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J R Soc Med 2005;98:296
doi:10.1258/jrsm.98.6.296-a
© 2005 Royal Society of Medicine

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J R Soc Med 2005;98:296
© 2005 The Royal Society of Medicine

Letters

Myocardial infarction after aspirin treatment, and Kounis syndrome

Nicholas G Kounis Sophia N Kouni   Constantinos M Koutsojannis

Section of Medical Sciences, Patras Highest Institute of Education and Technology, 7 Aratou Street, Queen Olga's Square, Patras, Greece

E-mail: ngkounis{at}otenet.gr

Dr Fox and his colleagues (January 2005 JRSM1) describe the case of a patient who developed coronary vasospasm after a dose of aspirin, to which she had a history of allergy. The concurrence of allergic reactions with acute coronary syndromes has been well described previously. Sometimes the allergic angina syndrome (Kounis syndrome) progresses to myocardial infarction.2 Various foods and drugs have been incriminated.

This syndrome is caused by release of inflammatory mediators during mast cell degranulation. These compounds include preformed mediators such as histamine, neutral proteases (tryptase, chymase) and platelet activating factor and also newly synthesized mediators such as leucotrienes and thromboxane which have been incriminated clinically and experimentally in production of coronary spasm and/or acute myocardial infarction. However, inflammatory mediators have also been reported increased in the blood or urine of patients with acute coronary syndromes of non-allergic aetiology;3-5 moreover, degranulated mast cells have been found abundant in the coronary plaque rupture areas of such patients with recent myocardial infarction.6 For these reasons, we have suggested the existence of a final common pathway for allergic and non-allergic coronary syndromes.7

If mast cells do contribute to non-allergic coronary events, there is scope for therapy with stabilizing drugs such as sodium cromoglicate or ketotifen and with monoclonal antibody to IgE. Experimentally, Nemmar et al.8 have succeeded in abrogating late thrombotic events by stabilizing mast cell membrane with sodium cromoglicate and reducing inflammation with dexamethasone. We urge the research community to explore this possible final common pathway in allergic and non-allergic coronary syndromes.

REFERENCES

  1. Fox DJ, Gray TP, Fath-Ordoubadi F. Myocardial infarction after aspirin treatment. J R Soc Med2005; 98:21 -3[Free Full Text]

  2. Kounis NG, Zavras GM: Allergic angina and allergic myocardial infarction. Circulation1996; 94:1789

  3. Clejan S, Japa S, Clemetson C, et al. Blood histamine is associated with coronary artery disease, cardiac events and severity of inflammation and atherosclerosis. J Cell Mol Med2002; 6:583 -92[Medline]

  4. Takase B, Maruyama T, Kurita A, et al. Arachidonic acid metabolites in acute myocardial infarction. Angiology1996; 47:649 -61

  5. Filipiak KJ, Tarchsalska-Krynska B, Opolski G, et al. Tryptase levels in patients with acute coronary syndromes: the potential new marker in unstable plaque? Clin Cardiol2003; 26:366 -72[Medline]

  6. Kovanen PT, Kaartinen M, Paavonen T. Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction. Circulation1995; 92:1083 -8[Free Full Text]

  7. Zavras GM, Papadaki PJ, Kokkinis SE, et al. Kounis syndrome secondary to allergic reaction following shellfish ingestion. Int J Clin Pract2003; 57:622 -4[Medline]

  8. Nemmar A, Hoet PHM, Vermylen J, et al. Pharmacological stabilization of mast cells abrogates late thrombotic events induced by diesel exhaust particles in hamsters. Circulation2004; 110:1670 -7[Abstract/Free Full Text]


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