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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.

Kounis syndrome is the concurrence of acute coronary syndromes with conditions associated with mast cell activation, such as allergies or hypersensitivity and anaphylactic or anaphylactoid insults that can involve other interrelated and interacting inflammatory cells behaving as a 'ball of thread'â. It is caused by inflammatory mediators such as neutral proteases including tryptase and chymase, arachidonic acid products, histamine, platelet activating factor and a variety of cytokines and chemokines released during the activation process. Platelets with FCεεRI and FCεεRII receptors also participate in the above cascade. Vasospastic allergic angina, allergic myocardial infarction and stent thrombosis with occluding thrombus infiltrated by eosinophils and/or mast cells constitute the three reported variants of this syndrome. Kounis syndrome is a ubiquitus disease that represents a magnificent natural paradigm and nature'âs own experiment, in a final trigger pathway implicated in cases of coronary artery spasm and plaque rupture. Kounis syndrome can complicate anesthesia, vaccination, medical therapy and stent implantation and it seems to be associated with coronary allograft vasculopathy and takotsubo syndrome, it can often be confused with hypersensitivity myocarditis and can be the cause of unexplained sudden death. Kounis syndrome has revealed that the same mediators released from the same inflammatory cells are present in acute coronary events of nonallergic etiology. These cells are not only present in the culprit region before plaque erosion or rupture but they release their contents just before an actual coronary event. Therefore, does Kounis syndrome represent a magnificent natural paradigm and nature'âs own experiment in a final trigger pathway implicated in cases of coronary artery spasm and plaque rupture showing a novel way towards our effort to prevent acute coronary syndromes? Drugs, substances targeting the stem cell factor that is essential for mast cell development, proliferation, survival, adhesion and homing as well as monoclonal antibodies and natural molecules that protect mast cell surface and stabilize mast cell membrane could emerge as novel therapeutic ways capable to prevent acute coronary and acute cerebrovascular events.

Introduction and importance Kounis syndrome, also known as allergic angina syndrome, is defined as the occurrence of an acute coronary syndrome concomitantly with a hypersensitivity reaction. It is a very important diagnosis and missing it may be fatal to the patient. This is a medical emergency, and immediate treatment should be initiated. The treatment of Kounis syndrome is challenging because treatment of either acute coronary syndrome and hypersensitivity reaction can lead to the worsening of the other injury. This case is the first reported case of Kounis syndrome following coronavirus disease 2019 vaccination in Sri Lanka according to our knowledge. Case presentation We discuss a 54-year-old female Sri Lankan patient who developed Kounis syndrome following Oxford AstraZeneca COVID-19 vaccination. The patient initially developed anaphylaxis following the AstraZeneca COVID-19 vaccine and subsequently developed acute coronary syndrome secondary to anaphylaxis. The patient was treated appropriately and eventually recovered from her condition. Conclusion This syndrome should be suspected when there is a concurrent acute coronary syndrome with allergic reactions. This is an often under- or misdiagnosed condition, and physicians should be educated about it. Caregivers should be aware of its pathophysiology, as treatment of either of the two may worsen the other injury.

Kounis syndrome is a type of acute coronary syndrome that occurs when a chemical mediator produced by mast cell activation leads to coronary artery vasospasm. This can happen due to anaphylaxis, anaphylactoid reactions, allergies, or hypersensitivities. There are three variants of Kounis syndrome, including vasospastic allergic angina, an atheromatous disease with plaque eruption, and stent thrombosis. In this case, the patient developed type 2 Kounis syndrome after consuming a fish meal, which caused him to present with a non‐ST elevation myocardial infarction (NSTEMI) at our hospital.

Acute coronary syndromes can develop with an unusual and challenging presentation. Kounis syndrome is a mostly overlooked Acute Coronary Syndrome (ACS) in the setting of anaphylactic or anaphylactoid reactions in response to an allergic insult that can lead to severe complications including cardiac arrest. A 52-yearold- man presented to the emergency department of our hospital because of acute transient loss of consciousness that developed some minutes after almonds ingestion. The complex diagnostic workup led to the diagnosis of vasospastic Kounis syndrome, an infrequent type of acute coronary syndrome, mostly overlooked, with challenging diagnostic and therapeutic features. Peculiarities on clinical presentation, the approach adopted by the emergency physician and the consultant cardiologist to achieve the correct diagnosis and our proposed management with a brief revision of the literature will be reported. Unusual clinical presentations of acute coronary syndromes represent part of the pitfalls that an emergency physician can face during the everyday practice. Prompt identification of these conditions is always struggling but of crucial importance to improve patient prognosis with a correct diagnostic work-up and therapeutic management.

