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High-sensitivity C-reactive protein and lipoprotein-associated phospholipase A2 stability before and after stroke and
Mitchell S V Elkind1, Vladimir Leon, Yeseon P Moon
1Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, NY, USA. mse13@columbia.edu
Insights
High-sensitivity C-reactive protein (hsCRP) and lipoprotein-associated phospholipase A2 (Lp-PLA2) levels change after myocardial infarction (MI) and stroke. hsCRP increases, while Lp-PLA2 levels decrease, impacting long-term risk assessment.
Area of Science:
- Biomarkers
- Cardiovascular Disease
- Inflammation
Background:
- High-sensitivity C-reactive protein (hsCRP) and lipoprotein-associated phospholipase A2 (Lp-PLA2) are investigated as systemic inflammation and cardiovascular risk biomarkers.
- Limited data exist on the longitudinal stability of these markers and the impact of acute vascular events.
Purpose of the Study:
- To assess the long-term stability of hsCRP and Lp-PLA2 mass and activity levels.
- To determine the effect of acute myocardial infarction (MI) and stroke on these biomarker levels.
Main Methods:
- Serum samples from 52 participants were collected annually over 4 years.
- hsCRP and Lp-PLA2 mass/activity were measured. Longitudinal stability was analyzed using random effects models.
- Samples from 37 participants were analyzed before and after stroke or MI events.
Main Results:
- hsCRP and Lp-PLA2 activity remained stable over time.
- Lp-PLA2 mass showed a modest annual decrease of 5%.
- Following stroke and MI, hsCRP levels significantly increased, while Lp-PLA2 mass and activity levels significantly decreased.
Conclusions:
- hsCRP and Lp-PLA2 activity are stable biomarkers over time.
- Acute vascular events like stroke and MI alter hsCRP and Lp-PLA2 levels.
- Post-event measurements may not accurately reflect baseline risk for long-term stratification.
Background And Purpose:
High-sensitivity C-reactive protein (hsCRP) and lipoprotein-associated phospholipase A2 (Lp-PLA2) are hypothesized to be biomarkers of systemic inflammation and risk of myocardial infarction (MI) and stroke. Little is known, however, about the stability of these markers over time, and in particular, about the effects of acute vascular events on these marker levels.
Methods:
Serum samples were collected at 4 annual intervals in 52 stroke-free participants from the Northern Manhattan Study (NOMAS) and assayed for hsCRP and Lp-PLA2 mass and activity levels using standard techniques. Log transformation of levels was performed as needed to stabilize the variance. Stability of marker levels over time was assessed using random effects models unadjusted and adjusted for demographics and other risk factors. In addition, samples from 37 initially stroke-free participants with stroke (n=17) or MI (n=20) were available for measurement before and after the vascular event (median 5 days, range 2 to 40 days). Levels before and after events were compared using nonparametric tests.
Results:
HsCRP and Lp-PLA2 activity levels were stable over time, whereas Lp-PLA2 mass levels decreased on average 5% per year (P=0.0015). Using accepted thresholds to define risk categories of Lp-PLA2 mass, there was no significant change over time. HsCRP increased after stroke (from median 2.2 mg/L prestroke to 6.5 mg/L poststroke; P=0.0067) and MI (from median 2.5 mg/L pre-MI to 13.5 mg/L post-MI; P<0.0001). Lp-PLA2 mass and activity levels both decreased significantly after stroke and MI (for Lp-PLA2 mass, from median 210.0 ng/mL to 169.4 ng/mL poststroke, P=0.0348, and from median 233.0 ng/mL to 153.9 post-MI, P<0.0001).
Conclusion:
Lp-PLA2 mass levels decrease modestly, whereas hsCRP and Lp-PLA2 activity appear stable over time. Acutely after stroke and MI, hsCRP increases whereas Lp-PLA2 mass and activity levels decrease. These changes imply that measurements made soon after stroke and MI are not reflective of prestroke levels and may be less reliable for long-term risk stratification.
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