| Literature DB >> 28215109 |
Parveen K Garg1, Neal W Jorgensen2, Robyn L McClelland2, Nancy S Jenny3, Michael H Criqui4, Matthew A Allison4, Philip Greenland5,6, Robert S Rosenson7, David S Siscovick8, Mary Cushman3,9.
Abstract
Prospective studies supporting a relationship between elevated lipoprotein-associated phospholipase A2 (Lp-PLA2) and incident peripheral arterial disease (PAD) are limited. We evaluated the association of Lp-PLA2 with incident PAD in a multi-ethnic cohort without clinical cardiovascular disease. A total of 4622 participants with measurement of Lp-PLA2 mass and Lp-PLA2 activity and an ankle-brachial index (ABI) between 0.9 and 1.4 were followed for the development of PAD (median follow-up = 9.3 years), defined as an ABI ⩽0.9 and decline from baseline ⩾0.15. There were 158 incident PAD events during follow-up. In adjusted logistic regression models, each higher standard deviation of both Lp-PLA2 activity and mass did not confer an increased risk of developing PAD [odds ratios, (95% confidence intervals)]: 0.92 (0.66-1.27) for Lp-PLA2 activity and 1.06 (0.85-1.34) for mass. Additionally, no significant interaction was found according to ethnicity: p=0.43 for Lp-PLA2 activity and p=0.55 for Lp-PLA2 mass. We found no evidence of an association between Lp-PLA2 and incident PAD.Entities:
Keywords: ankle–brachial index; inflammation; lipoprotein-associated phospholipase A2; peripheral arterial disease (PAD)
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Year: 2016 PMID: 28215109 DOI: 10.1177/1358863X16671424
Source DB: PubMed Journal: Vasc Med ISSN: 1358-863X Impact factor: 3.239