Inflammation, Proinflammatory Mediators and Myocardial Ischemia-reperfusion Injury

Jakob Vinten-Johansen, Rong Jiang, James G. Reeves, James Mykytenko, Jeremiah Deneve, Lynetta J. Jobe

Research output: Contribution to journalReview article

53 Scopus citations

Abstract

Ischemic myocardium must be reperfused to terminate the ischemic event; otherwise the entire myocardium involved in the area at risk will not survive. However, there is a cost to reperfusion that may offset the intended clinical benefits of minimizing infarct size, postischemic endothelial and microvascular damage, blood flow defects, and contractile dysfunction. There are many contributors to this reperfusion injury. Targeting only one factor in the complex web of reperfusion injury is not effective because the untargeted mechanisms induce injury. An integrated strategy of reducing reperfusion injury in the catheterization laboratory involves controlling both the conditions and the composition of the reperfusate. Mechanical interventions such as gradually restoring blood flow or applying postconditioning may be used independently in or conjunction with various cardioprotective pharmaceuticals in an integrated strategy of reperfusion therapeutics to reduce postischemic injury.

Original languageEnglish (US)
Pages (from-to)123-145
Number of pages23
JournalHematology/Oncology Clinics of North America
Volume21
Issue number1
DOIs
Publication statusPublished - Feb 1 2007

    Fingerprint

ASJC Scopus subject areas

  • Hematology
  • Oncology

Cite this

Vinten-Johansen, J., Jiang, R., Reeves, J. G., Mykytenko, J., Deneve, J., & Jobe, L. J. (2007). Inflammation, Proinflammatory Mediators and Myocardial Ischemia-reperfusion Injury. Hematology/Oncology Clinics of North America, 21(1), 123-145. https://doi.org/10.1016/j.hoc.2006.11.010