Inhibition of sPLA2-IIA, C-reactive protein or complement: new therapy for patients with acute myocardial infarction?

Paul A J Krijnen, Christof Meischl, Remco Nijmeijer, Cees A Visser, C Erik Hack, Hans W M Niessen

Research output: Contribution to journalReview articleAcademicpeer-review

31 Citations (Scopus)


Reperfusion of ischemic myocardium after acute myocardial infarction (AMI) induces a local activation of inflammatory reactions that results in ischemia/reperfusion (I/R)-injury. I/R-injury contributes considerably to the total cell damage in the heart after AMI. Secretory phospolipase A2-IIA (sPLA2-IIA), C-reactive protein (CRP) and complement are inflammatory mediators that have been demonstrated to play key roles in I/R injury. From studies by us and others a mechanism emerged in which sPLA2-IIA binds to reversibly damaged cardiomyocytes and subsequently induces cell death, partly by potentiating binding of CRP and subsequent complement activation. Next to this, sPLA2-IIA also has a direct toxic effect, independent of CRP or complement. Therefore, these studies indicate a crucial role of inflammatory mediators in ischemia/reperfusion injury. This review will focus on the pathogenic effects of sPLA2-IIA, CRP and complement and on the putative therapeutic effects of inhibitors of these inflammatory mediators in acute myocardial infarction.

Original languageEnglish
Pages (from-to)113-23
Number of pages11
JournalCardiovascular & hematological disorders drug targets
Issue number2
Publication statusPublished - Jun 2006


  • Animals
  • C-Reactive Protein
  • Complement Inactivating Agents
  • Complement System Proteins
  • Enzyme Inhibitors
  • Group II Phospholipases A2
  • Humans
  • Journal Article
  • Myocardial Infarction
  • Myocardial Reperfusion Injury
  • Phospholipases A
  • Research Support, Non-U.S. Gov't
  • Review

Cite this