Kounis syndrome (allergic angina and allergic myocardial infarction): A natural paradigm? (original) (raw)

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...

Allergic myocardial infarction

Cardiology journal, 2008

In the literature there are very few well-documented cases of myocardial ischemia with pathomechanism accompanying allergic reaction. It is defined as Kounis syndrome, i.e. angina pectoris or infarction with allergic etiology. It is suggested, that few few cases of myocardial ischemia after a Hymenoptera sting reported thus far represent only a minute percentage of the total number of allergic reactions which occur in the circulatory system. It is difficult to make a credible decision whether allergic mechanisms are responsible for a greater number of deaths than we suspect. In the light of the literature, this review deals with current views regarding pathomechanisms of myocardial ischemia in the course of anaphylactic reaction and presents the clinical manifestation of myocardial ischemia with an allergic background, pointing out that allergic reactions involving cardiac muscle are not limited to the development of ischemia. The term organ anaphylaxis, in relation to the heart, al...

Kounis syndrome: a narrative review

Southern African Journal of Anaesthesia and Analgesia, 2016

Inflammatory mediators released from activated mast cells and basophils during hypersensitivity reactions have direct pathological effects on the myocardium and coronary vasculature. It was traditionally thought that cardiovascular signs and symptoms in anaphylaxis are largely due to peripheral vasodilation and increased vascular permeability. However, there is extensive evidence of primary cardiac involvement during hypersensitivity reactions, most notably coronary vasoconstriction as well as atherosclerotic plaque erosion and rupture, leading to angina pectoris and acute coronary syndromes. Furthermore, mast cells are well established as effector cells in atherosclerosis, through their effects on atherosclerotic plaque progression and destabilisation. It was noted over 30 years ago that cardiac patients have a markedly higher concentration of biologic amines (especially histamine) in their coronary vasculature, and, additionally, are hyper-reactive to the effects thereof. This is borne out by the disproportionate mortality rate of those with cardiac disease that suffer a hypersensitivity reaction. Kounis syndrome refers to angina pectoris or an acute coronary syndrome secondary to a hypersensitivity reaction, with the subtypes dependent on the underlying state of the coronaries and presence of a drug-eluting stent or not. This review will focus mainly on the aetiology, pathophysiology, diagnoses and treatment of this important syndrome.

Coronary Stents, Hypersensitivity Reactions, and the Kounis Syndrome

Journal of Interventional Cardiology, 2007

The use of drug-eluting stents (DES) for the treatment of coronary stenosis has increased sharply and now accounts for more than 75% of all coronary stents utilized. However, concern has been increasing that DES could be associated with stent thrombosis, paradoxical coronary vasoconstriction, and hypersensitivity reactions. Components of currently used DES have been reported to induce, either separately or synergistically, hypersensitivity reactions and possibly lead to cardiac events. DES-activated intracoronary mast cells could release histamine, arachidonic acid metabolites, proteolytic enzymes, as well as a variety of cytokines, chemokines, and platelet-activating factor (PAF) leading to local inflammation and thrombosis. These events may be more common than suspected because it is hard to document them, unless they become systemic, in which case they manifest themselves as the "Kounis syndrome," characterized by the concurrence of acute coronary events with hypersensitivity reactions. Recognition of this problem may lead to better vigilance, as well as new DES with mast cell blocking molecules that may also be disease modifying.