PMID- 23936148 OWN - NLM STAT- MEDLINE DCOM- 20140305 LR - 20211021 IS - 1932-6203 (Electronic) IS - 1932-6203 (Linking) VI - 8 IP - 7 DP - 2013 TI - Effect of folic acid supplementation on levels of circulating Monocyte Chemoattractant Protein-1 and the presence of intravascular ultrasound derived virtual histology thin-cap fibroatheromas in patients with stable angina pectoris. PG - e70101 LID - 10.1371/journal.pone.0070101 [doi] LID - e70101 AB - BACKGROUND: Virtual Histology Intravascular Ultrasound (VH-IVUS) may be used to detect early signs of unstable coronary artery disease. Monocyte Chemoattractant Protein-1 (MCP-1) is linked with coronary atherosclerosis and plaque instability and could potentially be modified by folic acid treatment. METHODS: In a randomized, prospective study, 102 patients with stable angina pectoris (SAP) received percutaneous coronary intervention and established medical treatment as well as either homocysteine-lowering folic acid/vitamin B12 (+/- B6) or placebo (+/- B6) for 1 year before VH-IVUS was performed. The presence of VH-Thin-Cap Fibroatheroma (VH-TCFA) in non-intervened coronary vessels was registered and serum levels of MCP-1 were measured. The patients were subsequently followed for incident myocardial infarction (MI). RESULTS: Patients treated with folic acid/vitamin B12 had a geometric mean (SD) MCP-1 level of 79.95 (1.49) versus 86.00 (1.43) pg/mL for patients receiving placebo (p-value 0.34). VH-TCFA lesions were present in 7.8% of patients and did not differ between intervention arms (p-value 0.47). Serum levels of MCP-1 were 1.46 (95% CI 1.12 to 1.92) times higher in patients with VH-TCFA lesions than in those without (p-value 0.005). Afterwards, patients were followed for median 2.1 years and 3.8% experienced a myocardial infarction (MI), which in post-hoc Cox regression analyses was independently predicted by both MCP-1 (P-value 0.006) and VH-TCFA (p-value 0.01). CONCLUSIONS: In patients with SAP receiving established medical treatment, folic acid supplementation is not associated with either presence of VH-TCFA or levels of MCP-1. MCP-1 is however associated with VH-TCFA, a finding corroborated by increased risk for future MI. ClinicalTrials.gov Identifier: NCT00354081. FAU - Loland, Kjetil H AU - Loland KH AD - Department of Clinical Science, University of Bergen, Bergen, Norway. kjetil.loland@gmail.com FAU - Bleie, Oyvind AU - Bleie O FAU - Strand, Elin AU - Strand E FAU - Ueland, Per M AU - Ueland PM FAU - Nordrehaug, Jan E AU - Nordrehaug JE FAU - Garcia-Garcia, Hector M AU - Garcia-Garcia HM FAU - Serruys, Patrick W AU - Serruys PW FAU - Nygard, Ottar AU - Nygard O LA - eng SI - ClinicalTrials.gov/NCT00354081 PT - Journal Article PT - Randomized Controlled Trial PT - Research Support, Non-U.S. Gov't DEP - 20130725 PL - United States TA - PLoS One JT - PloS one JID - 101285081 RN - 0 (CCL2 protein, human) RN - 0 (Chemokine CCL2) RN - 935E97BOY8 (Folic Acid) SB - IM MH - Aged MH - Angina, Stable/complications/diagnostic imaging/*diet therapy/pathology MH - Chemokine CCL2/*blood MH - Coronary Vessels/diagnostic imaging/*pathology MH - *Dietary Supplements MH - Female MH - Folic Acid/*administration & dosage MH - Humans MH - Male MH - Middle Aged MH - Myocardial Infarction/diagnostic imaging/etiology/pathology/*prevention & control MH - Percutaneous Coronary Intervention MH - Plaque, Atherosclerotic/complications/diagnostic imaging/*diet therapy/pathology MH - Prospective Studies MH - Risk Factors MH - Ultrasonography PMC - PMC3723764 COIS- Competing Interests: Alpharma Inc provided the study capsules, generated the randomization sequence, and concealed the randomization code free of charge and rendered a limited grant to finance the initial phase of the trial. However, Alpharma Inc had no role in the design or implementation of the trial, had no access to study data, and did not participate in data analysis or interpretation or in the preparation, review, or approval of the manuscript. This does not alter our adherence to all the PLOS ONE policies on sharing data and materials. EDAT- 2013/08/13 06:00 MHDA- 2014/03/07 06:00 PMCR- 2013/07/25 CRDT- 2013/08/13 06:00 PHST- 2013/04/19 00:00 [received] PHST- 2013/06/15 00:00 [accepted] PHST- 2013/08/13 06:00 [entrez] PHST- 2013/08/13 06:00 [pubmed] PHST- 2014/03/07 06:00 [medline] PHST- 2013/07/25 00:00 [pmc-release] AID - PONE-D-13-17226 [pii] AID - 10.1371/journal.pone.0070101 [doi] PST - epublish SO - PLoS One. 2013 Jul 25;8(7):e70101. doi: 10.1371/journal.pone.0070101. Print 2013.