Abstract 4468: Coronary Vasomotion is Linked to Markers of Cellular Inflammation and Atherothrombosis
Background and Objectives. Abnormal endothelial function in atherosclerosis is associated with altered profiles of circulating adhesion molecules and cytokines. To date, no study has compared coronary vascular function with cellular indices of inflammation and atherothrombosis. We explored the relationship between pacing induced coronary vasomotion and cellular markers in atherosclerotic and angiographically normal vessels.
Methods. Twenty-five 25 patients (pts) with stable atherosclerosis and 10 pts with angiographically smooth coronary arteries with no history or risk factors for atherosclerosis were studies. Pts underwent right atrial pacing starting at 90 bpm followed by 20 bpm increments up to maximal rate of 150 bpm, each step for 2 min. Endothelial independent vasomotion was assessed after intracoronary nitroglycerine (NTG, 0.2mg). % maximal vasodilatation was calculated as net change in mean luminal diameter from baseline to peak pacing, expressed as a % of NTG-induced luminal diameter in the given segment. Whole blood was sampled from the guiding catheter in the coronary artery prior to the procedure. Flow cytometry was used to quantify expression of platelet surface P-selectin, monocyte surface CD11b and CD40, and platelet-monocyte binding.
Results (see Table⇓). Twenty-eight patients showed vasodilation and 7 pts vasoconstriction in response to pacing. Subjects with coronary vasoconstrictor responses showed elevated levels of platelet-monocyte binding (PMB), and monocyte surface CD40, but not of platelet P-selectin or monocyte CD11b. In the entire population, a significant inverse relationship was noted between coronary vasomotion and PMB (r2=0.29, p=0.001), and monocyte surface CD40 expression(r2=0.22, p=0.0045).
Conclusions. Coronary endothelial dysfunction is associated with leukocyte activation and adhesion. The extent of coronary endothelial dysfunction appears inversely related to platelet-monocyte binding.