Role of inflammation in cardiovascular disease: how to use C-reactive protein in clinical practice

James S Zebrack1, Jeffrey L Anderson

  • 1University of Utah School of Medicine, Department of Internal Medicine, Division of Cardiology, Salt Lake City, UT, USA. mmzebrack@pol.net

Insights

Inflammation drives atherosclerosis, leading to heart attacks and strokes. High-sensitivity C-reactive protein (hs-CRP) is a key marker for cardiovascular risk, but its clinical use requires careful consideration.

Area of Science:

  • Cardiovascular Medicine
  • Immunology
  • Biochemistry

Background:

  • Atherosclerotic plaque disruption causes acute coronary syndromes, stroke, and sudden death.
  • Inflammation plays a critical role in the development and progression of atherosclerosis.
  • Systemic inflammation markers predict cardiovascular events, and treatments reduce these markers.

Purpose of the Study:

  • To review the role of inflammation in atherosclerosis pathogenesis.
  • To discuss inflammatory markers, focusing on C-reactive protein (CRP).
  • To explore the clinical utility and interpretation of CRP in cardiovascular risk assessment.

Main Methods:

  • Review of current medical research on inflammation and atherosclerosis.
  • Analysis of studies on inflammatory markers, particularly high-sensitivity C-reactive protein (hs-CRP).
  • Discussion of clinical scenarios and interpretation of hs-CRP levels.

Main Results:

  • High-sensitivity C-reactive protein (hs-CRP) is the most validated marker for cardiovascular risk assessment.
  • hs-CRP is central to atherosclerosis, with studies demonstrating its predictive value.
  • Factors influencing hs-CRP interpretation and potential anti-inflammatory therapies are discussed.

Conclusions:

  • Inflammation is integral to atherosclerosis, and hs-CRP is a key indicator of vascular inflammation and cardiovascular risk.
  • While hs-CRP is valuable, uncertainties remain regarding its optimal clinical application.
  • Future research should focus on assessing and modulating vascular inflammation to prevent atherosclerotic disease progression.

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