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Nicholas G Kounis - One of the best experts on this subject based on the ideXlab platform.
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covid 19 disease women s predominant non heparin vaccine induced thrombotic thrombocytopenia and Kounis Syndrome a passepartout cytokine storm interplay
Biomedicines, 2021Co-Authors: Nicholas G Kounis, Ioanna Koniari, Stelios F Assimakopoulos, Cesare De Gregorio, Dimitrios Velissaris, Mingyow Hung, Virginia Mplani, Luca Saba, Aikaterini Brinia, Sophia N KouniAbstract:Coronavirus disease 2019 (COVID-19) and severe acute respiratory Syndrome coronavirus 2 (SARS-CoV-2) constitute one of the deadliest pandemics in modern history demonstrating cardiovascular, gastrointestinal, hematologic, mucocutaneous, respiratory, neurological, renal and testicular manifestations and further complications. COVID-19-induced excessive immune response accompanied with uncontrolled release of cytokines culminating in cytokine storm seem to be the common pathogenetic mechanism of these complications. The aim of this narrative review is to elucidate the relation between anaphylaxis associated with profound hypotension or hypoxemia with pro-inflammatory cytokine release. COVID-19 relation with Kounis Syndrome and post-COVID-19 vaccination correlation with heparin-induced thrombocytopenia with thrombosis (HITT), especially serious cerebral venous sinus thrombosis, were also reviewed. Methods: A current literature search in PubMed, Embase and Google databases was performed to reveal the pathophysiology, prevalence, clinical manifestation, correlation and treatment of COVID-19, anaphylaxis with profuse hypotension, Kounis acute coronary Syndrome and thrombotic events post vaccination. Results: The same key immunological pathophysiology mechanisms and cells seem to underlie COVID-19 cardiovascular complications and the anaphylaxis-associated Kounis Syndrome. The myocardial injury in patients with COVID-19 has been attributed to coronary spasm, plaque rupture and microthrombi formation, hypoxic injury or cytokine storm disposing the same pathophysiology with the three clinical variants of Kounis Syndrome. COVID-19-interrelated vaccine excipients as polysorbate, polyethelene glycol (PEG) and trometamol constitute potential allergenic substances. Conclusion: Better acknowledgement of the pathophysiological mechanisms, clinical similarities, multiorgan complications of COVID-19 or other viral infections as dengue and human immunodeficiency viruses along with the action of inflammatory cells inducing the Kounis Syndrome could identify better immunological approaches for prevention, treatment of the COVID-19 pandemic as well as post-COVID-19 vaccine adverse reactions.
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Anaphylactic shock with methylprednisolone, Kounis Syndrome and hypersensitivity to corticosteroids: a clinical paradox
Italian Journal of Pediatrics, 2018Co-Authors: Nicholas G Kounis, Ioanna Koniari, George D Soufras, Emmanouil ChourdakisAbstract:Corticosteroids are widely used for the treatment of allergic reactions but paradoxically themselves may induce acute, delayed, local or systemic allergic reactions and even anaphylaxis with Kounis Syndrome. They can suppress the release of arachidonic acid from mast cell membranes, via phospholipase A2 and eicosanoid biosynthesis inhibition. Corticosteroids can promote cell apoptosis and mediate in annexin or lipocortin synthesis, substances that modulate inflammatory cell activation, adhesion molecule expression, transmigratory and phagocytic functions. Antigen-antibody reaction, hapten formation, and medication contaminants are some of the incriminated causes. Patients with atopic diathesis are particularly vulnerable. Complete and thorough previous history of drug reactions or allergies is necessary before administration of any particular medication including corticosteroids.
