title: Plasma asymmetric dimethylarginine concentrations in newly diagnosed patients with acute myocardial infarction or unstable angina pectoris during two weeks of medical treatment.
abstract: A high concentration of plasma asymmetric dimethylarginine (ADMA) has been associated with several risk factors for atherosclerosis, and this may increase the risk for acute coronary syndromes (ACSs). We measured plasma ADMA concentrations in patients who had newly diagnosed ACS (n = 48), and we followed the changes in ADMA concentrations during these patients' short-term medical therapy, which included various combination of drugs with or without percutaneous coronary interventions according to the needs of each patient. Concentrations of plasma ADMA were found to be high in patients who had ACS compared with 48 age-matched healthy control subjects (3.13 +/- 0.85 vs 1.57 +/- 0.85 mumol/L, p <0.0001). Follow-up measurements of ADMA showed dramatic decreases in plasma ADMA concentrations over 2 weeks of medical therapy for ACS (from 3.27 +/- 0.87 to 1.52 +/- 0.47 mumol/L, p <0.0001). Plasma ADMA at baseline showed a significant positive correlation with serum C-reactive protein and plasma insulin and a significant negative correlation with serum levels of high-density lipoprotein and plasma alpha-tocopherol. During therapy, changes in plasma ADMA concentrations were significantly correlated with changes in the ratio of total cholesterol to high-density lipoprotein cholesterol and in serum C-reactive protein concentrations but not with changes in insulin levels. This study provides the first evidence that plasma ADMA concentrations are significantly high in patients who have ACS and that ADMA concentrations rapidly decrease after short-term medical therapy.
authors.affiliation: Division of Cardiology, Samsung Medical Center & Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, South Korea.
authors.forename: Sung Won
authors.initials: SW
authors.lastname: Bae
authors.forename: Markus C
authors.initials: MC
authors.lastname: Stühlinger
authors.forename: Hwan Soo
authors.initials: HS
authors.lastname: Yoo
authors.forename: Kyung Hyun
authors.initials: KH
authors.lastname: Yu
authors.forename: Haing Kee
authors.initials: HK
authors.lastname: Park
authors.forename: Bo Yoon
authors.initials: BY
authors.lastname: Choi
authors.forename: Yun-Sun
authors.initials: YS
authors.lastname: Lee
authors.forename: Otmar
authors.initials: O
authors.lastname: Pachinger
authors.forename: Yoon-Ho
authors.initials: YH
authors.lastname: Choi
authors.forename: Sang Hoon
authors.initials: SH
authors.lastname: Lee
authors.forename: Jeong Euy
authors.initials: JE
authors.lastname: Park
mesh_terms: D000328:Adult; D000368:Aged; D000789:Angina, Unstable / Q000097:blood / Q000175:diagnosis* / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood*; D002097:C-Reactive Protein / Q000378:metabolism; D002317:Cardiovascular Agents / Q000627:therapeutic use*; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003131:Combined Modality Therapy; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood / Q000175:diagnosis* / Q000628:therapy; D004791:Enzyme Inhibitors / Q000097:blood*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007328:Insulin / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000175:diagnosis* / Q000628:therapy; D013223:Statistics as Topic; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood; D024502:alpha-Tocopherol / Q000097:blood
chemical_list: D002317:Cardiovascular Agents; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D004791:Enzyme Inhibitors; D007328:Insulin; D008075:Lipoproteins, HDL; D014280:Triglycerides; C018524:N,N-dimethylarginine; D002097:C-Reactive Protein; D001120:Arginine; D002784:Cholesterol; D024502:alpha-Tocopherol