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Do we need to consider inflammatory markers when we treat atherosclerotic disease?

Vasilios G Athyros1, Anna I Kakafika, Asterios Karagiannis

  • 1Second Propedeutic Department of Internal Medicine, Medical School, Aristotle University of Thessaloniki, Hippocration Hospital, Thessaloniki, Greece. athyros@med.auth.gr

Atherosclerosis
|April 19, 2008
PubMed

Insights

Monitoring inflammatory markers like C-reactive protein can guide drug selection for cardiovascular disease (CVD) risk. This approach may help manage atherosclerosis in high-risk patients, but requires further clinical trials for validation.

Area of Science:

  • Cardiology
  • Immunology
  • Pharmacology

Background:

  • Inflammation is implicated in the pathogenesis of atherosclerosis.
  • High-risk patient groups including those with acute coronary syndromes (ACS), stable coronary artery disease (CAD), diabetes mellitus (DM), metabolic syndrome (MetS), non-alcoholic fatty liver disease (NAFLD), and systemic autoimmune diseases (SAD) exhibit significant inflammatory activity.
  • Atherosclerosis severity and extent correlate with inflammatory processes in these populations.

Purpose of the Study:

  • To review the utility of monitoring inflammatory markers for guiding therapeutic drug selection in patients at high risk for cardiovascular disease (CVD).
  • To assess the role of inflammation in atherosclerosis within specific high-risk patient cohorts.
  • To evaluate the potential of using simple inflammatory markers to inform treatment strategies.

Main Methods:

  • A comprehensive review of clinical and experimental studies was conducted.
  • Studies focused on inflammation in patients with ACS, stable CAD, DM, MetS, NAFLD, and SAD.
  • Analysis of the role of inflammatory markers such as C-reactive protein and fibrinogen in disease progression and treatment selection.

Main Results:

  • Evidence supports a significant role for inflammation in the development and severity of atherosclerosis among high-risk individuals.
  • Cost-effective monitoring of simple inflammatory markers (e.g., C-reactive protein, fibrinogen) is feasible.
  • These markers may assist in selecting drugs that address both traditional CVD risk factors and underlying inflammation.

Conclusions:

  • Monitoring inflammatory markers offers a potential strategy to personalize drug selection for CVD prevention in high-risk patients.
  • Further well-designed clinical trials with relevant endpoints are necessary to confirm the clinical utility and impact of this approach.
  • Inflammation management, guided by marker monitoring, could be a key component in reducing cardiovascular risk.

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