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anaphylactic cardiovascular collapse and Kounis Syndrome systemic vasodilation or coronary vasoconstriction
Annals of Translational Medicine, 2018Co-Authors: Nicholas G Kounis, Ioanna Koniari, Gianfranco Cervellin, Laura Bonfanti, Periklis Dousdampanis, Nikolaos Charokopos, Stelios F Assimakopoulos, Stavros K Kakkos, Ioannis Ntouvas, George D SoufrasAbstract:The first reported human anaphylactic death is considered to be the Pharaoh Menes death, caused by a wasp sting. Currently, anaphylactic cardiovascular events represent one of most frequent medical emergencies. Rapid diagnosis, prompt and appropriate treatment can be life saving. The main concept beyond anaphylaxis lies to myocardial damage and ventricular dysfunction, thus resulting in cardiovascular collapse. Cardiac output depression due to coronary hypoperfusion from systemic vasodilation, leakage of plasma and volume loss due to increased vascular permeability, as well as reduced venous return, are regarded as the main causes of cardiovascular collapse. Clinical reports and experiments indicate that the human heart, in general, and the coronary arteries, in particular, could be the primary target of the released anaphylactic mediators. Coronary vasoconstriction and thrombosis induced by the released mediators namely histamine, chymase, tryptase, cathepsin D, leukotrienes, thromboxane and platelet activating factor (PAF) can result to further myocardial damage and anaphylaxis associated acute coronary Syndrome, the so-called Kounis Syndrome. Kounis Syndrome with increase of cardiac troponin and other cardiac biomarkers, can progress to heart failure and cardiovascular collapse. In experimental anaphylaxis, cardiac reactions caused by the intracardiac histamine and release of other anaphylactic mediators are followed by secondary cardiovascular reactions, such as cardiac arrhythmias, atrioventricular block, acute myocardial ischemia, decrease in coronary blood flow and cardiac output, cerebral blood flow, left ventricular developed pressure (LVdp/dtmax) as well as increase in portal venous and coronary vascular resistance denoting vascular spasm. Clinically, some patients with anaphylactic myocardial infarction respond satisfactorily to appropriate interventional and medical therapy, while anti-allergic treatment with antihistamines, corticosteroids and fluid replacement might be ineffective. Therefore, differentiating the decrease of cardiac output due to myocardial tissue hypoperfusion from systemic vasodilation and leakage of plasma, from myocardial tissue due to coronary vasoconstriction and thrombosis might be challenging during anaphylactic cardiac collapse. Combined antiallergic, anti-ischemic and antithrombotic treatment seems currently beneficial. Simultaneous measurements of peripheral arterial resistance and coronary blood flow with newer diagnostic techniques including cardiac magnetic resonance imaging (MRI) and myocardial scintigraphy may help elucidating the pathophysiology of anaphylactic cardiovascular collapse, thus rendering treatment more rapid and effective.
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Kounis Syndrome an update on epidemiology pathogenesis diagnosis and therapeutic management
Clinical Chemistry and Laboratory Medicine, 2016Co-Authors: Nicholas G KounisAbstract:Kounis Syndrome has been established as a hypersensitivity coronary disorder induced by various conditions, drugs, environmental exposures, foods and coronary stents. Allergic, hypersensitivity, anaphylactic and anaphylactoid reactions are associated with this Syndrome. Vasospastic allergic angina, allergic myocardial infarction and stent thrombosis with occluding thrombus infiltrated by eosinophils and/or mast cells constitute are the three reported, so far, variants of this Syndrome. Apart from coronary arteries, it affects the cerebral and mesenteric arteries. Its manifestations are broadening and its etiology is continuously increasing. Kounis Syndrome is a ubiquitous disease which represents a magnificent natural paradigm and nature's own experiment in a final trigger pathway implicated in cases of coronary artery spasm and plaque rupture. Kounis Syndrome seems to be not a rare disease but an infrequently diagnosed clinical entity which has revealed that the same mediators released from the same inflammatory cells are also present and in acute coronary events of non allergic 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, awareness of etiology, epidemiology, pathogenesis and clinical manifestations seems to be important for its prognosis, diagnosis, treatment, prevention.
