Simultaneous intracoronary velocity- and pressure-derived assessment of adenosine-induced collateral hemodynamics in patients with one- to two-vessel coronary artery disease

Abstract

Objectives: The purpose of this investigation in patients with poorly and well developed coronary collaterals was to assess the influence of collateral and collateral adjacent vascular resistances and, in part, a stenotic lesion of the collateral supplying vessel on the hemodynamic collateral responses to adenosine.

Background: In humans, little is known about the functional behavior of the coronary collateral circulation.

Methods: In 50 patients with one- and two-vessel coronary artery disease (CAD) undergoing percutaneous transluminal coronary angioplasty (PTCA), collateral flow index (CFI, no unit) changes and vascular resistance index (R, cm/mm Hg) changes of the collateral (R(coll)) and the distal collateral receiving (R4) vessel in response to adenosine (140 microg/min/kg IV) were measured by intracoronary (i.c.) Doppler and pressure guidewires. The variables were determined at baseline and during adenosine in patients with poor (angiographic collateral degree before PTCA <2 of 0 to 3) and good coronary collaterals.

Results: Pressure-derived CFI (CFI(p)) decreased under adenosine in patients with poor collaterals, and it increased in the group with good collaterals. There were inverse correlations between the adenosine-induced change in CFI(p) and the change in R(coll) (r = 0.61, p = 0.0001). In the group with good, but not with poor collaterals, there was also a significant correlation between CFI(p) increase and the decrease in R4, between the severity of the contralateral stenosis and CFI(p) augmentation and among the left versus right coronary artery as ipsilateral vessel and CFI(p) change.

Conclusions: Overall, patients with well, versus poorly developed coronary collaterals do better regarding the capacity to increase collateral flow in response to adenosine. In patients with good, but not poor, collaterals, an adenosine-induced collateral flow increase depends on the ipsilateral distal vascular resistance decrease, but is also directly influenced by the severity of a contralateral stenosis and probably by the size of the collateralized vascular bed.