European Heart Journal Advance Access originally published online on February 21, 2007
European Heart Journal 2007 28(6):699-704; doi:10.1093/eurheartj/ehl565
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Lipoprotein-associated phospholipase A2 does not predict mortality or new ischaemic events in acute coronary syndrome patients
1 Uppsala Clinical Research Center, Uppsala University Hospital, S-751 85 Uppsala, Sweden
2 Department of Medical Sciences, Clinical Chemistry, Uppsala University Hospital, S-751 85 Uppsala, Sweden
Received 21 June 2006; revised 22 January 2007; accepted 1 February 2007; online publish-ahead-of-print 21 February 2007.
* Corresponding author. Tel: +46 18 611 9502; fax: +46 18 506638. E-mail address: jonas.oldgren{at}ucr.uu.se
Aim Lipoprotein-associated phospholipase A2 (Lp-PLA2) has been suggested as an independent predictor of cardiovascular events in epidemiological studies. We sought to evaluate Lp-PLA2 as a risk factor for future cardiovascular events in patients with acute coronary syndromes (ACS) and to elucidate the relationship between Lp-PLA2 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-PLA2 (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-PLA2 levels. In the FRISC II patients and healthy controls, Lp-PLA2 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-PLA2 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-PLA2 at randomization. In FRISC II, the 1 year mortality was 4.2, 4.2, and 4.8% in the low, middle, and top Lp-PLA2 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-PLA2 tertiles, respectively, P = 0.5.
Conclusion ACS patients had higher Lp-PLA2 levels than healthy controls. Lp-PLA2 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-PLA2 levels in ACS patients. The biological role of Lp-PLA2 and its role as a risk marker in ACS patients still remain unclear.
Key Words: Acute coronary syndromes • Inflammation
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