Augmented vasodilator response to L-arginine after coronary angioplasty may attenuate restenosis.

Abstract

Nitric oxide (NO) plays an important role in the control of vascular tone as well as structure. This study examined the possibility that the extent of restenosis 3 months after percutaneous transluminal coronary angioplasty (PTCA) might be correlated with the magnitude of NO production at the PTCA sites on the day following PTCA. In 23 consecutive patients who underwent PTCA, we examined the coronary artery diameter response to intracoronary administration of L-arginine (1 microg/kg) and isosorbide dinitrate (ISDN, 40 microg/kg) at the sites of PTCA (n = 25) and at untreated sites distal to the PTCA sites approximately 18 h after PTCA. The coronary artery diameter at the PTCA site was determined 3 months after PTCA in all patients. Normalized vasodilator responses to L-arginine (responses to L-arginine/those to ISDN) were greater at the PTCA sites than at the untreated sites (P = 0.05), whereas vasodilator responses to ISDN did not differ between the PTCA and untreated sites. These results suggest a greater production of NO at the PTCA sites despite presumable loss of the endothelium due to the PTCA. Furthermore, the magnitude of normalized vasodilator responses to L-arginine examined at 18 h after PTCA correlated with the coronary artery diameter 3 months after PTCA (r = 0.592, P = 0.002). These results suggest that augmented NO production after PTCA may protect against the development of coronary restenosis. Treatment that enhances local NO production may be clinically useful in preventing restenosis after PTCA.