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Heart: dilated cardiomyopathy (DCM)
Introduction
- Cause: taurine deficiency; idiopathic.
- Signs: dyspnea, lethargy, reduced activity, inappetence.
- Diagnosis: radiography, ultrasound.
- Treatment: rest, diuretics, vasodilators, digoxin; taurine.
- Prognosis: good if taurine related; very poor if idiopathic.
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Presenting signs
- Dyspnea.
- Depression.
- Pleural effusion.
- Exercise intolerance.
- Decreased appetite.
- Recent weight loss.
- Apparently sudden onset.
- Ascites.
- Syncope.
- Signs of thromboembolism Thromboembolism: aorta .
Acute presentation
- Severe dyspnea and collapse.
Age predisposition
- Middle-aged to older.
Breed/Species predisposition
- Domestic shorthair (DSH) British shorthair.
- Burmese.
- Siamese Siamese.
- Abyssinian Abyssinian.
Special risks
- Anesthesia Anesthesia: in cardiovascular insufficiency.
- Sedation Sedation or sedative protocol.
- Restraint: excessive restraint → struggle → possible fatal respiratory compromise.
- Radiology: dorsal recumbency → possible respiratory compromise.
Pathogenesis
Etiology
Undefined
- Idiopathic.
- May be end-stage of hypertrophic cardiomyopathy Heart: hypertrophic cardiomyopathy, or other unclassified forms of cardiomyopathy Heart: restrictive cardiomyopathy.
Metabolic
- Taurine deficiency Taurine deficiency: canned/dried foods → destruction of taurine. Feeding an unfortified diet, eg dog food, can → low blood levels which have been associated with DCM, retinal degeneration Taurine.
- Need 1000-1500 mg/kg dry matter taurine in dry foods and 2000-2500 mg/kg dry matter taurine in canned foods.
Predisposing factors
General
Factors which worsen congestive failure
- Exertion.
- Stress.
- Sudden increase in salt intake.
Specific
- Age.
Pathophysiology
- Poorly understood or unknown.
- Metabolic or biochemical lesion affecting cardiac myocyte → failure of contractility/increased work for myocardium → chronic hypovolemic shock response Shock:
- Right-sided failure due to myocardial involvement or secondary to the left backward failure → ascites, hepatomegaly, jugular pulse, pleural effusion, pericardial effusion.
- Salt and water retention by kidney due to poor renal perfusion → sympathetic drive and RAAS (aldosterone) leads to increased venous return (preload) and venous pressure, further stretch of myocardium and predisposition to edema.
- Increased end-diastolic left ventricular volume and pressure → dilation and non-compensatory hypertrophy (La Place relationship) of left ventricle → compromized papillary muscle function and passive dilation of atrioventricular annulus causing mitral regurgitation → increased left atrial pressures → left atrial enlargement → increased pulmonary venous (capillary wedge) pressure and pulmonary edema +/- pleural effusion → pleural effusion.
Note pleural effusion will occur with left-sided as well as right-sided failure in cats. - Poor cardiac output (CO) due to decreased stroke volume (SV) → sympathetic drive → increased heart rate (HR).
- Reduced cardiac output with arteriolar contraction to increase vascular resistance (mediated through sympathetic tone, active renin-angiotension-aldosterone system (RAAS) and increased vasopressin release); also venoconstriction → increased venous return → increased stretch of myocardium (preload).
- Arteriolar constriction increases afterload (left ventricle wall stress) and myocardial workload → further myocardial dysfunction, further dilation.
- Signs of poor systolic function and vasoconstricted state: poor pulse, pale mucous membranes, delayed capillary refill time, cold extremities, etc.
- Left atrial stretch may → supraventricular dysrhythmias, eg atrial fibrillation.
- Increased myocardial wall stress, poor coronary perfusion of myocardium and diseased myocytes may result in ventricular dysrhythmias.
Timecourse
- Weeks-months from onset of signs.
- Usually weeks-months survival after diagnosis.
Diagnosis
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Treatment
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Prevention
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Outcomes
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Further Reading
Publications
Refereed papers
- Recent references from PubMed and VetMedResource.
- Van Israël N (2004) Feline cardiomyopathies: diagnostic approach. UK Vet 9 (5), 35-42.
- Bright J M, Herrtage M E & Schneider J F (1999) Pulsed Doppler assessment of left ventricular diastolic function in normal and cardiomyopathic cats. JAAHA 35 (4), 285-291 PubMed.
- Bright J M, Mears E (1997) Chronic heart disease and its management. Vet Clin North Am Small Animal Pract 27 (6), 1305-1329 PubMed.
- Novotny M J, Hogan P M, Flannigan G (1994) Echocardiographic evidence for myocardial failure induced by taurine deficiency in domestic cats. Can J Vet Res 58 (1), 6-12 PubMed.
- Lawler D F, Templeton A J, Monti K L (1993) Evidence for genetic involvement in feline dilated cardiomyopathy. J Vet Intern Med 7 (6), 383-387 PubMed.