摘要
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.
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.
