ABSTRACT
OBJECTIVES: We tested the hypothesis that cyclic alterations in coronary artery blood flow that occurred after coronary angioplasty could be attenuated or abolished by a monoclonal antibody to the platelet surface membrane GP IIb/IIIa receptor. BACKGROUND: Coronary artery cyclic flow variations may occur after coronary angioplasty in experimental animal models and humans. In animal models of coronary thrombosis, cyclic alterations in flow often have preceded thrombotic occlusion or reocclusion. Several agents that inhibit platelet function have been shown to attenuate or eliminate cyclic flow variations in these models. METHODS: We monitored coronary artery flow in 27 patients for 30 min after coronary angioplasty, using 0.018-in. (0.046 cm) coronary guide wires with pulsed wave Doppler ultrasound transducers on the distal tips. Clinical data were collected and quantitative analyses performed on coronary arteriograms made before and after the angioplasty procedures. We compared findings in patients with and without cyclic flow variations detected. RESULTS: There were 20 men and 7 women. Mean age was 58 years, and 63% had unstable angina. They received standard doses of nitrates, aspirin, heparin, calcium channel antagonists and other medications clinically indicated. Nevertheless, we detected cyclic flow variations in five patients (19%). Four of these patients had stable flow restored with intravenous injection of 0.25 mg/kg normal body weight of monoclonal antibody c7E3 Fab to the platelet GP IIb/IIIa receptor. In one patient, stable flow was restored by repeat dilation when an immediate angiogram revealed renarrowing. Patients developing cyclic alterations in flow had longer lesions (18.7 +/- 7.5 mm vs. 13.1 +/- 5.7 mm, p < 0.05) that had responded less well to angioplasty (stenosis postangioplasty 47 +/- 13% vs. 33 +/- 15%, p < 0.05). CONCLUSIONS: Cyclic alterations in coronary artery blood flow may occur in some patients after coronary angioplasty, despite the use of standard antiplatelet, antithrombotic and antivasospastic medications. We found that they could be eliminated by this monoclonal antibody that blocks the final common event of platelet aggregation.