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after administration of intravenous epinephrine for bee sting induced anaphylaxis Kounis Syndrome or epinephrine effect
Chinese Medical Journal, 2016Co-Authors: Nicholas G Kounis, George D Soufras, Dimitrios Lianas, Nicholas PatsourasAbstract:To the Editor: In the very important report published in Chinese Medical Journal,[1] a 50-year-old male patient, stented with a bare metal stent followed by 3 overlapping drug-eluting stents, developed anaphylactic reaction following a bee sting that was treated with intravenous 0.1 mg epinephrine at a 1:100,000 together with intravenous methylprednisolone, chlorpheniramine maleate, and ranitidine. He developed, immediately after, an anterior wall myocardial infarction, and subsequent coronary arteriography revealed total occlusion in the proximal left anterior descending stent and 90% stenosis with tissue growth in the mid-stent. The authors concluded that the acute myocardial infarction occurred due to acute stent thrombosis caused by exogenous epinephrine administration. This report, however, raises important questions related to the cause and pathophysiology of these events. First, could bee sting anaphylaxis be aggravated by concurrent anti-allergic therapy in atopic diathesis individuals? The described patient was given intravenously, apart from epinephrine, methylprednisolone, chlorpheniramine maleate, and ranitidine. These 4 drugs that are given to treat anaphylaxis have been incriminated, paradoxically, as inducing mild or severe allergic reactions! Indeed, most epinephrine preparations contain sulfite as a preservative and antioxidant, which itself may trigger anaphylaxis in atopic individuals.[2,3] We must always bring in mind that allergens have additive effects and the more allergens an atopic patient is exposed to, the easier and quicker anaphylactic shock and Kounis Syndrome appear.[3] Second, the administration of epinephrine was the cause of stent thrombosis or the anaphylactic reaction? The described patient was stented with a bare metal stent followed by 3 overlapping drug-eluting stents. Bare metal and drug-eluting stents have components namely stainless steel that is a combination of nickel, chromium, titanium, manganese, molybdenum, polymer coating, and eluted antiproliferative drugs such as paclitaxel, zotarolimus, and accompanying antiplatelet therapy that constitute an allergenic complex. This allergenic complex embedded in the coronary intima is applying continuous, persistent, and chronic hypersensitivity inflammation able to induce stent thrombosis manifesting as the Kounis hypersensitivity coronary Syndrome.[4] Several reports have shown that stents attract, such as magnet eosinophils and mast cells that release inflammatory mediators locally and in the systemic circulation able to induce coronary spasm and stent thrombosis. For example, acute myocardial infarction, in the stented area, manifesting as Kounis Syndrome has coincided with allergic reactions from contrast material, insect and larvae stings, nonsteroidal anti-inflammatory agents, and even with allergy to clopidogrel the drug that is given to prevent stent thrombosis![5,6] Third, can we always give epinephrine intravenously? Epinephrine is the cornerstone of treatment for anaphylaxis but it can aggravate the ischemia, prolong QTc interval, promote platelet aggregation, and induce coronary vasospasm and arrhythmias. According to the current guidelines, there is no absolute contraindication to epinephrine use in anaphylaxis. However, the use of intravenous epinephrine is still controversial in severe allergic reactions. It should be considered in patients with severe hypotension or cardiac arrest who do not respond to aggressive fluid resuscitation. Intramuscular use of epinephrine is the safer and preferred route of administration unless the patient has severe anaphylaxis.[7] All above support the view that the described patient's acute myocardial infarction due to stent thrombosis following the intravenous epinephrine for bee sting-induced anaphylaxis was due to Kounis Syndrome rather than to intravenous epinephrine administration. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
Teri Millane - One of the best experts on this subject based on the ideXlab platform.
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Kounis Syndrome presenting as st segment elevation myocardial infarction following a hymenoptera bee sting
International Journal of Cardiology, 2009Co-Authors: Jaspal Taggar, Timothy Watson, Kashif Musarrat, Teri MillaneAbstract:We described a patient presenting with acute myocardial infarction after sustaining a hymenoptera (bee) sting. Cardiac catheterisation confirmed significant intra-coronary thrombosis in the left anterior descending artery with minimal underlying plaque disease. A unifying diagnosis of Kounis Syndrome secondary to hymenoptera envenomation was made. This is followed by a brief review of the pathophysiology of acute myocardial infarction in the context of Kounis Syndrome.
Adnan Abaci - One of the best experts on this subject based on the ideXlab platform.
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Kounis Syndrome secondary to amoxicillin clavulanic acid use
International Journal of Cardiology, 2008Co-Authors: Yusuf Tavil, Murat Turfan, Sedat Turkoglu, Adnan AbaciAbstract:Myocardial injury and acute coronary Syndrome have been rarely associated with amoxicillin/clavulanic acid intake. The responsible pathogenetic mechanism is described by an amplified mast cell degranulation inducing coronary artery spasm and/or acute myocardial infarction in susceptible individuals which is called Kounis Syndrome. We report here a case of Kounis Syndrome presented with acute coronary Syndrome due to amoxicillin/clavulanic acid use. All other etiologies, including ischemic reinfarction were appropriately ruled out.
Asuman Kaftan - One of the best experts on this subject based on the ideXlab platform.
