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Nonocclusive thrombus on preexisting plaques, dynamic obstruction, progressive obstruction, inflammation and/or infection, and secondary unstable angina seem to be the 5 not mutually exclusive causes of the unstable angina syndrome. These were suggested in the excellent editorial by E. Braunwald. 1 In this editorial, it was pointed out that vasospastic angina, which is a form of unstable angina, is rarely caused by allergic reactions via mediators such as histamine or leukotrienes acting on coronary vascular smooth muscle.We have suggested that the coincidental occurrence of chest discomfort with characteristic clinical symptoms, signs, and laboratory findings of angina pectoris together with acute or chronic allergic processes constitutes a new clinical entity, which was named allergic angina. 2 Furthermore, this can progress to acute myocardial infarction, which was named allergic myocardial infarction. 3 We believe that allergic angina and allergic myocardial infarction represent a magnificent natural paradigm that might have profound clinical and therapeutic implications. This is based on clinical and laboratory findings.It is almost certain today that the majority of cases of unstable angina and acute myocardial infarction are the result of combined coronary artery spasm and atheromatous plaque erosion or rupture followed by thrombus formation.Allergic or hypersensitivity reactions are associated with mast cell degranulation and release of mediators including histamine, leukotrienes, and neutral proteases, such as tryptase and chymase. Histamine and leukotrienes are powerful coronary vasoconstrictors, and tryptase and chymase are metalloproteinase activators that can trigger degradation of collagen and induce plaque erosion or rupture, thus initiating an acute coronary event. Indeed, plasma histamine concentration in coronary circulation was found to be elevated in patients with variant angina, 4 and infiltration of activated mast cells at the site of erosion or rupture was shown in patients with recent acute myocardial infarction. 5 Therefore, the same substances released during allergic episodes are found in patients with acute coronary episodes. The reported causes to date that are capable of inducing allergic angina and allergic myocardial infarction include conditions such as food allergy; bronchial asthma; serum sickness; urticaria; angioedema; drugs such as antibiotics, contrast media, corticosteroids, dextran, nonsteroidal antiinflammatory drugs, skin disinfectants, streptokinase, tetanus toxoid, glaphenine, and zomepirac; and wasp stings and viper venoms. If we consider that these causes are commonly encountered, then one can think that a common pathogenetic basis might exist.In 2 studies we have in progress, we have preliminarily seen that mast cell content is elevated in blood plasma of patients with acute myocardial infarction and that coronary events are reduced in patients receiving mast cell-stabilizing drugs for bronchial asthma.Is therefore allergic angina nature's own experiment, manifesti...

Percutaneous transluminal coronary angioplasty with coronary stent implantation is a lifesaving medical procedure that has become, nowadays, the most frequent performed therapeutic procedure in medicine. Plain balloon angioplasty, bare metal stents, first and second generation drug-eluting stents, bioresorbable and bioabsorbable scaffolds have offered diachronically a great advance against coronary artery disease and have enriched our medical armamentarium. Stented areas constitute vulnerable sites for endothelial damage, endothelial dysfunction, flow turbulence, hemorheologic changes, platelet dysfunction, coagulation changes and fibrinolytic disturbances. Implant surface attracts several proteins such as albumin, fibronectin, fibrinogen, and complement that lead to complement system activation. Macrophages recognize the implant as foreign substance due to protein adsorption and its continuous presence results in macrophage differentiation and fusion into foreign body giant cells. Polymer coating, stent metallic platforms and the released drugs can act as strong antigenic complex that apply continuous, repetitive, persistent and chronic hypersensitivity irritation to the coronary intima. The concomitant administration of oral antiplatelet drugs and environmental exposures can induce hypersensitivity inflammation. A class of platelets, activated via high-affinity and low-affinity IgE hypersensitivity receptors FCγRI, FCγRII, FCεRI and FCεRII, can induce Kounis hypersensitivity-associated thrombotic syndrome inside the stented coronaries. Type III variant of this syndrome is diagnosed when coronary artery stent thrombosis is associated with thrombus infiltrated by eosinophils or mast cells and/or when coronary intima, media and adventitia adjacent to stent, is infiltrated by eosinophils or mast cells. Careful history of hypersensitivity reactions to all implanted materials and concomitant drugs with monitoring of inflammatory mediators as well as lymphocyte transformation studies to detect hypersensitivity must be undertaken in order to avoid disastrous consequences. Food and Drug Administration recommendations for coronary stent implantation should be applied also to bioresorbable scaffolds. Further studies with inert and non-allergenic implants are necessary.

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