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(Circulation. 2002;106:435.)
© 2002 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Clinic for Internal Medicine III, Friedrich-Schiller-University, Jena, Germany.
Correspondence to Gerald S. Werner, MD, Klinik für Innere Medizin III, Friedrich-Schiller-Universität, Erlanger Allee 101, D-07740 Jena, Germany. E-mail gerald.werner{at}med.uni-jena.de
Background Coronary steal can occur in collateral-dependent myocardium during pharmacologically induced vasodilation. This study assessed coronary steal invasively in chronic total coronary occlusions (TCOs).
Methods and Results In 35 consecutive patients with a percutaneous transluminal coronary angioplasty of a TCO (duration >4 weeks), coronary flow velocity (APV) by a Doppler wire and distal pressure (PD) by a pressure wire were assessed in the collateral-dependent vascular bed before dilatation. Indexes of peripheral resistance (RP) and for the collateral pathway, including the donor artery segment (RCP), were calculated. Changes of these parameters were assessed during intravenous adenosine (140 µg · kg-1 · min-1). Adenosine caused a decrease of APV, ie, coronary steal, in 13 patients (37%; group S), an increase in 11 patients (group R), and no change in 11 patients (group N). Angiographic analysis of collateral pathways showed no difference between the groups, except that in group S all collateral connections were continuously visible but no large collaterals (>0.5 mm) were found. In group N, collaterals were least developed. The increase of APV in group R was associated with a decrease of RP, whereas RCP remained unchanged. In contrast, group S showed no change in RP but a significant increase of RCP, indicating an increased resistance of the donor segment.
Conclusions Coronary steal is observed in about one third of TCOs and is associated with specific hemodynamic changes of RP and RCP. Steal occurred only with well-developed angiographically visible collaterals but not with very large collaterals.
Key Words: collateral circulation coronary disease vasodilation
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