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ABSTRACT An acute coronary syndrome due to mast-cell activation in the presence of an allergen is known as Kounis Syndrome (KS). This relatively new entity of KS is being increasingly recognized among allergists, cardiologists, and emergency physicians; however, it is not well-known among anesthesiologists. We report here, a case of type 2 KS due to antibiotic administration causing sudden perioperative cardiac arrest.

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.

Background: Kounis syndrome (KS), also known as allergic myocardial infarction, presents in three variants. This condition is often underrecognized due to limited knowledge and its variable presentation. To address these limitations, the present review aims to describe the triggers, types, management, and patient outcomes of KS. Methods: In this systematic review, PubMed and Scopus were used to identify publications of clinical case reports; variables included sociodemographic characteristics, clinical manifestations, triggers, treatments, and outcomes. Data from the articles´ abstracts were assessed by two corresponding authors, and subsequently, each case was analyzed by two coauthors, validated and analyzed with Stata 12. To categorize each Kounis type, mean and proportion comparison tests were performed, and measures of association were obtained using logistic regression and expressed as odds ratios. Results: A global distribution was identified, with predominance in the Northern Hemisphere. Type I KS was the most reported variant, and most of the patients were adult men. Most of the patients presented variability in the treatment and outcomes. Conclusions: KS may represent a diagnostic challenge, and underdiagnosis could explain the lack of uniformity in the diagnostic and assessment process. Our results highlight a need for improved approaches based on patient history for correct diagnosis and preventing recurring events.

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.

Kounis syndrome is defined by the occurrence of an acute coronary syndrome (ACS) in the setting of an allergic, hypersensitivity or anaphylactic condition. Degranulation of mast cells and platelet activation leading to the release of multiple inflammatory mediators are thought to make the arterial circulation susceptible to acute cardiac events. It is an often underdiagnosed entity in the emergency setting, due to lack of awareness among emergency providers. Identifying Kounis syndrome is critical, since managing ACS differs from that of a classical acute myocardial infarction. We present the case of a 72-year old male patient with a history of stable coronary disease who presented to the emergency department with a diffuse pruritic rash and chest pain. Electrocardiogram showed ST elevation myocardial infarction. Urgent coronary angiography revealed total occlusion of the mid left anterior descending coronary artery which was treated with a drug eluting stent with an excellent outcome. The pruritic rash responded to treatment with intravenous corticosteroids and antihistamines; No allergens were identified. The patient’s symptoms resolved and he had an uneventful hospitalization. The diagnosis of Kounis syndrome can complicate the management of acute allergic reactions. Special precautions should be taken by emergency physicians with regards to the administration of beta blockers, morphine and vasodilators, which may be detrimental in this setting.

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.

Two cases of allergic angina and allergic myocardial infarction (Kounis syndrome) following penicillin administration are described. The patients suffered from lung and mandible neoplasms and had previously received several courses of antineoplastic therapy without any sequelae. One patient had normal coronary arteries (type I variant of the syndrome) and the other had coronary artery disease with previous myocardial infarction (type II variant of the syndrome). The allergic reaction following penicillin administration seemed to have triggered the development of an acute coronary artery spasm in the first patient and an acute myocardial infarction in the second. This report shows that susceptible individuals expressing a magnified mast cell degranulation effect may be more vulnerable to coronary artery spasm and plaque erosion or rupture.

This case report discusses a rare occurrence of type II Kounis syndrome, characterised by an acute myocardial infarction triggered by an allergic reaction. The patient, a young adult male, experienced urticaria soon after eating oysters, which quickly escalated to severe chest discomfort. Despite lacking typical cardiac risk factors, the electrocardiogram showed indications of ST-elevation myocardial infarction. This condition was further complicated by ventricular fibrillation, necessitating urgent life-saving measures. This case demonstrates the intricate and often overlooked relationship between hypersensitivity reactions and cardiovascular events. It highlights the necessity for increased vigilance and rapid diagnostic and treatment approaches in handling Kounis Syndrome, especially in emergency situations. The case underscores the importance of considering allergic causes in acute cardiac scenarios, particularly in patients who do not have standard risk factors for coronary artery disease.

Asthma, a chronic inflammatory airway disease, is characterized by airway hyperresponsiveness and structural changes. Accurate postmortem diagnosis is crucial because of legal and insurance implications, necessitating differentiation from other causes of sudden death. Thymus and activation-regulated chemokine (TARC) is a chemokine that potentially acts as a biomarker of asthma. This study evaluated the diagnostic value of serum TARC combined with immunoglobulin E (IgE) levels as biomarkers in forensic settings. The subjects were 100 autopsy cases, categorized into fatal asthma (n = 25), acute myocardial infarction (AMI) (n = 37), and traumatic deaths (n = 38). TARC levels were significantly elevated in asthma (525.68 ± 801.87 pg/mL) compared with AMI (180.35 ± 109.37 pg/mL) and trauma (173.26 ± 105.01 pg/mL) cases. Similarly, serum IgE levels were higher in asthma (3363.72 ± 7023.46 KU/L) than in AMI (130.92 ± 260.79 KU/L) and trauma (134.53 ± 195.41 KU/L) cases. ROC curve analysis showed that serum TARC had a sensitivity of 68.0 % and specificity of 73.6 % (AUC 0.763, cut-off value of 225 pg/mL). In comparison, serum IgE had a sensitivity of 80 % and specificity of 86.1 % (AUC 0.881, cut-off value of 307 KU/L). The combined use of TARC and IgE increased the diagnostic specificity to 95.8 %. Serum TARC and IgE are valuable biomarkers for diagnosing fatal asthma in forensic settings. While serum TARC levels correlate with Th2-mediated inflammation, the combined measurement of TARC and IgE enhances the diagnostic accuracy, providing significant specificity for confirming asthma diagnosis. •Serum TARC is a potential biomarker of diagnosis in fatal asthma.•TARC levels are reliable if the postmortem interval is within 72 hours.•TARC cut-off for asthma diagnosis is 225 pg/mL, and IgE cut-off is 307 KU/L.•Serum TARC, in combination with IgE, reaches diagnostic specificity to 95.8 %.