Introduction

• Although many patients suffering from cardiovascular disease are identified during routine examination or present with mild clinical signs, a subset will present on an emergency basis with severe, life-threatening congestive heart failure.
• These patients often require aggressive therapy and intensive monitoring to achieve a successful outcome.
• Despite their critical status at presentation many will survive for prolonged periods if the acute episode is successfully managed.

Pathogenesis

Etiology

• Etiologies behind development of feline HCM and RCM are not totally understood.
• A mutation in the myosin binding protein-C gene has been associated with HCM in a family of Maine Coons.
• Nutritional taurine deficiency Taurine deficiency is well-described cause of feline myocardial failure (dilated cardiomyopathy). Adequate dietary taurine supplementation found in virtually all cat foods has greatly reduced the incidence this disease. Currently, the occasional cases of feline DCM that are detected are usually not taurine related, do not respond to supplementation, and are idiopathic with respect to etiology.

Pathophysiology

• Following the initial cardiac insult and a reduction in cardiac output there are short-term compensatory mechanisms that become activated to facilitate circulatory homeostasis, including:
  • Sympathetic nervous system.
  • Renin-angiotensin-aldosterone system (RAAS).
  • Release of arginine-vasopressin.
  • Renal sodium and water retention.
• Feline cardiomyopathies (HCM, RCM) are primarily diseases of diastolic dysfunction, in which concentric hypertrophy or myocardial fibrosis limits the ability of the heart to relax during diastole.
• Feline dilated cardiomyopathy (DCM Heart: dilated cardiomyopathy (DCM)) is similar in pathophysiology to canine DCM, in which there is progressive loss of systolic function.
• Ultimately pulmonary capillary pressures rise promoting the development of pulmonary edema  Lung: pulmonary edema, pleural effusion Pleural effusion, or ascites (rare in cats) while pronounced increase in afterload diminishes effective forward blood and increases myocardial oxygen demands.

Timecourse

• Time until development of decompensated heart failure is difficult to predict based on today's diagnostic modalities.
• Some patients live for years with significant cardiovascular disease but never develop nor require treatment for heart failure.
• Predisposing factors that may quickly shift a patient with compensated heart failure to a decompensated state include:
  • The development of arrhythmias Heart: dysrhythmia, especially atrial fibrillation Atrial fibrillation.
  • Abrupt discontinuation of prescribed medications.
  • Stress.
  • Corticosteroid administration.

Diagnosis

Treatment

Outcomes