Differentiating Primary Myocardial From Secondary Myocardial Diseases in Dogs
World Small Animal Veterinary Association World Congress Proceedings, 2011
Christophe W. Lombard, Dr.med.vet, DACVIM (Cardiology)
Vetsuisse Faculty, University of Bern, Bern, Switzerland


Myocardial disease and cardiomyopathy are terms that unfortunately are often used interchangeably in clinical medicine. This is not necessarily correct, but without great consequences. The term cardiomyopathy however should be reserved for the primary myocardial disease of large breed dogs, with an unknown (idiopathic) etiology, but strong suspicion of a genetic cause because of a high familial incidence in certain breeds. This disease is also called dilated cardiomyopathy (DCM) because of its typical patho-anatomical changes, i.e., dilation of all 4 cardiac chambers. It carries a bad prognosis and leads invariably to the death of the affected dogs. Myocardial disease is a very general term indicating some acquired damage or metabolic derangement of the myocardium. Secondary myocardial disease may be defined as some often reversible, inflammatory, metabolic, toxic, or infiltrative disease of the myocardium with a known etiology or causative agent. This definition will cover the majority of the frequent forms of secondary myocardial diseases such as myocarditis, and myocardial disease secondary to endocrine abnormalities, electrolyte imbalances, trauma and the gastric dilatation/volvulus (GDV) complex, and neoplasias. Secondary myocardial diseases are frequently classified by their known or suspected etiology.

History and Clinical Presentation

The suspicion of myocardial disease is a relatively simple clinical diagnosis that includes a history of recent onset of exercise intolerance or weakness, from mild to most severe, possibly leading to collapse or syncope. These clinical signs may have been chronic and progressive, or are of acute onset, depending on the etiology. On physical examination, signs of diminished cardiac performance (diminished pulse quality, prolonged CRT, low blood pressure) and frequently cardiac arrhythmias are usually present. Loud heart murmurs are usually absent and would point towards major valvular regurgitation from degenerative valvular disease, vegetative endocarditis, or possible previously undiscovered cardiac malformations.

Further Clinical Work-up

The usual work-up should include an ECG, radiographs of the chest, a complete echocardiogram as well as some laboratory work. The hemogram, especially the presence of a leukocytosis, serves to point towards some inflammatory disease, concomitant or causative. The chemistry profile serves to rule out any major electrolyte disturbances (especially hypokalemia, hypercalcemia) that could facilitate the development of (usually ventricular) cardiac arrhythmias. Determination of cardiac troponins (cTnI or cTnT) is very useful when suspecting secondary myocardial disease. Elevated values indicate damaged myocardial cells that are leaking these enzymes. Troponin-measurement is particularly useful when the history includes a possible acute damage to the heart, as with trauma (car accident), toxic effects (myocardial depression factor with the gastric dilatation volvulus complex, snake or toad envenomation, heavy metal poisoning etc.) The severity and therapeutic resistance of the noticed arrhythmias (multifocal ventricular premature beats and ventricular tachycardia) follows somewhat the elevation of the troponins; additionally, the elevation should render the clinician more attentive to the possibility of intermittent and severe arrhythmias (possibly leading to sudden cardiac death) and lead to more intensive monitoring and more aggressive therapy, as well as the formulation of a more guarded prognosis.


Ventricular tachyarrhythmias are the usual indicator of myocardial disease, but can't differentiate primary from secondary forms. Only the Doberman and Boxer breeds have a very high incidence of VPC's and V. tach. with idiopathic DCM. In the other large breeds with idiopathic DCM, supraventricular tachyarrhythmias, especially atrial fibrillation (AF) dominate. AF is almost always a reliable sign of DCM. In some dogs, "lone AF" without cardiac dilatation is found. We believe that these are early forms of idiopathic DCM, with the cardiac deterioration and dilatation developing at a later time.

Cardiac Imaging

On thoracic radiographs with secondary myocardial disease, there may be cardiomegaly, but more commonly, none or only mild degrees are seen. The etiology, duration and pathophysiology of the underlying disease will determine the development of cardiac enlargement. For example, metabolical causes (hypothyroidism, deficiencies of vitamin E/selenium, carnitine, taurine etc.) damage the heart slowly and progressively and allow some compensatory dilatation of the cardiac chambers. Cardiac neoplasms, especially the common 3 forms (hemangiosarcoma, mesothelioma and chemodectoma) most often lead to pericardial effusions with the corresponding radiographic image. Other neoplasms (lymphoma, myomas and myosarcomas) most often grow into the cardiac walls and cavities and cause little radiographic cardiomegaly. With acute or subacute myocardial disease, there is simply not enough time to develop cardiomegaly.

