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Lipoprotein-associated phospholipase A2 does not predict mortality or new ischaemic events in acute coronary syndrome patients
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , UCR-Uppsala Clinical Research center. (UCR)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , UCR-Uppsala Clinical Research center. (UCR)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , UCR-Uppsala Clinical Research center. (UCR)
2007 (English)In: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 28, no 6, 699-704 p.Article in journal (Refereed) Published
Abstract [en]

AIM: Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) has been suggested as an independent predictor of cardiovascular events in epidemiological studies. We sought to evaluate Lp-PLA(2) as a risk factor for future cardiovascular events in patients with acute coronary syndromes (ACS) and to elucidate the relationship between Lp-PLA(2) and other known risk markers in ACS patients and healthy control subjects. METHODS AND RESULTS: Blood samples were obtained at randomization in a random subset of ACS patients in the FRISC II (n = 1362) and GUSTO IV (n = 904) studies and in 435 apparently healthy controls of similar age and gender. Median Lp-PLA(2) (mass) levels were 305 ng/mL (FRISC II), 373 ng/mL (GUSTO IV), and 254 ng/mL (healthy controls). Time delay from symptom onset did not influence Lp-PLA(2) levels. In the FRISC II patients and healthy controls, Lp-PLA(2) was significantly correlated with cholesterol (r = 0.3), low-density lipoprotein (r = 0.4 and r = 0.3, respectively), and C-reactive protein (r = 0.08 and r = 0.1, respectively), all P < 0.01. Lp-PLA(2) was not correlated with age, interleukin-6, troponin T, or NT-proBNP in any of the three cohorts. There was no difference in the composite of death and myocardial infarction at 30 days (GUSTO IV) or 180 days (FRISC II) in relation to low, middle, and top tertiles of Lp-PLA(2) at randomization. In FRISC II, the 1 year mortality was 4.2, 4.2, and 4.8% in the low, middle, and top Lp-PLA(2) tertiles, respectively, P = 0.8. In GUSTO IV, 1 year mortality was 7.0, 8.3, and 9.6% in the low, middle, and top Lp-PLA(2) tertiles, respectively, P = 0.5. CONCLUSION: ACS patients had higher Lp-PLA(2) levels than healthy controls. Lp-PLA(2) was significantly correlated to lipid levels but only weakly correlated or unrelated to other well-established risk markers in ACS. The risk of future cardiovascular events or mortality was not related to Lp-PLA(2) levels in ACS patients. The biological role of Lp-PLA(2) and its role as a risk marker in ACS patients still remain unclear.

Place, publisher, year, edition, pages
2007. Vol. 28, no 6, 699-704 p.
Keyword [en]
Acute coronary syndromes, Inflammation
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-14781DOI: 10.1093/eurheartj/ehl565ISI: 000244960400016PubMedID: 17314110OAI: oai:DiVA.org:uu-14781DiVA: diva2:42552
Available from: 2008-01-31 Created: 2008-01-31 Last updated: 2017-12-11Bibliographically approved

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Oldgren, JonasJames, StefanSiegbahn, AgnetaWallentin, Lars

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