Kounis syndrome leading to triple-vessel coronary artery ischaemia due to simultaneous coronary spasm, plaque erosion, and multiple stent thrombosis: a case report

Abstract

Background Kounis syndrome (KS) is an acute coronary syndrome (ACS) induced by allergic reactions. Currently, there are three variants of KS based on the mechanism and onset of ACS. We report a rare case of KS, wherein ACS was caused by all KS variants. Case summary A 68-year-old man with a history of percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction of the left anterior descending artery 16 days ago underwent a staged PCI for the mid-left circumflex artery (LCx) stenosis under optical coherence tomography (OCT) guidance using low-molecular-weight dextran (LMWD). During OCT examination, the LMWD induced an anaphylactic reaction. The patient was immediately administered medications to manage the anaphylaxis; however, he complained of chest discomfort. Coronary angiography and subsequent intravascular ultrasound revealed a newly developed coronary thrombus in the proximal LCx. Furthermore, coronary spasm or multiple stent thromboses occurred sequentially in all coronary arteries, resulting in triple-vessel coronary artery ischaemia. Balloon angioplasty was performed under intra-aortic balloon pumping, which could rescue the patient. The patient was discharged without any complications 11 days post-KS, under a 7-day anti-histamine regimen. No further cardiovascular events had occurred by 1-year follow-up. Discussion This case documented the clinical course of KS caused by LMWD, wherein all KS variants occurred sequentially. Early recognition of KS and appropriate management with anaphylaxis medication and balloon angioplasty under mechanical circulatory support effectively prevent vascular morbidity. Interventionalists should be aware of this rare and serious complication of PCI.

Identification of the biological processes, immune cell landscape, and hub genes shared by acute anaphylaxis and ST-segment elevation myocardial infarction

“…In anaphylactic patients with pre-existing atherosclerosis, STEMI is associated with allergic factors-triggered atheromatous plaque erosion or stent thrombosis, which culminates in coronary occlusion and myocardial damage ( Sakaue et al, 2020 ; Engheta et al, 2021 ; Yamamoto et al, 2022 ). While in patients with angiographically normal coronary arteries and no risk factors for coronary artery disease, prolonged coronary spasm appears to be the leading cause of acute STEMI following anaphylaxis ( Goto et al, 2016 ; Li et al, 2018 ).…”

“…While in patients with angiographically normal coronary arteries and no risk factors for coronary artery disease, prolonged coronary spasm appears to be the leading cause of acute STEMI following anaphylaxis ( Goto et al, 2016 ; Li et al, 2018 ). Mast cells, distributed around coronary arteries and plaques, have been proposed to be implicated in anaphylaxis complicated with STEMI ( Marone et al, 2014 ; Li et al, 2018 ; Yamamoto et al, 2022 ). Upon activation, mast cells secrete inflammatory mediators such as histamine ( Galli and Tsai, 2012 ; Galli et al, 2020 ), which regulates coronary artery tone and vascular permeability, thus affecting hemodynamic stress and coronary blood flow ( Matsuyama et al, 1990 ; Kounis and Zavras, 1991 ; Mikelis et al, 2015 ).…”

“…A nationwide epidemiological study in the United States reported that among 235,420 patients hospitalized for allergy, hypersensitivity, or anaphylaxis, 0.2% of patients experienced STEMI ( Desai et al, 2019 ). Acute STEMI following anaphylaxis is associated with allergic mediators-induced coronary spasms, plaque erosion/rupture, or stent thrombosis ( Li et al, 2018 ; Sakaue et al, 2020 ; Yamamoto et al, 2022 ). Inflammatory responses elicited by mast cell-released vasoactive substances appears to be involved in this process and aggravate myocardial injury ( Galli and Tsai, 2012 ; Abdelghany et al, 2017 ; Li et al, 2018 ; Yamamoto et al, 2022 ).…”

“…Acute STEMI following anaphylaxis is associated with allergic mediators-induced coronary spasms, plaque erosion/rupture, or stent thrombosis ( Li et al, 2018 ; Sakaue et al, 2020 ; Yamamoto et al, 2022 ). Inflammatory responses elicited by mast cell-released vasoactive substances appears to be involved in this process and aggravate myocardial injury ( Galli and Tsai, 2012 ; Abdelghany et al, 2017 ; Li et al, 2018 ; Yamamoto et al, 2022 ). Clinically, anaphylaxis complicated with STEMI is one of the most serious emergencies without effective predictors and medications.…”

Tea for histamine anti-allergy: component analysis of tea extracts and potential mechanism for treating histamine anti-allergy

“…When allergic reaction occurs in tissues, it will cause the rupture of basophilic granulocytes and mast cells to release histamine, and induce keratinocytes to secrete inflammatory cytokines IL-1β and NGF ( Lipnik-Stangelj et al, 2013 ). In addition, it will also cause dilation of capillaries and venules and increase permeability of tube walls, smooth muscle spasm, and enhancement of glandular secretion activities, resulting in local skin tissue showing congestion, erythema, and swelling ( Maria Arin et al, 2017 ; Gao et al, 2018 ; Yamamoto et al, 2022 ). Existing studies have shown that histamine secretion can stimulate the body to produce ROS and trigger oxidative stress in the body ( Hassanen et al, 2023 ), and promote the release of inflammatory factors through the NF- κ B pathway ( Park et al, 2014 ).…”