Echocardiography is the method of choice to differentiate primary and secondary myocardial diseases. Admittedly, this will only be feasible once the DCM has advanced to a moderate degree. Highlights of DCM are excentric dilatation of all 4 cardiac chambers, concomitant thinning of the ventricular walls, and ventricular hypokinesis; some dogs have primarily left sided dilatation, and the right sided dilatation is often classified as arrhythmogenic right ventricular cardiomyopathy (ARVC). As the DCM has a long occult phase without clinical signs, early forms will only be detected by prospective screening of individuals from breeds with a high prevalence. Upper limits for normal ventricular dimensions have been published for the Doberman breed; similar reliable data recognized and validated by the community of veterinary cardiologists appears to be lacking for other commonly affected breeds. Hypokinesis alone is by no means sufficient to cast the diagnosis of DCM with heavy consequences on an individual dog. Lack of preload, hypothyroidism, negative inotropic drugs are examples whereby reduced shortening fractions are encountered without concomitant ventricular and atrial dilatation and other signs of myocardial disease. Therefore, screening populations for DCM should be performed by a specialist. Interestingly, mild elevations of troponin T in the group-mean of large dogs with the prodromal stage of DCM has been found, in comparison with the group-mean of healthy dogs that didn't develop DCM, even at a later stage. The differences however were too small to provide a cut-off with sufficient sensitivity and specificity. On the other hand, incidence of quite a low number of ventricular premature contractions (VPC, less than 50–100 per 24hr period on Holter recordings) has shown to have excellent predictive value for later development of DCM in the lives of Dobermans. In Boxers, with classical DCM or ARVC, ventricular tachyarrhythmias are also frequent and likely predictive of a later dilatation and development of congestive heart failure, unless these individuals die before because of a fatal arrhythmia (sudden cardiac death, SCD).

Progression into congestive heart failure is the usual development of the idiopathic DCM. Secondary myocardial diseases almost never progress to CHF, but die from arrhythmias (sudden cardiac death = SCD).


Once CHF is present, aggressive therapy with diuretics, Pimobendan and vasodilators is warranted. To maintain optimal diuresis in advanced chronic cases, sequential nephron blockade with furosemide and spironolactone may be necessary. Aldosterone-inhibition is also suspected to reduce the fibrosing process in the ventricular myocardium and therefore brings additional benefits.

Ventricular tachyarrhythmias should be treated judiciously. In cases with suspected secondary myocardial disease, near normal contractile shortening and dangerous forms (fast V. tach, multifocal VPC's, R-on-T phenomenon), aggressive intravenous therapy with constant rate infusions (lidocaine, sotalol, amiodarone) is necessary, while trying to combat the underlying disease that caused the arrhythmia. In Boxers and Dobermans with idiopathic DCM however, the therapeutic goal may be a simple a reduction of the arrhythmia to a lower, less dangerous grade on the Lown-classification scheme. Atrial fibrillation is best suppressed with a combination of digoxin and diltiazem, or digoxin and a beta-blocker. Goal of this therapy is a reduction of the ventricular rate into a range between 100 and 130/min at rest at home, monitored ideally with a Holter ECG. Some large dogs with "lone" AF can benefit from electric cardioversion into sinus rhythm after pretreatment with sotalol.

Table 1. Differentiation of secondary from primary myocardial disease.





Peracute to acute trauma, intoxication, GDV
Subacute to chronic: hypothyroidism, taurine-, carnitine deficiency, cor pulmonale

Slow development, acute onset of CHF is possible, usually in the late stages

Affected breeds

All breeds, Amer. Cocker

Large and giant breeds, Boxer, Doberman, Portuguese Water Spaniel

Age at onset

Any age

Severe forms at 3 to 5 years, milder forms at 6 to 10 yrs


Weakness, arrhythmias, CHF infrequent

Exercise intolerance, tachydyspnea, weakness to syncope, CHF frequent

Blood pressure

Rarely normal, frequently low, depend. upon etiology

Most often normal until CHF develops


Elevated with trauma, GDV, pericardial effusion, renal failure, sepsis, myocarditis/ pericarditis. Other etiologies not known yet

Mild elevation in populations of "preclinical" DCM
Boxers with ARVC. Individual elevation with CHF


Inflammatory changes with certain etiologies, stress leukograms

Usually normal, mild anemias possible in chronic CHF


From normal to severely abnormal, dependent upon etiology

Mostly normal. Hyponatremia and - chloremia with high doses of diuretics, hypokalemia with anorexia


VPC's and V. tach, almost never AF
Bradycardias, AV-Blocks with hypothyroidism or degenerative disease of conduction system, QT- and T-wave changes with electrolyte disturbances

Boxer/Doberman: VPC, V. tach
Other large breeds: Atrial fibrillation
Progressive QRS-prolongation and ST-deviations


Acute: Essentially normal dimensions, various degrees of hypokinesis. Some etiologies may be visible (infiltrations).
Chronic: Mild chamber dilatation and wall thinning, valves usually normal

Classic: various degrees of eccentric dilatation of chambers with thinning of walls and hypokinesis. Normal valve-morphology, functional AV-regurgitation


Speaker Information
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Christophe W. Lombard, Dr.med.vet, DACVIM Cardiology
Vetsuisse Faculty
University of Bern
Bern, Switzerland

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