Paradoxical increase in microvascular resistance during tachycardia downstream from a severe stenosis in patients with coronary artery disease - Reversal by angioplasty

Background-The pathophysiology of microvascular response to a severe corona ry stenosis has not been conclusively identified. The aim of this study was to characterize the human vasomotor response to pacing-induced ischemia of both the stenotic arterial segment and the distal microcirculation. Methods and Results-Sixteen patients with stable angina and single-vessel d isease were studied. Blood flow velocity and transstenotic pressure gradien t were monitored at baseline, after intracoronary adenosine (2 mg), and dur ing ischemia induced by atrial pacing with and without adenosine. At the en d of this protocol, the study was repeated after intracoronary phentolamine in 7 patients and after angioplasty in 9. Stenosis resistance was calculat ed as the ratio between mean pressure gradient and mean flow, and microvasc ular resistance as the ratio between mean distal pressure and mean flow; va lues were expressed as percent of baseline. Adenosine decreased (P <0.05) b aseline microvascular resistance to 52 +/- 17%, but not stenosis resistance . Pacing increased both stenosis and microvascular resistances (244 +/- 96% and 164 +/- 60% of baseline. respectively, P <0.05). Addition of adenosine to pacing decreased both stenosis (143 +/- 96% of baseline, P <0.05 versus ischemia) and microvascular (51 +/- 17% of baseline, P <0.05 versus baseli ne and ischemia) resistances. Phentolamine did not affect coronary resistan ce at any step of the protocol. Angioplasty and stenting restored a progres sive decline in microvascular resistance during pacing (51 +/- 19% of basel ine, P <0.05 versus baseline). Conclusions-In patients with coronary artery disease, tachycardia-induced i schemia was associated with elevated resistance of both the stenotic segmen t and the microvasculature. Revascularization prevents this paradoxical beh avior.