Determinants of Coronary Steal in Chronic Total Coronary Occlusions: Donor Artery, Collateral, and Microvascular Resistance

Determinants of Coronary Steal in Chronic Total Coronary Occlusions: Donor Artery, Collateral, and Microvascular Resistance

Gerald S. Werner, Michael Fritzenwanger, Dirk Prochnau, Gero Schwarz, Markus Ferrari, Wilbert Aarnoudse, Nico H. J. Pijls, Hans R. Figulla

The mechanisms of coronary steal were studied in 56 patients during recanalization of a chronic coronary occlusion. The pressure and flow velocity in the donor artery and distal to the occlusion were recorded with Doppler and pressure wires before recanalization to assess resistance components within the collateral system. These measurements were repeated during systemic adenosine infusion. Adenosine caused an increase in donor artery resistance in patients with steal, but microvascular resistance did not respond, whereas in patients without steal, donor artery resistance remained low and microvascular resistance decreased. Patients with steal had more severe regional dysfunction indicating an adverse influence on myocardial function.

Objectives

We aimed to assess the mechanisms of coronary steal by direct hemodynamic measurements of the collateral circulation in chronic total coronary occlusions (CTO).

Background

Coronary steal may cause ischemia despite well-developed collaterals in coronary artery disease.

Methods

Fifty-six patients were studied during recanalization of a CTO. Before recanalization, the fractional flow reserve in the donor artery (FFRD) at the takeoff of the collaterals and the coronary flow reserve were recorded. After crossing the occlusion, the distal coronary flow velocity was measured by a Doppler wire (APVOccl), and distal pressure by a pressure wire. Changes of these parameters were assessed during intravenous adenosine (140 μg/kg/min). Resistance indexes for the donor artery (RD), collaterals (RC), and microcirculation (RP) were calculated.

Results

Adenosine caused a decrease of APVOccl (i.e., coronary steal, in 26 patients [group S], an increase in 19 patients [group R], and no change in 11 patients). The FFRD was lower in group S. RD and RC increased in group S, while RD did not change significantly and RC decreased in group R. Patients with steal had more severe regional dysfunction. Patients with steal but without an FFRD <0.8 tended to have an impaired microvascular function.

Conclusions

We could demonstrate that coronary steal in man is mainly due to a hemodynamically significant donor artery lesion, but can also occur due to an impaired vasodilatory reserve of the microcirculation in the absence of a donor artery lesion. Coronary steal may have an adverse influence on the preservation of myocardial function by collaterals.