Clonidine in congestive heart failure: a vasodilator with negative inotropic effects.

Published

Journal Article

Fourteen patients with moderately severe congestive heart failure (CHF) were given clonidine orally (0.2 and 0.4 mg doses) to determine the hemodynamic effects of a typical centrally acting vasodilator. The 0.2 mg dose significantly reduced mean systemic (15%) and mean pulmonary artery (20%) pressure; the corresponding reductions in vascular resistance were not as great because of a diminished cardiac output. Pulmonary capillary wedge pressure decreased significantly (27%). Heart rate decreased 11% and stroke volume remained unchanged. At a higher dose (0.4 mg), clonidine augmented these reductions but increased stroke volume modestly (15%). Isovolumic developed pressure/duration of isovolumic contraction and the duration of the preejection period were used as indexes of inotropy. After both doses, isovolumic developed pressure/duration of isovolumic contraction decreased dramatically (greater than or equal to 33%) and the preejection period increased substantially (greater than or equal to 18%) (both p less than 0.05). Compared with currently employed vasodilating agents, the centrally acting agent clonidine appears unique in that the drug-induced systemic and pulmonary arterial vasodilation are not accompanied by a commensurate improvement in ventricular systolic function. This lack of improvement appears to be a result of negative inotropic effects.

Full Text

Duke Authors

Cited Authors

  • Hermiller, JB; Magorien, RD; Leithe, ME; Unverferth, DV; Leier, CV

Published Date

  • March 1, 1983

Published In

Volume / Issue

  • 51 / 5

Start / End Page

  • 791 - 795

PubMed ID

  • 6829440

Pubmed Central ID

  • 6829440

International Standard Serial Number (ISSN)

  • 0002-9149

Digital Object Identifier (DOI)

  • 10.1016/s0002-9149(83)80135-0

Language

  • eng

Conference Location

  • United States