Kounis syndrome: a manifestation of drug-eluting stent thrombosis associated with allergic reaction to contrast material.

Stent components acting as potential antigens and promoting intracoronary mast cell activation can lead to catastrophic intrastent thrombosis. Patients with drug-eluting stent (DES) implantation are prone to hypersensitivity reactions from five potential antigens namely, nickel strut, polymer coating, eluted drug, as well as, concomitant drugs clopidogrel and aspirin. These events may be more common than suspected because it is hard to document them, unless they become systemic, in which case they manifest themselves as the Kounis syndrome characterized by the concurrence of acute coronary events with hypersensitivity reactions. This report concerns of a patient with implanted DES who developed an acute myocardial infarction in the stent area following an allergic reaction to contrast material.

Kounis syndrome associated with hypersensitivity to hymenoptera stings.

Hymenoptera stings can induce acute coronary syndromes by different pathogenetic mechanisms including direct action of the venom constituents on the coronary endothelium or allergic reaction with mediators acting on the coronary vasculature. Two patients were stung by wasps and honeybees and developed Kounis syndrome as a consequence of allergic reaction. Kounis syndrome is the concurrence of acute coronary syndromes with mast cell activation induced by allergic or hypersensitivity and anaphylactic of anaphylactoid reactions. It is caused via inflammatory mediators released through mast cell activation. The patients had pre-existing coronary artery disease (type II variant of Kounis syndrome) and the allergic reaction induced by hymenoptera stings seems to have triggered inflammatory mediator release. The pathophysiology and clinical implications of this association are discussed.

Severe thrombocytopenia after heparin therapy in a patient with unstable angina and recent stent implantation.

Heparin-induced thrombocytopenia represents a serious side effect of heparin therapy. Immune-mediated platelet activation results in thrombocytopenia, endothelial thrombin release and development of thrombosis, mainly venous. We report the case of a man with a history of coronary artery disease and recent stent implantation. This patient developed severe heparin-induced thrombocytopenia type II after low molecular weight heparin administration because of unstable angina which occurred two months after stent implantation. The patient was treated with a new anticoagulant regimen, fondaparinux sodium. There were no complications and platelet counts were restored to normal levels.