Skip Navigation

Cardiovascular Research 2001 49(3):600-608; doi:10.1016/S0008-6363(00)00175-9
© 2001 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Billinger, M.
Right arrow Articles by Seiler, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Billinger, M.
Right arrow Articles by Seiler, C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2001, European Society of Cardiology

Collateral and collateral-adjacent hyperemic vascular resistance changes and the ipsilateral coronary flow reserve

Documentation of a mechanism causing coronary steal in patients with coronary artery disease

Michael Billinger, Martin Fleisch, Franz R. Eberli, Bernhard Meier and Christian Seiler*

University Hospital, Swiss Cardiovascular Center Bern, Cardiology, Bern, Switzerland

* Corresponding author. Tel.: +41-31-632-3693; fax: +41-31-632-4299 christian.seiler.cardio{at}insel.ch

Objectives: The goal of this clinical study was to assess the influence of hyperemic ipsilateral, collateral and contralateral vascular resistance changes on the coronary flow velocity reserve (CFVR) of the collateral-receiving (i.e. ipsilateral) artery, and to test the validity of a model describing the development of collateral steal. Methods: In 20 patients with one- to two-vessel coronary artery disease (CAD) undergoing angioplasty of one stenotic lesion, adenosine induced intracoronary (i.c.) CFVR during vessel patency was measured using a Doppler guidewire. During stenosis occlusion, simultaneous i.c. distal ipsilateral flow velocity and pressure (Poccl, using a pressure guidewire) as well as contralateral flow velocity measurements via a third i.c. wire were performed before and during intravenous adenosine. From those measurements and simultaneous mean aortic pressure (Pao), a collateral flow index (CFI), and the ipsilateral, collateral, and contralateral vascular resistance index (Ripsi, Rcoll, Rcontra) were calculated. The study population was subdivided into groups with CFI<0.15 and with CFI≥0.15. Results: The percentage-diameter coronary artery stenosis (%-S) to be dilated was similar in the two groups: 78±10% versus 82±12% (NS). CFVR was not associated with %-S. In the group with CFI≥0.15 but not with CFI<0.15, CFVR was directly and inversely associated with Rcoll and Rcontra, respectively. Conclusions: A hemodynamic interaction between adjacent vascular territories can be documented in patients with CAD and well developed collaterals among those regions. The CFVR of a collateralized region may, thus, be more dependent on hyperemic vascular resistance changes of the collateral and collateral-supplying area than on the ipsilateral stenosis severity, and may even fall below 1.

KEYWORDS CAD, coronary artery disease; CFI, collateral flow index; CF(V)R, coronary flow (velocity) reserve; CVP, central venous pressure; Pao, mean aortic pressure; Poccl, distal coronary occlusive (wedge) pressure; PTCA, percutaneous transluminal coronary angioplasty; Rcoll, collateral resistance index; Rcontra, contralateral resistance index; Ripis, ipsilateral resistance index; Vioccl, distal velocity time integral during vessel occlusion; Viø-occl, distal velocity time integral during vessel patency


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.