Kounis syndrome: A primary cause for the anaphylactic shock

Kounis, Nicholas G.; Soufras, George D.

doi:10.5603/cj.2014.0012

Cited by 3 publications

(2 citation statements)

References 7 publications

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“…Indeed, mediators released by activated mast cells can induce coronary artery spasm, plaque rupture, and thrombosis, leading to a clinical picture of Kounis syndrome. On the other hand, all the cells involved in the process activate and co-activate each other, creating a sort of "vicious circle of inflammation" [12,[33][34][35][36][37][38][39][40][41][42]. Three variants of Kounis syndrome have been described thus far: in the type I variant, coronary spasm in normal or nearly normal coronary arteries associated with hypersensitivity reaction can progress to myocardial infarction.…”

Section: Discussionmentioning

confidence: 99%

Postmortem IgE determination in coronary artery disease

Lambert

Tse

Tettamanti

et al. 2019

Journal of Forensic and Legal Medicine

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Allergic inflammation is thought to play a role in atherogenesis and atherosclerotic disease progression. IgE may activate mast cells and macrophages located within atheromatous lesions, which may contribute to local inflammation and disease progression. On the other hand, increased IgE levels in individuals with acute myocardial infarction might also be the consequence of immunological reactions to damaged coronary arteries or myocardium. In this study, total IgE and mast cell tryptase were measured in a series of forensic autopsy cases showing various degrees of coronary artery disease, in order to correlate laboratory results with morphological findings and compare them to conclusions reported in the clinical setting. A total of 84 subjects were selected and two study groups were retrospectively formed, a non-allergic, cardiac death group (42 cases) and a non-allergic, non-cardiac control group (42 cases). Our findings indicated that a portion of acute coronary syndromes and coronary deaths characterized by coronary atherosclerotic lesions of various severities are also characterized by increased total IgE and mast cell tryptase levels, thus corroborating the data previously reported in both clinical and forensic literature on this topic as well as the necessity of combining morphological investigations focusing on the heart and coronary arteries with biochemical analyses.

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Section: Discussionmentioning

confidence: 99%

Postmortem IgE determination in coronary artery disease

Lambert

Tse

Tettamanti

et al. 2019

Journal of Forensic and Legal Medicine

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“…In response to ovalbumin administration, the sensitized rat hearts of anaphylaxis group demonstrated a decrease in coronary blood flow, and in the maximum rate of systolic left ventricular pressure (dP/dtmax) and an increment in coronary vascular resistance, as evidence of coronary spasm. The authors concluded that these results may suggest that left ventricular dysfunction during anaphylaxis can be attributed mainly to coronary vasoconstriction and the inducible myocardial ischemia (57,58). (VIII) In other experimental models, anaphylaxis was induced by ovalbumin antigen injection into open-chest of artificially ventilated sensitized mice.…”

Section: Experimental Evidencementioning

confidence: 99%

Anaphylactic cardiovascular collapse and Kounis syndrome: systemic vasodilation or coronary vasoconstriction?

et al. 2018

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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 socalled 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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Vaccination and anaphylaxis: a forensic perspective

2017

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AimTo review the available literature pertaining to fatalities following vaccine administration and, in particular, cases of vaccine-related fatal anaphylaxis.MethodThe MEDLINE database was systematically searched up to March 2016 to identify all relevant articles pertaining to fatal cases of anaphylaxis following vaccine administration.ResultsSix papers pertaining to fatal anaphylaxis following vaccination were found relevant. Mast cell tryptase and total IgE concentration was assessed exclusively in one case. Laryngeal edema was not detected in any of these cases, whereas eosinophil or mast cell infiltration was observed in lymphoid organs. In one case, immunohistochemical investigations using anti-tryptase antibodies allowed pulmonary mast cells and degranulating mast cells with tryptase-positive material outside to be identified.ConclusionIn any suspected IgE-mediated fatal anaphylactic cases, biochemical investigations should be systematically performed for forensic purposes. Splenic tissue should be routinely sampled for immunohistochemical investigations in all suspected anaphylaxis-related deaths and mast cell/eosinophil infiltrations should be systematically sought out in the spleen, myocardium, and coronary artery wall. The hypothesis of fatal anaphylaxis following vaccination should be formulated exclusively when circumstantial data, available medical records, laboratory investigations, and autopsy or histology findings converge in a consistent pattern. The reasonable exclusion of alternative causes of death after all postmortem investigations is also imperative in order to establish or rule out a cause-and-effect relationship between vaccine administration and any presumptive temporarily-related death.

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Kounis syndrome: A primary cause for the anaphylactic shock

Cited by 3 publications

References 7 publications

Postmortem IgE determination in coronary artery disease

Postmortem IgE determination in coronary artery disease

Anaphylactic cardiovascular collapse and Kounis syndrome: systemic vasodilation or coronary vasoconstriction?

Vaccination and anaphylaxis: a forensic perspective

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