TY - JOUR
T1 - Relation between serum sodium concentration and the hemodynamic and clinical responses to converting enzyme inhibition with captopril in severe heart failure
AU - Packer, M.
AU - Medina, N.
AU - Yushak, M.
N1 - Funding Information:
From the Division of Cardiology, Department of Medicine, The Mount Sinai School of Medicine of The City University of New York, New York, New York. Dr. Packer is the recipient of a Young Investigators' Research Award (R23-HL-25055) from the National Heart, Lung, and Blood Institute, Bethesda, Maryland. Manuscript received June 14, 1983; revised manuscript received November 2, 1983, accepted November 4, 1983.
PY - 1984
Y1 - 1984
N2 - The relation between pretreatment serum sodium concentration and the early and late effects of captopril was examined in 77 consecutive patients with severe chronic heart failure, in whom cardiac catheterization was performed during initiation of treatment and after 2 to 8 weeks. Two groups of patients were defined: 37 patients had hyponatremia (serum sodium<135 mEq/liter, group A) and 40 patients had a normal serum sodium concentration (〉-135 mEq/liter, group B). With first doses of captopril, patients in group A showed more marked hemodynamic responses than did patients in group B (p<0.02). The changes in mean arterial pressure and left ventricular filling pressure seen with first doses of the drug varied linearly and inversely with the pretreatment serum sodium concentration (r = -0.58 and r = -0.53, respectively); this was likely related to the finding that, before administration of captopril, the serum sodium concentration varied linearly and inversely with the logarithm of the plasma renin activity (r = ‒0.78). However, the pretreatment serum sodium concentration did not predict the long-term hemodynamic or clinical responses to converting enzyme inhibition. Symptomatic hypotension occurred early in the course of therapy (within 24 hours of initiating captopril therapy) in 9 (12°10) of the 77 patients; 8 of these 9 had severe hyponatremia (serum sodium <130 mEq/liter) and comprised 53°10 of the 15 patients in our study with such low serum sodium concentrations. In contrast, symptomatic hypotension occurring late during therapy (after 1 to 4 weeks) was related to an excessive long-term reduction in left ventricular filling pressure (!s~ 14 mm Hg) and not to serum sodium concentration. In conclusion, patients with severe heart failure complicated by severe hyponatremia are more than 30 times more likely to develop symptomatic hypotension during initiation of therapy with captopril than are patients with a serum sodium concentration of 130 mEq/liter or greater. Patients with severe hyponatremia merit particular caution during initiation of treatment with converting enzyme inhibitors.
AB - The relation between pretreatment serum sodium concentration and the early and late effects of captopril was examined in 77 consecutive patients with severe chronic heart failure, in whom cardiac catheterization was performed during initiation of treatment and after 2 to 8 weeks. Two groups of patients were defined: 37 patients had hyponatremia (serum sodium<135 mEq/liter, group A) and 40 patients had a normal serum sodium concentration (〉-135 mEq/liter, group B). With first doses of captopril, patients in group A showed more marked hemodynamic responses than did patients in group B (p<0.02). The changes in mean arterial pressure and left ventricular filling pressure seen with first doses of the drug varied linearly and inversely with the pretreatment serum sodium concentration (r = -0.58 and r = -0.53, respectively); this was likely related to the finding that, before administration of captopril, the serum sodium concentration varied linearly and inversely with the logarithm of the plasma renin activity (r = ‒0.78). However, the pretreatment serum sodium concentration did not predict the long-term hemodynamic or clinical responses to converting enzyme inhibition. Symptomatic hypotension occurred early in the course of therapy (within 24 hours of initiating captopril therapy) in 9 (12°10) of the 77 patients; 8 of these 9 had severe hyponatremia (serum sodium <130 mEq/liter) and comprised 53°10 of the 15 patients in our study with such low serum sodium concentrations. In contrast, symptomatic hypotension occurring late during therapy (after 1 to 4 weeks) was related to an excessive long-term reduction in left ventricular filling pressure (!s~ 14 mm Hg) and not to serum sodium concentration. In conclusion, patients with severe heart failure complicated by severe hyponatremia are more than 30 times more likely to develop symptomatic hypotension during initiation of therapy with captopril than are patients with a serum sodium concentration of 130 mEq/liter or greater. Patients with severe hyponatremia merit particular caution during initiation of treatment with converting enzyme inhibitors.
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U2 - 10.1016/S0735-1097(84)80364-2
DO - 10.1016/S0735-1097(84)80364-2
M3 - Article
C2 - 6323565
AN - SCOPUS:0021326617
SN - 0735-1097
VL - 3
SP - 1035
EP - 1043
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 4
ER -