Kounis syndrome (allergic angina and allergic myocardial infarction): A natural paradigm? (original) (raw)
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Internal and emergency medicine, 2012
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 mec...
Kounis syndrome: myocardial infarction secondary to an allergic insult--a rare clinical entity
Acta cardiologica, 2011
The association of an acute coronary syndrome with mast cell activation secondary to allergen exposure is known as the Kounis syndrome. We present two cases of the Kounis syndrome: (i) one was misdiagnosed as acute ST elevation myocardial infarction and treated with thrombolytics; (ii) the second diagnosis was made after a recurrence two months after the first incident.
Type 2 Kounis syndrome in an allergic woman: An uncommon presentation of acute coronary syndrome
Journal of Cardiology Cases, 2013
Acute coronary syndromes secondary to allergy-induced coronary vasospasm are known as "Kounis syndrome." The main pathophysiological mechanism of coronary spasm in Kounis syndrome is the release of inflammatory mediators during a hypersensitivity reaction triggered by food, insect bites, or drugs. Here, we report a case of an acute coronary syndrome secondary to allergic reaction following levofloxacin administration in a 68-year-old female without a prior history of coronary artery disease. Our patient's coronary angiography revealed moderate lesions in the coronary vasculature and she was diagnosed as having a type II variant Kounis syndrome. Type II variant includes patients in whom the acute release of inflammatory mediators due to mast cell degranulation such as histamine, serotonin, and leukotrienes can induce either coronary artery spasm with normal cardiac enzymes and troponins or plaque erosion or rupture manifesting as acute myocardial infarction. According to our knowledge, this is the first case report of Kounis syndrome attributed to levofloxacin administration.
Kounis Syndrome - Allergic Myocardial Infarction. A Case Report
Wiadomości Lekarskie, 2019
Kounis syndrome or allergic myocardial infarction is an acute coronary syndrome in the course of an allergic reaction. In allergic patients in response to a specific condition - nourishment, inhalation, environmental substances, drug or insect bite there is an allergic reaction involving many different cells and mediators that can cause coronary artery spasm or initiate the process of rupture and activation of atherosclerotic plaque resulting in acute coronary syndrome. The paper describes a case of a young man with allergy to pollen and confirmed sensitization to nuts, who developed a full-blown anaphylactic shock after eating the nut mix and experienced a rapidly passing acute coronary syndrome with troponin up to 4.7 μg/L. An increased concentration of tryptase (15 μg/L), total IgE (> 3,000 IU/mL) and specific anti-nut IgE (55.1 kUA/L) were found. Based on the course of the disease and the results of allergic and cardiac tests, allergic type 1 myocardial infarction, i.e. cause...
Kounis Syndrome—not a Single-organ Arterial Disorder but a Multisystem and Multidisciplinary Disease
Balkan Medical Journal, 2019
Coronary symptoms associated with conditions related to mast cell activation and inflammatory cell interactions, such as those involving T-lymphocytes and macrophages, further inducing allergic, hypersensitivity, anaphylactic, or anaphylactic insults, are currently referred to as the Kounis syndrome. Kounis syndrome is caused by inflammatory mediators released during allergic insults, postinflammatory cell activation, and interactions via multidirectional stimuli. A platelet subset of 20% with high-and low-affinity IgE surface receptors is also involved in this process. Kounis syndrome is not just a single-organ but also a complex multisystem and multiorgan arterial clinical condition; it affects the coronary, mesenteric, and cerebral arteries and is accompanied by allergy-hypersensitivityanaphylaxis involving the skin, respiratory, and vascular systems in the context of anesthesia, surgery, radiology, oncology, or even dental and psychiatric medicine; further, it has significantly influences both morbidity and mortality. Kounis syndrome might be caused by numerous and continuously increasing causes, with broad clinical symptoms and signs, via multi-organ arterial system involvement, in patients of any age, thereby demonstrating predominant anaphylactic features in terms of a wide spectrum of mast cell-association disorders. Cardiac symptoms, such as chest pain, coronary vasospasm, angina pectoris, myocardial infarction, stent thrombosis, acute cardiac failure, and sudden cardiac death associated with subclinical, clinical, acute, or chronic allergic reactions, constitute the clinical manifestations of this syndrome. Since its first description, a common pathway between allergic and non-allergic coronary events has been demonstrated. The hypothesis is based on the existence of a much higher degree of mast cell degranulation at plaque erosion or rupture sites compared with at the adjacent areas or even more distant segments in post-acute myocardial infarction of non-allergic etiology. Although mast cell activation, differentiation, and mediator release takes days or weeks, the mast cell degranulation may occur just before any acute coronary event, further resulting in coronary artery vasoconstriction and atheromatous plaque rupture. It seems that medications and natural molecules stabilizing the mast cell membrane as well as monoclonal antibodies protecting the mast cell surface can emerge as novel therapeutic modalities for acute coronary and cerebrovascular event prevention.
An Atypical Presentation of Allergic Myocardial İnfarction
Acute coronary syndromes secondary to hypersensitivity reactions related with allergic factors are defined as Kounis syndrome. Doxycycline is an antibiotic commonly used in clinical practice. In this report, we described an atypical presentation of Kounis syndrome in a patient who was admitted to the emergency service complaining of chest pain, generalized rash and fever. She was taking doxycycline for 3 days because of urinary tract infection. Non specific ST-T changes were seen on electrocardiography, positive troponin levels were detected and global left ventricular wall motion abnormalities were defined by echocardiography. The patient had no conventional risk factor for acute coronary syndrome. Normal coronary angiography results, improved left ventricular functions and symptoms by antihistaminic and steroid treatments were consistent with Kounis syndrome. All patients admitted with the concurrence of chest pain and allergic symptoms should be asked about exposure to allergens.
Anaphylaxis and cardiovascular disease: therapeutic dilemmas
Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2015
Cardiovascular disease (CVD) increases the risk of severe or fatal anaphylaxis. Some medications used to treat CVD can exacerbate anaphylaxis. To review anaphylaxis and the heart, the potential impact of medications for CVD on anaphylaxis and anaphylaxis treatment, and the cardiovascular effects of epinephrine; to examine the therapeutic dilemmas arising from these issues and propose a way forward. PubMed searches were performed for the years 1990-2014 inclusive, using terms such as angiotensin-converting enzyme (ACE) inhibitors, adrenaline, allergic myocardial infarction, anaphylaxis, angiotensin-receptor blockers (ARBs), beta-adrenergic blockers, epinephrine, and Kounis syndrome. Cardiac mast cells are key constituents of atherosclerotic plaques. Mast cell mediators play an important role in acute coronary syndrome (ACS). Patients with CVD have an increased risk of developing severe or fatal anaphylaxis. Medications used in CVD treatment, including beta-adrenergic blockers and ACE...