L-arginine attenuates lymphocyte activation and anti-oxidized LDL antibody levels in patients undergoing angioplasty.
BACKGROUND
Patients with acute coronary syndromes exhibit evidence of peripheral T lymphocyte activation, elevated acute phase proteins and enhanced oxidative stress. Nitric oxide (NO) has been recognized as one of the relaxant factors synthesized and released by normal endothelium, and acts as a double-edged sword on the immune system. L-arginine ameliorates experimental atherosclerosis and restenosis as well as endothelial dysfunction. We sought to investigate the effect of L-arginine administration on the extent of lymphocyte activation and anti-oxLDL antibodies in patients with unstable angina undergoing PCI with stent placement.


METHODS
Patients with unstable angina were randomized to treatment with L-arginine (6g per day; n = 13) or none (n = 16) for 1 month starting immediately on the day of stent deployment. Lymphocyte activation was assayed by FACS employing double staining with a common lymphocyte marker (CD3) and an activation marker HLA-DR, on the day of the procedure and 1 month later. Anti-oxLDL antibodies were assayed by ELISA.


RESULTS
Patients with unstable angina not receiving L-arginine exhibited a significant 43% rise in the percentage of activated peripheral T lymphocytes, 1 month after stent deployment. Patients treated with L-arginine exhibited a fall albeit not significant in the fraction of peripheral lymphocytes bearing the activation marker. Antibodies to anti-oxLDL rose significantly between baseline and 1 month follow-up. L-arginine treatment significantly attenuated the rise in anti-oxLDL antibody levels.


CONCLUSIONS
L-arginine attenuates the systemic rise in peripheral lymphocyte activation and oxidative stress markers induced by vessel wall injury following PCI. These effects may contribute to a favorable effect of the drug in patients with acute coronary syndromes undergoing PCI.
George
Jacob
J
The Department of Cardiology, Tel Aviv Medical Center (affiliated to the Sackler Faculty of Medicine), 6 Weizman Street, Tel Aviv University, Tel Aviv, Israel. jacobg@post.tau.ac.il
Shmuel
Sigal Ben
SB
Roth
Arie
A
Herz
Itzhak
I
Izraelov
Sabina
S
Deutsch
Varda
V
Keren
Gad
G
Miller
Hylton
H
D000368:Aged; D000789:Angina, Unstable / Q000175:diagnosis / Q000628:therapy*; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects / Q000379:methods*; D000888:Antibodies, Anti-Idiotypic / Q000032:analysis / Q000276:immunology; D001120:Arginine / Q000008:administration & dosage*; D016516:CD4-CD8 Ratio; D023903:Coronary Restenosis / Q000517:prevention & control; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D008077:Lipoproteins, LDL / Q000276:immunology / Q000378:metabolism*; D008213:Lymphocyte Activation / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism*; D011336:Probability; D011379:Prognosis; D015607:Stents; D016896:Treatment Outcome
D000888:Antibodies, Anti-Idiotypic; D008077:Lipoproteins, LDL; C099252:oxidized low density lipoprotein; D009569:Nitric Oxide; D001120:Arginine