Abstract
The syndrome of congestive heart failure is responsible for substantial morbidity and mortality.
1
Patients with heart failure have shortness of breath and a limited capacity for exercise, have high rates of hospitalization and rehospitalization, and die prematurely. The primary mode of therapy for this syndrome is based on antagonism of neurohormonal pathways (notably, the sympathetic nervous system
2
and the renin–angiotensin–aldosterone axis
3
,
4
) activated in the failing cardiovascular system. Drugs that antagonize these pathways decrease mortality and morbidity
2
–
4
and in some cases improve the underlying structural abnormalities of the heart, a process termed “reverse remodeling.”
5
On the basis of . . .
