Papers of the Week

Coronary syndromes associated with conditions related to mast cell activation and inflammatory cell interaction, such as T-lymphocytes and macrophages, further inducing allergic or hypersensitivity and anaphylactic or anaphylactoid insults are referred today as Kounis syndrome. Kounis syndrome is caused by inflammatory mediators released during an allergic insult post inflammatory cell activation and interaction via multidirectional stimuli. A platelet subset, of 20%, with high and low affinity IgE surface receptors are also involved in this process. Kounis syndrome is not simply a single organ disease, but a complex multi-system and multi organ arterial clinical syndrome, affecting coronary, mesenteric and cerebral arteries accompanied by allergy-hypersensitivity-anaphylaxis, involving skin, respiratory and vascular systems in the context of anesthesia, surgery, radiology, oncology, or even dental and psychiatric medicine with significant influence on both morbidity and mortality. Kounis syndrome might be caused by numerous and continuously increasing causes accompanied with broadening clinical symptoms and signs via multi organ arterial system involvement, in patients of any age, demonstrating predominant anaphylaxis features in terms of a wide spectrum of mast cell-association disorders. Cardiac symptoms as chest pain, coronary vasospasm, angina pectoris, myocardial infarction, stent thrombosis, acute cardiac failure, and sudden cardiac death, associated with subclinical, clinical, acute or chronic allergic reactions constitute clinical manifestations of this syndrome. Since its first description, a common pathway between allergic and non allergic coronary events has been demonstrated. The hypothesis is based on the existence of a much higher mast cell degranulation degree at the sites of plaque erosion or rupture compared to adjacent areas or even to more distant segments in post acute myocardial infarction of non allergic etiology patients. Mast cell activation, differentiation and mediator release takes days or weeks, therefore mast cell degranulation could be performed just before any acute coronary event, further resulting in coronary artery vasoconstriction and atheromatous plaque rupture. It seems that medications and natural molecules stabilizing mast cell membrane as well as monoclonal antibodies by protecting mast cell surface could emerge as novel therapeutic modalities for acute coronary and cerebrovascular event prevention.