Key result
Intracoronary L-arginine significantly increased the basal diameter of all coronary segments and stenoses but did not change the magnitude of atrial pacing-induced dilatation.
Why the study?
Does intracoronary L-arginine improve flow-mediated dilatation induced by atrial pacing in patients with coronary artery disease and stable angina?
Does intracoronary L-arginine improve flow-mediated dilatation induced by atrial pacing in patients with coronary artery disease and stable angina?
L-arginine dilates coronary segments and stenoses but does not enhance flow-mediated dilatation induced by atrial pacing in diseased epicardial coronary arteries.
Does not augment pacing-induced dilatation in CAD; leaves open L-arginine's role in endothelial modulation.
OBJECTIVE: To examine the effects of L-arginine on basal coronary tone and flow mediated dilatation induced by atrial pacing in patients with coronary artery disease and stable angina. DESIGN: Atrial pacing was performed during intracoronary infusions of normal saline and L-arginine (150 micromol/min) in 8 patients with coronary artery disease and stable angina. The luminal diameter of epicardial coronary arteries was assessed by quantitative angiography. RESULTS: L-arginine administration significantly increased the diameter of all the coronary segments and stenoses. During atrial pacing with saline infusion, luminal diameter of the proximal, distal, and stenosis reference segments increased significantly (p < 0.01 versus saline) but stenosis diameter did not change. L-arginine administration did not change the magnitude (NS) of atrial pacing induced dilatation in proximal and distal segments and in coronary stenoses and their reference segments. CONCLUSIONS: Non-stenotic segments of diseased coronary arteries dilate in response to atrial pacing but stenoses do not. L-arginine dilates coronary segments and stenoses but does not increase the magnitude of the response to atrial pacing in proximal and distal segments and in coronary stenoses and their reference segments. These findings provide evidence that the shear stress responsive mechanism is absent at stenoses but present in non-stenotic segments of diseased coronary arteries. They also indicate a relative deficiency of L-arginine, except in the shear response mechanism.
No takes yet. Share an insight, caveat, or question.
Dimitris Tousoulis (2003) studied Coronary artery disease and stable angina (n=8). L-arginine vs. Normal saline was evaluated on Luminal diameter of epicardial coronary arteries assessed by quantitative angiography (p=< 0.01). Intracoronary L-arginine significantly increased the basal diameter of all coronary segments and stenoses but did not change the magnitude of atrial pacing-induced dilatation.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: