Hemodynamic effects of renin inhibition by enalkiren in chronic congestive heart failure

Gerald W. Neuberg, Marrick L. Kukin, Joshua Penn, Norma Medina, Madeline Yushak, Milton Packer

Research output: Contribution to journalArticle

40 Scopus citations

Abstract

Previous efforts to block the renin-angiotensin system in patients with chronic congestive heart failure (CHF) have focused on 2 distal sites in the system, the angiotensin-converting enzyme and the angiotensin II receptor. Recent work, however, has led to the development of agents that directly inhibit renin, the proximal step in the cascade. In this study, we investigated the hemodynamic effects of renin Inhibition In 9 patients with chronic CHF by using enalkiren, a primate-selective, dipeptide renin inhibitor, which has been previously shown to suppress plasma renin activity and to lower blood pressure in hypertensive patients. The acute intravenous administration of enalkiren (1.0 mg/kg) produced increases in cardiac index (2.0 ± 0.3 to 2.3 ± 0.1 liter/min/m2) and stroke volume index (26 ± 3 to 34 ± 4 ml/m2) and decreases in left ventricular filling pressure (31 ± 3 to 25 ± 3 mm Hg), mean right atrial pressure (15 ± 1 to 13 ± 2 mm Hg), heart rate (78 ± 5 to 72 ± 6 beats/min) and systemic vascular resistance (2,199 ± 594 to 1,339 ± 230 dynes·s·cm-5) (all p < 0.01 to 0.05). These observations indicate that renin inhibition produces hemodynamic benefits in patients with chronic CHF and could potentially provide a novel approach to interfering with the renin-angiotensin system in patients with this disorder.

Original languageEnglish (US)
Pages (from-to)63-66
Number of pages4
JournalThe American journal of cardiology
Volume67
Issue number1
DOIs
StatePublished - Jan 1 1991

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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