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12. Canine Cardiomyopathy and Bacterial Endocarditis
12.1 Cardiomyopathy
Dilated cardiomyopathy, literary means disease of the heart muscle, is commonly seen in dogs and cats. The cardiomyopathy is of three types, viz., dilated cardiomyopathy, hypertrophic cardiomyopathy, and restrictive cardiomyopathy. Since their exact etiology is not fully understood, these are generally referred as idiopathic cardiomyopathy. Dilated cardiomyopathy is more common in dogs, while hypertrophic cardiomyopathy is more common in cats.
12.1.1 Dilated Cardiomyopathy (DCM)
It is primary disease of myocardium of dogs, occurring in middle age, predominantly seen in males of large breeds (Great Dane, Doberman Pinscher, Irish wolfhound, Dalmatians, Cocker Spaniels, Saint Bernard, and Bull Mastiffs). It does not mean that dilated cardiomyopathy is not seen in female or other breeds of the dogs. Atypical form has also been recognized in Boxer and English Cocker Spaniels. Causes of dilated cardiomyopathy are not well defined. Nutritional deficiency of carnitine or taurine has been speculated. Dilated cardiomyopathy is characterized by poor contractility with or without arrhythmias leading to weakness, lethargy, anorexia, weight loss, tachycardia, chest wall heaves, subcutaneous edema, abdominal distension, tachypnea, orthopnea, dyspnea, cough, syncope, or sudden death.
12.1.1.1 Causes
Idiopathic or primary.
Genetic factors in Doberman Pinschers, Boxers, and Cocker Spaniels.
Secondary causes include nutritional deficiencies (taurine, carnitine) and toxins (doxorubicin, ethyl alcohol, plant toxins, cocaine, anesthetic drugs, cobalt, catecholamine, and monensin). Though hypothyroidism, and diabetes mellitus reduces myocardial function, may not lead to clinical heart failure. Gastric dilatation-volvulus, acute pancreatitis, and shock have been associated with microscopic myocardial necrosis. Myocardial damage has also been recorded in excessive sympathetic stimulation, hyperthermia, irradiation, and electric shock.
12.1.1.2 Diagnostic Profile
- 1.
Clinical signs
Clinical manifestations in dilated cardiomyopathy are highly variable and are related to heart failure. The clinical signs are enumerated below.
Weakness.
Lethargy.
Exercise intolerance.
Coughing.
Anorexia.
Chronic muscle wasting.
Abdominal distension/ascites.
Muddy colored mucus membranes.
Weak femoral pulse.
Jugular distension/pulse.
Tachypnea or dyspnea.
- 2.
Physical Examination
Physical examination in cases of dilated cardiomyopathy provides very useful information with regard to the heart and lung. The following information may be obtained on physical examination in dogs with dilated cardiomyopathy.
Nature of the pulse. Pulse deficit can be detected.
Nature of cardiac rhythm. It may be chaotic on auscultation if serious arrhythmias such as atrial fibrillation, atrial, or ventricular premature complexes are associated.
Murmurs. Various grades of systolic murmurs (grades 1–3) may be detected.
Variations (increase or decrease) in lung sound.
Pulmonary crackles/rales. These may be heard in dorso-caudal region of the lungs if pulmonary edema has set in due to left heart failure.
Changed character of heart sound. Heart sounds are muffled if there are effusions in pericardium or pleura.
Nature of cardiac apex beat. It is very pronounced.
- 3.
Electrocardiography
Electrocardiographic examination is not very specific to diagnose cardiomyopathy. It provides information regarding heart rhythm and rate, conduction disturbances, enlargement of the atrium and ventricles, variations in segments and intervals, etc. The following changes in electrocardiogram are generally seen in cases of dilated cardiomyopathy.
Electrocardiogram may be normal.
Tall and/or broad “P” wave with or without morphological changes.
Atrial fibrillation (Fig. 12.1). Commonly seen in giant breeds.
Ventricular tachycardia.
“R” wave alternans.
Increased amplitude of “R” wave.
Decreased amplitude of “R” wave.
Low-voltage complex (Fig.12.1).
Broad and slurred “QRS.”
Ventricular premature complexes. Commonly seen in large breeds of dog and Dobermans.
Paroxysmal ventricular tachycardia.
Depression of S-T segment.
Notched QRS complex if associated with microscopic intramural myocardial infarction (MIMI).
- 4.
Radiography
Radiographic examination of thorax provides valuable information regarding size of the heart, shape of the heart, lung congestion, position of trachea, and size of the large vessels. The following changes in radiographs are generally seen in dogs with cardiomyopathy:
Generalized cardiac enlargement.
Reduced angle of trachea with spine.
Left ventricle touching diaphragm.
Right ventricle touching sternum.
Increased size of pulmonary veins.
Interstitial pulmonary or alveolar edema (Fig.12.2a, b).
Left atrial enlargement (left heart failure).
Changed cardiac silhouette due to more pleural fluid.
