Neuroendocrine evaluation of cardiac disease

Heart failure is a complex clinical syndrome wherein reduced systolic or diastolic performance of the heart results in increased activity of the adrenergic nervous system, overexpression of atrial (ANP) and brain (BNP) natriuretic peptides, activation of the renin-angiotensin-aldosterone system (RAAS), increased synthesis and release of endothelin and arginine vasopressin (AVP), and amplified expression of proinflammatory cytokines, such as tumor necrosis factor-alpha, interleukin-1, and interleukin-6 [1,2]. Neuroendocrine responses to developing heart failure have been well documented in human patients, and recently conducted studies support the assertion that qualitatively similar responses operate in dogs and cats with heart disease. Understanding these complex systems is vital to understanding the modern treatment of heart failure, which is largely based on the concept of blunting or otherwise modifying the excessive operation of certain maladaptive neuroendocrine responses, such as the adrenergic system and the RAAS. It is becoming increasingly evident that measurement of particular neuroendocrine markers offers diagnostic, prognostic, and therapeutic information not easily obtained by routine clinical evaluation, sophisticated imaging, or hemodynamic assessments.