Low levels of IgM antibodies against phosphorylcholine are associated with fast carotid intima media thickness progression and cardiovascular risk in men.

Gigante B, Leander K, Vikström M, Baldassarre D, Veglia F, Strawbridge RJ, McLeod O, Gertow K, Sennblad B, Shah S, Zabaneh D, Humphries SE, Kauhanen J, Rauramaa R, Smit AJ, Mannarino E, Giral P, Tremoli E, Hamsten A, Frostegård J, de Faire U, IMPROVE Study Group

Atherosclerosis 236 (2) 394-399 [2014-10-00; online 2014-08-05]

Low levels of IgM anti-phosphorylcholine (anti-PC) increase the risk of cardiovascular events (CVE). Here we investigate the association of low anti-PC with the progression of carotid intima media thickness (C-IMT) and incidence of CVE in a large cohort of individuals at high risk of CVE, the IMPROVE, a prospective multicenter European study. 3711 subjects (54-79 years) with at least three established cardiovascular risk factors were enrolled. Baseline serum levels of IgM anti-PC were measured by ELISA. Carotid ultrasound investigations were performed at baseline and after 15 and 30 months of follow-up. The risk of C-IMT progression and ischemic CVE associated with low anti-PC levels was tested by logistic regression and Cox regression analysis, respectively. Risk estimates were adjusted by center and conventional cardiovascular risk factors. 3670 study participants were included in the present analysis and 213 CVE were recorded during a 3 year follow up. Anti-PC levels (U/ml) were classified into quartiles [Q1≤ 40, Q2 >40-≤64, Q3 >64-≤102, Q4 >102]. In men, low levels of anti-PC (Q1) were associated with the highest (>90th) percentile of the fastest C-IMT progression, i.e. the segment showing the fastest progression over 30 months in the whole carotid tree, with an OR of 1.41 (95%CI, 1.02-1.9) and with an increased risk of CVE with a multivariable adjusted HR of 1.85 (95%CI, 1.1-3.1). No significant associations were found in women. Low anti-PC levels increase the risk of CVE in men. This effect may be partly mediated by a fast C-IMT progression.

Affiliated researcher

PubMed 25150937

DOI 10.1016/j.atherosclerosis.2014.07.030

Crossref 10.1016/j.atherosclerosis.2014.07.030

pii: S0021-9150(14)01306-9

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