Kounis syndrome

Kounis syndrome is a group of symptoms that manifests as unstable vasospastic, nonvasospastic angina, or acute myocardial infarction and is triggered by the release of inflammatory mediators following an allergic insult.

Kounis syndrome is defined as "the concurrence of acute coronary syndromes with conditions associated with mast cell activation, involving interrelated and interacting inflammatory cells, and 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 and chemokines released during the activation process. 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 as a cause of 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, 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.

It has been shown that the same mediators, released during acute allergic episodes, are increased in blood or urine of patients suffering from acute coronary syndromes of nonallergic etiology. Consequently, the same substances from the same cells are present in both acute allergic episodes and acute coronary syndromes.

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 either 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

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