Chronic stimulation of neurohormonal systems leads to worsening left ventricular function, indicating that new pharmacological therapies must address neurohormonal and hemodynamic interactions.
Chronic neurohormonal activation drives heart failure progression, underscoring the need for pharmacological treatments that target these pathways beyond mere hemodynamic correction.
Traditionally, the pathophysiology of heart failure was viewed as a derangement in hemodynamic factors. Impairment in cardiac function resulted in decreased cardiac output and end-organ hypoperfusion triggering compensatory increases in heart rate, blood pressure and cardiac contractility. While initially beneficial, these mechanisms placed additional stress on the failing heart. Unfortunately, pharmacologic therapies that restored hemodynamic balance failed to halt disease progression. The activation of neurohormonal responses, including those of the renin-angiotensin-aldosterone system, the sympathetic nervous system and the arginine vasopressin system, has been implicated in the progression of heart disease. In acute heart failure, their effects help to restore cardiovascular homeostasis. However, the chronic stimulation of these systems eventually leads to worsening left ventricular function. Drug treatments that activate neurohormonal systems may have long-term clinically deleterious outcomes, and therefore new pharmacological therapies for cardiovascular disease must take into account the interaction between neurohormonal activation and hemodynamic factors.
Peter E. Pool (Thu,) conducted a review in Congestive Heart Failure. Chronic stimulation of neurohormonal systems leads to worsening left ventricular function, indicating that new pharmacological therapies must address neurohormonal and hemodynamic interactions.