Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 2003;107:290-293
Published online before print December 16, 2002, doi: 10.1161/01.CIR.0000045666.04794.14
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
107/2/290    most recent
01.CIR.0000045666.04794.14v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Vittorio, T. J.
Right arrow Articles by Jorde, U. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Vittorio, T. J.
Right arrow Articles by Jorde, U. P.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*CARVEDILOL
*METOPROLOL
Medline Plus Health Information
*Heart Failure
Related Collections
Right arrow Congestive
Right arrow Cardiovascular Pharmacology

(Circulation. 2003;107:290.)
© 2003 American Heart Association, Inc.


Clinical Investigation and Reports

Vasopressor Response to Angiotensin II Infusion in Patients With Chronic Heart Failure Receiving ß-Blockers

Timothy J. Vittorio, MD; Chim C. Lang, MD; Stuart D. Katz, MD; Milton Packer, MD; Donna M. Mancini, MD; Ulrich P. Jorde, MD

From the Division of Circulatory Physiology, Columbia Presbyterian Medical Center, New York, NY.

Correspondence to Ulrich P. Jorde, MD, Division of Circulatory Physiology, Department of Medicine, Columbia Presbyterian Medical Center, 177 Fort Washington Ave, Milstein Hospital Bldg 5-435, New York, NY 10032. E-mail upj1{at}columbia.edu

Background— A synergistic interaction between the angiotensin II (Ang II) type 1 receptor and {alpha}1-adrenergic receptors has been described. We hypothesized that the nonselective ß-antagonist carvedilol, through its {alpha}1-adrenergic blocking properties, may modulate vascular reactivity to Ang II in patients with chronic heart failure (CHF). Accordingly, we compared the vasopressor response to infused Ang II in patients treated with carvedilol and metoprolol, a selective ß-antagonist.

Methods and Results— All subjects were treated with carvedilol or metoprolol for at least 3 months. ACE inhibitor therapy was standardized to enalapril 40 mg/d or the maximally tolerated dose. Exogenous Ang II was administered as sequential intravenous bolus injections (2.5 to 30 ng/kg) titrated to a rise in radial artery systolic pressure of >=20 mm Hg. The dose of Ang II required to elicit a change of 20 mm Hg in radial artery systolic pressure (PD20) defined the vasopressor response to Ang II. Twenty subjects with CHF (mean left ventricular ejection fraction 28±9%, New York Heart Association class II [n=13] and III [n=7]) were studied. There was no correlation between plasma Ang II levels and PD20. However, the PD20 was significantly higher in patients treated with carvedilol than in those treated with metoprolol (20 [range 2.5 to 30] versus 5 [range 2.5 to 10] ng/kg, P=0.019).

Conclusions— The vasopressor response to Ang II infusion in patients treated with carvedilol was significantly lower than in patients treated with metoprolol. Whether this is due to the {alpha}1-adrenergic blocking or other ancillary properties of carvedilol warrants further investigation.


Key Words: congestive heart failure • angiotensin • adrenergic receptors