Kounis Nicholas G, Stefanidis Alexandros, Hung Ming-Yow, Özkan Uğur, de Gregorio Cesare, Ceasovschih Alexandr, Mplani Virginia, Gogos Christos, Assimakopoulos Stelios F, Chatzigrigoriadis Christodoulos, Plotas Panagiotis, Dousdampanis Periklis, Kouni Sophia N, Tsigkas Grigorios, Patsouras Nicholas, Calogiuri Gianfranco, Pourmasumi Soheila, Koniari Ioanna
Department of Medicine, Division of Cardiology, University Hospital of Patras, 26500 Patras, Greece.
First Cardiology Department, General Hospital of Nikea, Agios Panteleimon Piraeus, 3 D Mantouvalou Street, 18454 Piraeus, Greece.
J Cardiovasc Dev Dis. 2025 Aug 25;12(9):325. doi: 10.3390/jcdd12090325.
This narrative review explains the history of anaphylactic or hypersensitivity reactions, their connection to the cardiovascular system, and Kounis syndrome, which is linked to hypersensitivity. Additional subjects discussed include immunoglobulin E and serum tryptase, common pathways of allergic and nonallergic cardiovascular events, current perspectives on Kounis syndrome, allergic myocardial infarction, allergic angina, and the impact of COVID-19 and its vaccination on Kounis syndrome. Kounis syndrome is a distinct kind of acute vascular disease that affects the coronary, cerebral, mesenteric, peripheral, and venous systems. Kounis syndrome is currently used to describe coronary symptoms linked to disorders involving mast cell activation and inflammatory cell interactions, such as those involving T-lymphocytes and macrophages, which further induce allergic, hypersensitive, anaphylactic, or anaphylactic insults. Platelet activating factor, histamine, neutral proteases like tryptase and chymase, arachidonic acid products, and a range of cytokines and chemokines released during the activation process are among the inflammatory mediators that cause it. Proinflammatory cytokines are primarily produced by mast cells in COVID-19 infections. Mast cell-derived proteases and eosinophil-associated mediators are also more prevalent in the lung tissues and sera of COVID-19 patients. As a modern global threat to civilization, COVID-19 is linked to chemical patterns that can activate mast cells; therefore, allergic stimuli are usually the reason. Virus-associated molecular patterns can activate mast cells, but allergic triggers are typically the cause. By activating SARS-CoV-2 and other toll-like receptors, a variety of proinflammatory mediators, including IL-6 and IL-1β, are released, potentially contributing to the pathology of COVID-19.
这篇叙述性综述解释了过敏或超敏反应的历史、它们与心血管系统的联系以及与超敏反应相关的库尼斯综合征。讨论的其他主题包括免疫球蛋白E和血清类胰蛋白酶、过敏性和非过敏性心血管事件的常见途径、库尼斯综合征的当前观点、过敏性心肌梗死、过敏性心绞痛以及COVID-19及其疫苗接种对库尼斯综合征的影响。库尼斯综合征是一种独特的急性血管疾病，可影响冠状动脉、脑动脉、肠系膜动脉、外周动脉和静脉系统。目前，库尼斯综合征用于描述与涉及肥大细胞活化和炎症细胞相互作用的疾病相关的冠状动脉症状，例如涉及T淋巴细胞和巨噬细胞的疾病，这些疾病会进一步引发过敏、超敏、过敏反应或过敏样损伤。炎症介质包括血小板活化因子、组胺、类胰蛋白酶和糜蛋白酶等中性蛋白酶、花生四烯酸产物以及在激活过程中释放的一系列细胞因子和趋化因子。在COVID-19感染中，促炎细胞因子主要由肥大细胞产生。肥大细胞衍生的蛋白酶和嗜酸性粒细胞相关介质在COVID-19患者的肺组织和血清中也更为普遍。作为对文明的现代全球威胁，COVID-19与可激活肥大细胞的化学模式有关；因此，过敏刺激通常是原因。病毒相关分子模式可激活肥大细胞，但过敏触发因素通常是病因。通过激活SARS-CoV-2和其他Toll样受体，会释放包括IL-6和IL-1β在内的多种促炎介质，这可能会导致COVID-19的病理过程。
