Coronary vasoconstriction during myocardial ischemia induced by rises in metabolic demand in patients with coronary artery disease.
BACKGROUND
In patients with coronary artery disease, a maximal vasodilation of the coronary microcirculation is generally assumed to occur during myocardial ischemia induced by rises in metabolic demand. However, vasoconstriction has been documented during severe prolonged ischemia in animals. The aim of this study was to investigate coronary vasomotor tone during pacing-induced ischemia in humans.


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 resistance index was calculated as the ratio between mean arterial pressure and flow velocity. Measurements were obtained at baseline, after intracoronary 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 patients (25 +/- 7% of baseline versus 61 +/- 19%; P < .01). Coronary resistance 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 ischemic patients displayed increased coronary resistance at maximal heart rate (221 +/- 131% of baseline; P < .01 versus baseline, P < .01 versus control subjects). At this stage, adenosine decreased coronary resistance to 44 +/- 20% of values observed before injection. Additionally, it reduced ST-segment depression in 5 of 8 patients.


CONCLUSIONS
In patients with coronary artery disease, transient myocardial ischemia induced by increased metabolic demand is not associated with maximal vasodilation. Rather, an inappropriate severe microvascular vasoconstriction is present that can be abolished by intracoronary adenosine.
Sambuceti
G
G
CNR Institute of Clinical Physiology, Pisa, Italy. battesto@po.ifc.pi.cnr.it
Marzilli
M
M
Marraccini
P
P
Schneider-Eicke
J
J
Gliozheni
E
E
Parodi
O
O
L'Abbate
A
A
D000241:Adenosine; D001783:Blood Flow Velocity; D003326:Coronary Circulation / Q000502:physiology; D003327:Coronary Disease / Q000378:metabolism*; D003331:Coronary Vessels / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000175:diagnosis / Q000503:physiopathology*; D013610:Tachycardia / Q000503:physiopathology; D014655:Vascular Resistance; D014661:Vasoconstriction; D014665:Vasodilator Agents
D014665:Vasodilator Agents; D000241:Adenosine