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Cholesterol, C-reactive protein, and cerebrovascular events following intensive and moderate statin therapy

Jessica L Mega1, David A Morrow, Christopher P Cannon

  • 1TIMI (Thrombolysis in Myocardial Infarction) Study Group, Boston, Massachusetts 12114, USA. jmega@partners.org

Journal of Thrombosis and Thrombolysis
|June 21, 2006
PubMed

Insights

Intensive statin therapy did not significantly alter cerebrovascular event (CVE) rates. However, elevated C-reactive protein (CRP) levels, a marker of inflammation, independently predicted higher CVE risk, underscoring inflammation's role in stroke.

Area of Science:

  • Cardiovascular Medicine
  • Neurology
  • Pharmacology

Background:

  • Statins are known to reduce cerebrovascular events (CVE).
  • The interplay between cholesterol, C-reactive protein (CRP), and CVE under different statin regimens requires further investigation.

Purpose of the Study:

  • To investigate the relationship between cholesterol, CRP, and CVE in patients receiving intensive versus moderate statin therapy.
  • To assess the impact of achieved lipid and non-lipid biomarker levels on CVE risk.

Main Methods:

  • Analysis of the PROVE IT-TIMI 22 randomized trial data.
  • Involved 4,162 patients with acute coronary syndromes treated with intensive (atorvastatin 80 mg) or moderate (pravastatin 40 mg) statin therapy.
  • Serial biomarker measurements, including lipids and CRP, were assessed over 24 months.

Main Results:

  • No significant difference in CVE rates between intensive and moderate statin therapy groups (2.1% vs. 1.9%, P=0.62).
  • Patients with CVE exhibited higher CRP levels at 30 days and 4 months post-treatment compared to those without CVE (P=0.012, P=0.005).
  • Day 30 CRP levels independently predicted CVE risk, even after adjusting for other risk factors. Lower CRP (<2 mg/L) correlated with reduced event rates.

Conclusions:

  • Achieved low-density lipoprotein (LDL) cholesterol levels did not independently influence CVE rates in this cohort.
  • Elevated CRP levels were associated with a higher risk of CVE, highlighting inflammation's critical role.
  • Findings support the link between inflammation and cerebrovascular events, suggesting CRP as a potential risk marker.
Abstract

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