<unk>  is a group of symptoms that manifests as unstable vasospastic or nonvasospastic angina and even as acute myocardial infarction and is triggered by the release of inflammatory mediators following an allergic insult . The name was given  by a group of scientists from USA  and Greece  because Professor Nicholas G<unk> , cardiologist from Greece, was the first to discover that the same inflammatory mediators, released during acute allergic episodes, are also increased in blood or urine of patients suffering from acute coronary syndromes and that a common pathophysiologic pathway exists between hypersensitivity and acute coronary episodes. Taking  previously underrated, scattered and rarely diagnosed, clinical phenomena and  presenting their pathophysiology,  this scientist  described in 1991, for the first time,  the syndrome of "allergic angina" .
Allergic angina could progress to acute myocardial infarction which was named ‘‘allergic myocardial infarction’’ [5–7]. In 1995, Kovanen et al. examined specimens of coronary arteries from 20 patients who had died of acute myocardial infarction and found that the degree of mast cell degranulation was much higher (200 to 1 ratio) at the sites of plaque erosion or rup¬ture than in adjacent areas or in the more distant unaffected areas . He concluded that collagen-degrading proteases, from mast cells, could induce plaque erosion and/or rupture. Following this clinical description, Constantinides , in 1995, raised the possibility that ‘‘even ordinary allergic reactions could promote plaque disruption’’. This was based on Constantinides’s observation that circulating mast cell precursors could penetrate the open junctions between endothelial cells that line human atheromatous plaques in contrast to closed junctions over the normal arterial intima . Braunwald , in 1998, categorized allergic angina in a subgroup of dynamic coronary occlusion lesions by quoting that ‘‘allergic reactions with mediators such as histamine or leukotrienes acting on coronary vascular smooth muscle’’ can induce vasospastic angina.
Today, allergic angina and allergic myocardial infarction is a ubiquitous disease covering a wide spectrum of mast cell activation disorders which are associated with acute coronary syndromes and are  referred to as ‘‘Kounis syndrome’’ in the medical literature [12-17].<unk>  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 [18,19].
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.<unk> , 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 [18,19]. Consequently, the same substances from the same cells are present in both acute allergic episodes and acute coronary syndromes.
Does, therefore,<unk>  represent a magnificent natural paradigm and nature’s own experiment in a final trigger pathway implicated in cases of coronary artery spasm and plaque rupture? Drugs and natural molecules which stabilize mast cell membrane and monoclonal antibodies that protect mast cell surface could emerge as novel therapeutic modalities capable of preventing acute coronary and cerebrovascular events .
Kounis syndrome
Zunich-Kaye syndrome
Mounier-Kuhn syndrome
Yunis-Varon syndrome
Rotor syndrome
Klüver-Bucy syndrome
Ellis-van Creveld syndrome
Wildervanck syndrome