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I have completed bits of my EM training from India. Currently I am boarded with credentials from Christian Medical College, Vellore and also from the prestigious Royal College of Emergency Medicine, UK.  I am currently working in London as an A&E doctor, trying to appreciate the differences in the practise and culture of Emergency Medicine across different healthcare systems. I have always been an avid FOAMed supporter because FOAMed played an indispensable role during the days of my initial training. Through this blog, I aspire to disseminate knowledge and stay up to date with the EM literature. 

Monday, May 1, 2017

Allergic Myocardial Infarction - Kounis Syndrome

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 such as histamine, neutral proteases, arachidonic acid products, platelet activating factor and a variety of cytokines released during the activation process. 

In 1991, Kounis and Zavras described the syndrome of allergic angina as the concurrence of chest pain and allergic reactions, accompanied by clinical and laboratory findings of classical angina pectoris caused by inflammatory mediators released during the allergic insult. Allergic angina and allergic myocardial infarction are referred as “Kounis syndrome” .


Type I variant: includes patients with normal coronary arteries without predisposing factors for coronary artery disease in whom the acute release of inflammatory mediators can induce coronary artery spasm without increase of cardiac enzymes and troponins or coronary artery spasm progressing to acute myocardial infarction with raised cardiac enzymes and troponins
Type II variant: includes patients with culprit but quiescent pre-existing atheromatous disease in whom the acute release of inflammatory mediators can induce either coronary artery spasm with normal cardiac enzymes and troponins or plaque erosion or rupture manifesting as acute myocardial infarction
Type III variant: includes patients with coronary thrombosis (including stent thrombosis) in whom aspirated thrombus specimens stained with hematoxylin-eosin and Giemsa demonstrate the presence of eosinophils and mast cells respectively.

Causes of Kounis Syndrome

   Anti-histaminics (H1 and H2 blockers)
   Vasodilators (NTG) and routine ACS treatment

   Adrenaline is the drug of choice and can save lives in anaphylaxis, but in Kounis syndrome there is a chance of aggravating ischemia and worsen coronary vasospasm. Despite this risk, in severe reactions, adrenaline should be given as wide spread manifestations of Anaphylaxis are life-threatening. Sulfite free adrenaline is recommended when available. Glucagon may be considered for those who take beta blockers and do not respond to adrenaline. Fentanyl shows a slight mast cell activation as compared to morphine and should be the drug of choice when opioid analgesia is necessary.

Posted by:

     Lakshay Chanana
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine



  1. Kounis NG, Zavras GM. Histamine-induced coronary artery spasm: the concept of allergic angina. Br. J. Clin. Pract.45,121–128 (1991).
  2. Kounis NG, Zavras GM. Allergic angina and allergic myocardial infarction. Circulation94,1789 (1996).
  3. Kounis NG, Grapsas GM, Goudevenos JA. Unstable angina, allergic angina and allergic myocardial infarction. Circulation100,e156 (1999).

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