931-114 Effects of Inhibition of Nitric Oxide Synthesis in Proximal and Distal Segments in Patients with Normal Arteries and in Patients with Coronary Artery Disease

Inhibition of nitric oxide synthesis causes a decrease in basal diameter of distal epicardial coronary arteries in patients (pts) with normal coronary arteries (NCA). The effects of inhibition of nitric oxide synthesis with NG-monomethylL-arginine (LNMMA) in atheromatous coronary arteries was evaluated in 13 pts with chronic stable angina (aged 57±7 years, 11 males) due to angiographically documented coronary artery disease and in 8 pts (aged 50±5 years, 4 males) with angiographically NCA. LNMMA was infused intracoronary at 4,8 and 16μmol/min each for 4 minutes. In response to low LNMMA. 4μmol/min, there was a significant (p<0.05) reduction in luminal diameter of both proximal (from 3.49±0.28 to 3.35±0.28mm) and distal (from 1.33±0.07 to 1.23±0.06mm) segments in patients with NCA. In patients with atheromatous arteries there was a reduction in diameter of the distal segments (from 1.44±0.06 to 1.33±0.07mm) but no change occurred in the proximal segments (from 2.95±0.16 to 2.89±0.16mm). In response to high LNMMA. 16μmol/min, there was a significant (p<0.01) reduction in luminal diameter of both proximallfrom 2.53±0.27 to 2.33±0.26mm) and distal (from 1.10±0.06 to 0.99±0.06mm) segments in the pts with NCA. In the pts with atheromatous arteries the distal segments decreased in diameter (from 1.32±0.07 to 1.17±0.06mm) but no change occurred in the proximal segments (from 3.16±0.12 to 3.08±0.14mm). The magnitude of the distal vessel constriction was similar in both the patients with normal and in those with atheromatous arteries (–9.6±2.1% and –10.9±2.6% respectively, p=NS). In conclusion in pts with chronic stable angina due to coronary artery disease inhibition of basal nitric oxide synthesis causes distal coronary artery vasoconstriction, but it has no effect on proximal segment