utility of inflammatory biomarkers in secondary prevention, notably after ACS, is discussed fully in Chapters 17 and 18.
Beyond risk stratification, could inflammatory biomarkers add to the management of CVD by serving as targets or guides for therapy? Until recently, little evidence supported such utility. As one follows levels of LDL or blood pressure, serial measurement of CRP has little basis in evidence despite its plausibility. The recent analysis of PROVE IT (Pravastatin or Atorvastatin Evaluation and Infection Therapy)-TIMI 22 begins to provide justification for CRP as a target oftherapy (38). This study demonstrated better outcomes in survivors ofACS with not only below median LDL levels with statin treatment but also below median levels of hsCRP. Both variables were measured 1 mo after an ACS, obviating any artifactual changes owing to the acute-phase response. Although this prospective analysis ofa large clinical trial indicates a role for CRP as a new target for statin therapy, other studies will be required to extend this concept to other interventions. Further confirmatory studies could hasten incorporation of the concept of CRP as a target of therapy into practice, critical pathways, and guidelines.
Was this article helpful?