Relation of the Renin‐Angiotensin-Aldosterone System to Clinical State in Congestive Heart Failure

The status of the renin-angiotensin-aldosterone system (RAAS) in congestive heart failure (CHF) varies in many reports, in part because of the heterogeneity of the clinical status of the patients studied. To relate the RAAS to clinical state, we studied 23 patients with severe CHF (New York Heart Association functional classes III–IV): five had recent onset of severe pump failure with pulmonary edema (group 1), nine had recent cardiac decompensation superimposed on chronic CHF (group 2) and nine had chronic stable CHF (group 3). The severity of cardiac dysfunction in patients in group 3 was comparable to that in the other two groups (cardiac index, 1.6 ± 0.2 1/min/m2; ejection fraction, 19.3 ± 3%). Pulmonary wedge pressure was similar in all groups (29 ± 3, 28 ± 2 and 29 ± 5 mm Hg). Groups 1 and 2 had reduced mean blood pressure (71 ± 4 and 79 ± 4 mm Hg), increased plasma renin activity (PRA) (65 ± 12 and 29 ± 4 ng A I/ml/hour), plasma aldosterone (117 ± 19 and 59 ± 11 ng/dl) and serum creatinine (2.5 ± 0.5 and 3.0 ± 0.3 mg/dl). Serum sodium concentration was reduced only in group 2 (131 ± 2 mEq/l). These variables were normal in group 3. PRA and mean systemic blood pressure were inversely correlated in all patients (r = −0.48, p < 0.05), as were PRA and serum sodium concentration in patients in groups 2 and 3 (r = −0.51, p < 0.05). In four patients in group 2 who were followed longitudinally, PRA fell from 13.5 ± 1.3 to 3.9 ± 1.0 ng/ml/hour, plasma angiotensin II level from 177 ± 76 to 25 ± 11 pg/ml as their CHF was stabilized. In nine patients with an acute, apparently uncomplicated myocardial infarction, PRA was normal (5.0 ± 2.1 ng/ml/hour). The RAAS is markedly activated during decompensated cardiac failure but returns to normal with stabilization, even though evidence for severe cardiac dysfunction persists. A major stimulus for the activation of the RAAS in acute decompensation appears to be a decrease in systemic blood pressure associated with a decrease in cardiac output.

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