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acute st segment elevation myocardial infarction after sulbactam ampicilllin induced anaphylactic shock in an adult with significant coronary artery disease a case report
International Journal of Cardiology, 2009Co-Authors: Dogu Ismail Kilic, Harun Evrengul, Ali Vefa Ozcan, Halil Tanriverdi, Omer Cagliyan, Asuman KaftanAbstract:Abstract Myocardial injury may complicate allergic reactions caused by several medications. We evaluated a case of a myocardial injury with transient ST segment elevation in a 72 year-old man presenting with collapse caused by sulbactam–ampicilllin assumption. The purpose of this report is to present this interesting case and revise the classification of Kounis Syndrome.
Sophia N Kouni - One of the best experts on this subject based on the ideXlab platform.
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covid 19 disease women s predominant non heparin vaccine induced thrombotic thrombocytopenia and Kounis Syndrome a passepartout cytokine storm interplay
Biomedicines, 2021Co-Authors: Nicholas G Kounis, Ioanna Koniari, Stelios F Assimakopoulos, Cesare De Gregorio, Dimitrios Velissaris, Mingyow Hung, Virginia Mplani, Luca Saba, Aikaterini Brinia, Sophia N KouniAbstract:Coronavirus disease 2019 (COVID-19) and severe acute respiratory Syndrome coronavirus 2 (SARS-CoV-2) constitute one of the deadliest pandemics in modern history demonstrating cardiovascular, gastrointestinal, hematologic, mucocutaneous, respiratory, neurological, renal and testicular manifestations and further complications. COVID-19-induced excessive immune response accompanied with uncontrolled release of cytokines culminating in cytokine storm seem to be the common pathogenetic mechanism of these complications. The aim of this narrative review is to elucidate the relation between anaphylaxis associated with profound hypotension or hypoxemia with pro-inflammatory cytokine release. COVID-19 relation with Kounis Syndrome and post-COVID-19 vaccination correlation with heparin-induced thrombocytopenia with thrombosis (HITT), especially serious cerebral venous sinus thrombosis, were also reviewed. Methods: A current literature search in PubMed, Embase and Google databases was performed to reveal the pathophysiology, prevalence, clinical manifestation, correlation and treatment of COVID-19, anaphylaxis with profuse hypotension, Kounis acute coronary Syndrome and thrombotic events post vaccination. Results: The same key immunological pathophysiology mechanisms and cells seem to underlie COVID-19 cardiovascular complications and the anaphylaxis-associated Kounis Syndrome. The myocardial injury in patients with COVID-19 has been attributed to coronary spasm, plaque rupture and microthrombi formation, hypoxic injury or cytokine storm disposing the same pathophysiology with the three clinical variants of Kounis Syndrome. COVID-19-interrelated vaccine excipients as polysorbate, polyethelene glycol (PEG) and trometamol constitute potential allergenic substances. Conclusion: Better acknowledgement of the pathophysiological mechanisms, clinical similarities, multiorgan complications of COVID-19 or other viral infections as dengue and human immunodeficiency viruses along with the action of inflammatory cells inducing the Kounis Syndrome could identify better immunological approaches for prevention, treatment of the COVID-19 pandemic as well as post-COVID-19 vaccine adverse reactions.
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penicillin allergy in cancer patients manifesting as Kounis Syndrome
Heart and Vessels, 2005Co-Authors: George D Soufras, G M Zavras, P J Papadaki, Sophia N Kouni, Maria Batsolaki, Georgia V Gouveloudeligianni, Nicholas G Kounis, Panagiotis V Ginopoulos, Constantinos KoutsojannisAbstract: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.
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Kounis Syndrome secondary to allergic reaction following shellfish ingestion
International Journal of Clinical Practice, 2003Co-Authors: G M Zavras, P J Papadaki, Constantinos Kokkinis, K Kalokairinov, Sophia N Kouni, Maria Batsolaki, Georgia V Gouveloudeligianni, Constantinos KoutsojannisAbstract:: Two cases of allergic angina and allergic myocardial infarction (Kounis Syndrome) secondary to shellfish ingestion are described. The patients had pre-existing quiescent coronary artery disease (type II variant of the Syndrome) and the allergic reaction following eating shellfish seemed to have triggered the development of an acute myocardial infarction. The clinical implications are also discussed.
