Background: 

Stent implantation into atherosclerotic plaques releases, apart from particulate debris, soluble vasoconstrictor, thrombogenic and inflammatory substances which contribute to impaired microvascular perfusion. We now quantified the release of vasoconstrictors and tested the efficacy of coronary dilators to attenuate such vasoconstriction.

Methods: 

Using a distal protection/aspiration device, coronary arterial blood was retrieved before and during stent implantation in 22 patients with severe saphenous vein aorto-coronary bypass stenoses. Plasma concentrations of catecholamines, endothelin, serotonin, thromboxane B₂ and tumor necrosis factor a (TNFa) were measured. Vasoconstriction of rat mesenteric arteries with intact (+E) and denuded (-E) endothelium in response to coronary arterial or aspirate plasma was quantified and normalized to that by potassium chloride (KCl). Responses to adenosine, nitroprusside and verapamil against the constriction induced by coronary aspirate plasma were determined.

Results: 

The coronary arterial plasma withdrawn before stenting induced 21±5%, the coronary aspirate plasma after stenting induced 95±8% of maximum KCl-induced vasoconstriction. Serotonin, thromboxane B₂, and TNFa release into aspirate plasma increased by 1.9±0.2 mmol/l, 25.6±3.1 pg/ml and 19.7±6.1 pg/ml, respectively, during stenting. In arteries (+E; -E) constricted with aspirate plasma, the concentrations to induce half-maximal vasodilation were comparable for nitroprusside (3.3*10^-8mol/l; 1.9*10^-8mol/l) and verapamil (8.3*10^-8mol/l; 7.8*10^-8mol/l), and the vasoconstriction was eventually eliminated. The vasodilator response to adenosine was dependent on functional endothelium and weaker.

Conclusion: 

Serotonin and thromboxane are the main coronary vasoconstrictors after stenting. Nitroprusside and verapamil are more potent than adenosine to attenuate the aspirate plasma-induced vasoconstriction, and they are not dependent on functional endothelium.