CORONARY VASOCONSTRICTION DURING MYOCARDIAL-ISCHEMIA INDUCED BY RISESIN METABOLIC DEMAND IN PATIENTS WITH CORONARY-ARTERY DISEASE

In patients with coronary artery disease, a maximal vasodilation of th e coronary microcirculation is generally assumed to occur during myoca rdial ischemia induced by rises in metabolic demand. However, vasocons triction has been documented during severe prolonged ischemia in anima ls. The aim of this study was to investigate coronary vasomotor tone d uring pacing-induced ischemia in humans.Methods and Results The study included 11 patients with exercise-induced ischemia and single-vessel disease of the left anterior descending artery and 7 control subjects with normal coronary arteries. Blood flow velocity was monitored with a Doppler catheter in the left anterior descending artery. Coronary re sistance index was calculated as the ratio between mean arterial press ure and flow velocity. Measurements were obtained at baseline, after i ntracoronary adenosine (2 mg), and during maximal atrial pacing in the absence and presence of adenosine. After adenosine administration at rest, coronary resistance decreased more in control subjects than in p atients (25 +/- 7% of baseline versus 61 +/- 19%; P < .01). Coronary r esistance decreased in all control subjects (P < .01) both at maximal pacing (60 +/- 17% of baseline) and after administration of adenosine during tachycardia (31 +/- 13% of baseline). By contrast, all 10 ische mic patients displayed increased coronary resistance at maximal heart rate (221 +/- 131% of baseline; P < .01 versus baseline, P < .01 versu s control subjects). At this stage, adenosine decreased coronary resis tance to 44 +/- 20% of values observed before injection. Additionally, it reduced ST-segment depression in 5 of 8 patients. Conclusions In p atients with coronary artery disease, transient myocardial ischemia in duced by increased metabolic demand is not associated with maximal vas odilation. Rather, an inappropriate severe microvascular vasoconstrict ion is present that can be abolished by intracoronary adenosine.