Feline Cardiomyopathy

Chapter 37 Feline Cardiomyopathy





INTRODUCTION


Heart muscle disease is an important cause of morbidity and mortality in the cat. The various forms of myocardial disease account for virtually all acquired cardiac disorders in this species; disease that is primary to valvular structures, the pericardium, or specialized conduction system is uncommon. The nomenclature of myocardial disease is potentially problematic but evolving. Most recently, cardiomyopathy has been defined as a heart muscle disease that is associated with cardiac dysfunction.1 Myocardial diseases generally are defined by morphopathologic features or, when it is known, cause. Based on this classification scheme, there are four basic types of cardiomyopathy: (1) dilated cardiomyopathy, (2) hypertrophic cardiomyopathy (HCM), (3) restrictive cardiomyopathy (RCM), and (4) arrhythmogenic right ventricular cardiomyopathy.1 All of these forms are observed in the cat.2-6


Heart muscle diseases that are associated with a known causal agent, hemodynamic abnormality, or metabolic derangement are known as specific cardiomyopathies.1 In the cat, the most important disorders in this category are thyrotoxic cardiomyopathy and hypertensive HCM.7 In general, these secondary cardiomyopathies seldom result in clinical signs and are reversible when the underlying disorder resolves.8,9


This chapter addresses the clinical picture and therapy of cardiomyopathy that develop as a result of abnormalities that are primary to the myocardium. HCM is the most common heart disease in the cat and therefore is emphasized.




PATHOPHYSIOLOGY



Diastolic Dysfunction


The ability of the ventricle to fill at low diastolic pressures depends on the rate of the active, energy-requiring process known as myocardial relaxation, as well as on mechanical properties that determine chamber compliance.16 Impaired myocardial relaxation and diminished chamber compliance alter the pressure-volume relationship so that diastolic pressures are high when ventricular volume is normal or small. High diastolic pressures are reflected upstream, potentially resulting in atrial enlargement and venous congestion. In cases in which the end-diastolic volume is diminished, stroke volume may also be reduced. Therefore diastolic dysfunction can explain subnormal cardiac output as well as venous congestion.


Diastolic dysfunction is the predominant pathophysiologic mechanism responsible for clinical signs in HCM and RCM.7 With regard to HCM, intrinsic functional deficits of the cardiomyocytes and ischemia related to hypertrophy and abnormalities of the intramural coronary arteries are responsible for impaired myocardial relaxation. Hypertrophy and fibrosis stiffen the ventricle and explain diminished chamber compliance. The basis of cardiac dysfunction in feline RCM has been defined incompletely, although endomyocardial fibrosis likely plays an important role.


Systolic anterior motion (SAM) of the mitral valve is echocardiographically detected in approximately 65% of cats with HCM.2 The precise pathogenesis has been the subject of debate, but it is likely that abnormal drag forces are responsible for systolic movement of the valve leaflets toward the septum.17 Abnormal papillary muscle orientation and dynamic systolic ventricular performance provide a structural and functional substrate that predisposes to SAM.18 Movement of the mitral leaflets toward the septum results in dynamic—as opposed to fixed—left ventricular outflow tract obstruction and, usually, concurrent mitral valve regurgitation. It is relevant that SAM is a labile phenomenon. Decreases in preload and afterload or increases in contractility may provoke or augment SAM.19 The prognostic relevance of SAM in feline HCM has not been defined. Outflow tract obstruction due to SAM has been associated with poor prognosis in humans with HCM.20 Interestingly, the results of two retrospective studies of feline HCM suggest that SAM confers a more favorable prognosis than does its absence.2,21 Possibly this finding reflects the limitations of retrospective evaluation of a referral population but it is nonetheless interesting. SAM is likely the most important cause of cardiac murmurs in cats with HCM.



CLINICAL PRESENTATION



Patient History and Physical Findings


Clinical manifestations of feline cardiomyopathy result from CHF and arterial thromboembolism (ATE). Diagnosis and management of ATE are discussed elsewhere in this volume.When CHF is present, the observation of tachypnea or respiratory distress most commonly prompts the pet owner to seek veterinary evaluation. Cats with heart failure seldom cough. Nonspecific clinical signs such as lethargy, depression, and inappetence often are observed in patients with cardiomyopathy. Although the causative disorder is usually chronic, the onset of clinical signs associated with CHF is typically sudden.


Retrospectively evaluated case series have identified an association between the administration of glucocorticoids and the development of CHF in cats.21,22 Some affected cats may have had preexisting but clinically silent HCM, but this has not been established. This association is relevant, because the long-term prognosis for cats with glucocorticoid-associated CHF may be better than for those with CHF from more typical causes.22


Patients with CHF often are depressed, and hypothermia commonly is observed. The heart rates of cats with heart failure differ little from those of healthy cats,23 although bradycardia is occasionally evident. Many cats with HCM have a systolic murmur associated with SAM. The prevalence of murmurs in cats with other forms of heart disease is lower.5 A gallop rhythm is a subtle but important auscultatory finding. The third and fourth heart sounds are seldom audible in healthy cats. In general, auscultation of a gallop sound signifies diminished ventricular compliance in association with high atrial pressures. A gallop sound more specifically identifies cats with heart disease than does a murmur. It is important to recognize that the prevalence of murmurs in echocardiographically normal cats is not inconsequential. Because of this, the finding of a cardiac murmur is sometimes incidental to a clinical picture that results from noncardiac disease.


Crackles are sometimes heard in feline patients with cardiogenic edema, but it is likely that the auscultation of adventitious pulmonary sounds has low sensitivity and specificity for pulmonary edema. Patients in which pleural effusions are responsible for respiratory distress generally have quiet heart sounds as well as diminished, dorsally displaced bronchial tones.


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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Feline Cardiomyopathy

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