Canine idiopathic dilated cardiomyopathy. Part II: pathophysiology and therapy

Dilated cardiomyopathy (DCM) in dogs is characterized by ventricular and atrial enlargement, and systolic and diastolic dysfunction, with congestive heart failure (CHF) often developing at some stage. With greater understanding of the impact of neuroendocrine stimulation in heart disease, the understanding of the pathophysiology for CHF has changed considerably. It is no longer considered only to be a simple haemodynamic consequence of pump dysfunction, but is now characterized as a complex clinical syndrome with release of many neurohormones, which are believed to have impact on the progression of disease. This change in our understanding of the pathophysiology of CHF has important therapeutic implications. There are strong indications, although not yet proven, that drugs designed to influence the neuroendocrine activity, such as Angiotensin Converting Enzyme (ACE) inhibitors and beta-receptors antagonists, are efficacious as adjunct therapy of heart failure attributable to DCM in dogs. The benefits of drugs designed to influence the myocardial contractile state (positive inotropes) have not been fully evaluated. However, evidence has emerged in recent years indicating that new types of positive inotropes may be beneficial in dogs with DCM. This review focuses on the neuroendocrine aspects of DCM and their possible therapeutic implications and the place for long-term inotropic support in dogs with DCM.