Cephalosporins are an increasingly encountered cause of Kounis syndrome. The present study examined the clinical features of cephalosporin-induced Kounis syndrome and provided references for diagnosis, prevention, treatment, and prognosis. We collected cephalosporin-induced Kounis syndrome case reports by searching Chinese and English databases from the establishment of the database to October 31, 2021. Twenty-five patients (17 males and eight females) were included, with a median age of 61 years (range 33-92). Cephalosporins were administered via oral, intravenous and intramuscular routes. All reactions occurred within 30 min, except in two patients. Fourteen patients experienced chest pain, 19 experienced hypotension, 16 had cutaneous reactions, 10 had respiratory symptoms, and seven had gastrointestinal symptoms. Thirteen patients had elevated troponin levels, and eight patients had elevated serum tryptase levels. The electrocardiogram showed ST-segment elevation in 13 patients, depression in four patients, and elevation and depression in six patients. Coronary angiography showed normal results in 12 patients and abnormal results in 13 patients. The skin prick test was positive for cephalosporin in three patients. Twenty-four of the 25 patients recovered after being given anti-allergic and acute coronary syndrome treatment, and there was one death. Kounis syndrome is a serious adverse reaction to cephalosporin. Clinicians should consider Kounis syndrome in every patient receiving cephalosporin and presenting with acute chest pain or anaphylactic symptoms.

Inflammatory mediators, adhesion molecules of neutrophils and monocytes, have been shown to be increased in the plasma of patients presenting with acute coronary syndromes. Anaphylaxis is a systemic, immediate hypersensitivity reaction caused by rapid IgE-mediated release of mediators from mast cells and basophils. Kounis syndrome is the coincidental occurrence of these two distinct conditions accompanied by clinical and laboratory findings of angina pectoris caused by inflammatory mediators released during an allergic insult. Allergic angina can progress to acute myocardial infarction, which is termed 'allergic myocardial infarction'. There are several causes reported to be capable of inducing Kounis syndrome. These include a number of conditions, several drugs, foods and insect stings, among others. In this article, the clinical aspects, diagnosis, pathogenesis, incidence and epidemiology, related conditions and therapeutic management of this important syndrome are discussed.

The clinical picture of myocardial ischemia accompanying allergic reactions is defined in the cardiologic literature as Kounis syndrome (KS) or allergic angina/myocardial infarction. In PubMed, a search for “Kounis syndrome”, “allergic angina” or “allergic myocardial infarction” retrieves more than 100 results (among case reports, case series and reviews), most of which are published in cardiology/internal medicine/emergency medicine journals. In allergologic literature, heart involvement during anaphylactic reactions is well documented, but Kounis syndrome is hardly mentioned. Single case reports and small case series of angina triggered by allergic reactions have been reported for many years, and involvement of histamine and others mast cell mediators in the pathogenesis of coronary spasm has long been hypothesized, but the existence of an allergic acute coronary syndrome (ACS) is still questioned in the allergologic scientific community. Putative mechanisms of an allergic acute coronary syndrome include coronary spasm or heart tissue-resident mast cell activation (precipitating coronary spasm or inducing plaque rupture and coronary or stent thrombosis) due to systemic increase of allergic mediators, or heart tissue-resident mast cell activation by local stimuli. Indeed, the pathogenic mechanism of an ACS after an allergic insult might be related to direct effects of mast cell mediators on the myocardium and the atherosclerotic plaque, or to exacerbation of preexisting disease by the hemodynamic stress of the acute allergic/anaphylactic reaction. Which of these mechanisms is most important is still unclear, and this review outlines current views in the cardiologic and allergologic literature.

Abstract Background Although aspirin and adrenaline are the guideline-recommended treatments for acute coronary syndrome (ACS) and anaphylaxis, both regimens can contribute to clinical worsening in the setting of concurrent ACS and anaphylaxis which is called allergic angina or Kounis syndrome. Case summary A 62-year-old woman with food-dependent exercise-induced anaphylaxis developed ACS after intramuscular injection of adrenaline for the treatment of anaphylaxis, whereas administered aspirin for the treatment of ACS exacerbated anaphylaxis. Discussion Our case underlines the importance of tailored treatment based on the underlying pathophysiology of individual patients. Clopidogrel and glucagon might be a better alternative for the treatment of Kounis syndrome.

Kounis syndrome (KS) is an acute coronary syndrome secondary to allergic reactions and can be triggered by many factors. It is a rare condition that is difficult to diagnose, which delays the prognosis of the disease. KS can be classified into three subtypes. In this study, we report a 57-year-old patient with a history of anaphylaxis three times, one after using Moxifloxacin and the other two following a physical activity and an application of hair dye, which were released by an intramuscular adrenalin injection. The two different types of KS occurred at different times due to different causes in the same patient. Our patient was consistent with type 2 KS at the first attack and type 1 KS at the second attack. Therefore, clinicians should not misdiagnose myocardial ischaemia in patients who present with an allergy complaint.