Bridging Immunology and Cardiology: Current Perspectives on Kounis Syndrome

Kounis Syndrome (KS) is a distinct clinical manifestation in which Acute Coronary Syndromes (ACS) are associated with the occurrence of hypersensitivity or allergy. KS was initially described in 1991 as a range of acute myocardial ischemic events caused by mast cell activation and consequent release of inflammatory mediators in response to allergens, viz, drugs, insect stings, foods, and environmental agents. The pathophysiology of KS involves a complex interaction of histamine, tryptase, platelet-activating factor, and cytokines, resulting in coronary vasospasm, plaque rupture, and stent thrombosis. The syndrome has been classified into three variants: Type I, which is characterized by vasospasm and there is no underlying coronary disease; Type II, which is characterized by disruption of the plaque in the atherosclerotic plaque; and Type III, which is characterized by stent thrombosis, in which eosinophil and mast cell proliferation are prominent. Furthermore, the diagnosis requires a multimodal approach, which involves a clinical examination, biomarker testing (tryptase, IgE), echocardiography, and more advanced imaging, such as coronary angiography and MRI. However, due to complex pathophysiology and multimodal diagnosis, the management of KS is complex. To avoid exacerbation of allergic and ischemic processes in each other, a well-balanced anti-allergic and cardiovascular therapy is preferred, as well as using vasodilators, corticosteroids, antihistamines, and reasonable dosages of epinephrine and anticoagulants. Thus, the review focuses on symptoms and methods for early detection of KS to raise awareness and recognition for better patient outcomes associated with KS using case studies.