Enlarged caudal vena cava.
Ascites and hepatomegaly (right heart failure).
- 5.
Echocardiography
Echocardiographic examination is very valuable. It provides vital information about the size of the chambers, wall thickness, status of various valves, and large vessels. This is the only diagnostic tool that can differentiate between dilated and hypertrophic cardiomyopathy. Therefore confirmatory diagnosis of dilated cardiomyopathy can only be made on echocardiographic examination. The following changes in echocardiogram are generally seen in cases of dilated cardiomyopathy.
Heart enlargement (left atrium, left ventricle, right ventricle) (Fig. 12.3).
Decreased left ventricular shortening fraction (loss of contractility) and ejection fraction.
Thin left ventricular posterior wall and interventricular septum.
Irregular motion of mitral valve leaflets.
Increased E-point septal separation.
Diminished excursion of the aortic wall.
- 6.
Biochemical Examination
Examination of various biochemical indices provide additional information regarding the other associated changes.
Slight increase in the values of blood urea nitrogen and serum creatinine is suggestive of prerenal azotemia.
Serum albumin is decreased in chronic heart failure with ascites.
Moderate increase in serum alkaline phosphatase and alanine aminotransferase activities is suggestive of hepatic congestion and hypoperfusion.
Fall in arterial PO2 is indicative of increasing pulmonary edema.
Fall in venous PO2 is suggestive of diminished cardiac output.
Lower values of plasma carnitine may be seen in giant breeds and Boxers with cardiomyopathy.
Lower values of plasma taurine may be seen in Cocker Spaniels with cardiomyopathy.
Hyponatremia and hypochloremia in dogs with congestive heart failure may indicate poor prognosis.
- 7.
Cardiac Biomarkers
Recently some cardiac biomarkers are being advocated for detecting myocardial damage.
Increase in levels of cTn-I and NT-pro BNP (levels depend on extent of damage to cardiac muscle and heart failure) are suggestive of cardiac muscle damage.
Electrocardiogram (lead, II, sensitivity 1, speed 25 mm/s) of a 6-year-old female Labrador with exercise intolerance, dyspnea for 4 months showing ventricular heart rate as 120 bpm, atrial fibrillations, low-voltage R (0.2–0.25 mV) in all leads. Biochemical investigations revealed normal liver (SAP 96 U/L, ALT 44 IU/L, total bilirubin 1.2 mg%) and kidney (creatinine 1.4 mg%, BUN 26 mg%) functions and increased level of cTn-I (0.96 ng/mL) suggesting cardiomyopathy
(a) Right lateral radiograph of a 6-year-old female Labrador with exercise intolerance, dyspnea for 4 months showing edema in dorso-caudal region of the lung suggesting left heart failure. (b) Right lateral radiographs of a 10-year-old German Shepherd with severe dyspnea, panting, and exercise intolerance showing edema in dorso-caudal region of the lung suggesting left heart failure
(a–d) Echocardiogram of a dog with dilated cardiomyopathy showing apical four-chamber view, enlarged left atrium, and dilatation of both ventricles in M-mode. (These figures are with the courtesy of Dr. Neetu Saini, Associate Professor, Department of Medicine, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana)
12.1.1.3 Therapy
Restrict exercise.
Give low-salt diet.
Use diuretics.
Restrict exercise.
Milrinone or digitalis glycoside may be used.
Control edema with furosemide. Monitor dehydration with furosemide therapy.
Give low-salt diet.
In refractory cases consider the use of milrinone or digitalis or other vasodilators.
Cage rest.
Oxygen therapy.
Furosemide (every hour until diuresis is induced).
Nitroprusside IV with monitoring of blood pressure.
Oral hydralazine and topical nitroglycerine.
Manage arrhythmias with anti-arrhythmic drugs.
Pimobendan to deal with congestive heart failure.
12.1.1.4 Prognosis
Prognosis of the cases of dilated cardiomyopathy is very much variable. In established cases of dilated cardiomyopathy, survival rate varies from 2–3 months to 10–12 months. Survival rate in giant and large breed is low.
12.1.2 Hypertrophic Cardiomyopathy (HCM)
Hypertrophic cardiomyopathy is characterized by hypertrophy of the left ventricle. The hypertrophy of ventricular septum is not in proportion to the left ventricular free wall. The condition is more common in cats. However it has been reported in German Shepherds. Its etiology is uncertain. It is clinically manifested as development of cardiac failure leading to sudden death. Sometimes coughing, dyspnea, left apical systolic murmurs, syncope, or collapse are observed.
12.1.2.1 Diagnostic Profile
- 1.
Clinical Signs
Clinical signs in hypertrophic cardiomyopathy are not different from dilated cardiomyopathy. The signs are related to heart failure as are seen in other heart diseases.
Coughing.
Dyspnea with mild exercise.
Weak pulse.
Pale mucus membrane.
Murmurs.
Syncope/collapse.
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