier A, Wright N, Hamlin R (2001) Comparison of in-hospital versus 24-hour ambulatory electrocardiography for detection of ventricular premature complexes in mature Boxers. JAVMA 218, 222-224 PubMed.
  • Calvert C, Jacobs G, Smith D, Rathbun S, Pickus C (2000) Association between results of ambulatory electrocardiography and development of cardiomyopathy during long-term follow-up of Doberman Pinschers. JAVMA 216, 34-39 PubMed.

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