Kounis syndrome (allergic angina and allergic myocardial infarction): a natural paradigm?

Int J Cardiol. 2006 Jun 7;110(1):7-14. doi: 10.1016/j.ijcard.2005.08.007. Epub 2005 Oct 24.

Abstract

Inflammatory mediators including histamine, neutral proteases, arachidonic acid products, platelet activating factor and a variety of cytokines and chemokines are increased in blood or urine in both allergic episodes and acute coronary syndromes. The release of mediators during allergic insults has been incriminated to induce coronary artery spasm and/or atheromatous plaque erosion or rupture. A common pathway between allergic and non-allergic coronary syndromes seems to exist. Today, there is evidence that mast cells not only enter the culprit region before plaque erosion or rupture but they release their contents before an actual coronary episode. Kounis syndrome is the concurrence of acute coronary syndromes with conditions associated with mast cell activation including allergic or hypersensitivity and anaphylactic or anaphylactoid insults. It is caused by inflammatory mediators released through mast cell activation. Kounis syndrome, as consequence, of the above pathophysiologic association is regarded as nature's own experiment and magnificent natural paradigm showing novel way in an effort to prevent acute coronary syndromes. Drugs and natural molecules which stabilize mast cell membrane and monoclonal antibodies that protect mast cell surface could emerge as novel therapeutic modalities capable to prevent acute coronary and cerebrovascular events.

Publication types

  • Review

MeSH terms

  • Angina Pectoris / etiology*
  • Coronary Vasospasm / etiology*
  • Humans
  • Hypersensitivity / etiology*
  • Inflammation Mediators / adverse effects*
  • Mast Cells
  • Myocardial Infarction / etiology*
  • Syndrome

Substances

  • Inflammation Mediators