Kounis syndrome induced by oral intake of aspirin: case report and literature review

Hangouche, Abdelkader Jalil El; Lamliki, Ouiame; Oukerraj, Latifa; Dakka, Taoufiq; Doghmi, Nawal; Zarzur, Jamila; Cherti, Mohammed

doi:10.11604/pamj.2018.30.301.14948

Cited by 16 publications

(10 citation statements)

References 17 publications

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“… 23–25 (ii) The adverse effects of asthma and dyspnoea may lead to CAS and increase the occurrence of MACE or cardiogenic death with aspirin use. 26 27 (iii) The synthesis of prostacyclin, a well-known vasodilator released by endothelial cells, is inhibited by aspirin 28 and CAS is induced by aspirin. This could, in turn, cause recurrent angina leading to rehospitalisation, MI, and cardiac death.…”

Section: Discussionmentioning

confidence: 99%

Impact of aspirin use on clinical outcomes in patients with vasospastic angina: a systematic review and meta-analysis

et al. 2021

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ObjectivesThe use of aspirin to prevent cardiovascular disease in vasospastic angina (VSA) patients without significant stenosis has yet to be investigated. This study aimed to investigate the efficacy of aspirin use among VSA patients.DesignSystematic review and meta-analysis.Data sourcesPubMed, Web of Science and Cochrane Central Register of Controlled Trials were searched for relevant information prior to October 2020.Eligibility criteria for selecting studiesAspirin use versus no aspirin use (placebo or no treatment) among VSA patients without significant stenosis.Data extraction and synthesisTwo investigators extracted the study data. ORs and 95% CIs were calculated and graphed as forest plots. The Newcastle-Ottawa Quality Assessment Scale tool and Begg’s funnel plot were used to assess risk of bias.ResultsFour propensity-matched cohorts, one retrospective analysis and one prospective multicentre cohort, in total comprising 3661 patients (aspirin use group, n=1695; no aspirin use group, n=1966) were included in this meta-analysis. Aspirin use and the incidence of major cardiovascular adverse events with follow-up of 1–5 years were not significantly correlated (combined OR=0.90, 95% CI: 0.55 to 1.68, p=0.829, I2=82.2%; subgroup analysis: OR=1.09, 95% CI: 0.81 to 1.47, I2=0%). No significant difference was found between aspirin use and the incidence of myocardial infarction (OR=0.62, 95% CI: 0.09 to 4.36, p=0.615, I2=73.8%) or cardiac death (OR=1.73, 95% CI: 0.61 to 4.94, p=0.444, I2=0%) during follow-up.ConclusionAspirin use may not reduce the risk of future cardiovascular events in VSA patients without significant stenosis.PROSPERO registration numberCRD42020214891.

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Section: Discussionmentioning

confidence: 99%

Impact of aspirin use on clinical outcomes in patients with vasospastic angina: a systematic review and meta-analysis

et al. 2021

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“…Commonly used drugs, such as aspirin, antihypertensives, and corticosteroids as well as antibiotics and nonsteroidal anti-inflammatory drugs, constitute some of the main offenders. Aspirin alone (32) or in combination with underlying nasal polyps and asthma, known as the Samter–Beer triad (33), has been incriminated as a potential trigger for Kounis syndrome (34).…”

Section: Causalitymentioning

confidence: 99%

Kounis Syndrome—not a Single-organ Arterial Disorder but a Multisystem and Multidisciplinary Disease

Kounis¹,

Koniari²,

Velissaris³

et al. 2019

Balkan Med J

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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.

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“…18 In this case, the patient was exposed to aspirin and clopidogrel, while he had previously undergone deployment of a cobalt-chromium polymer-free metallic scaffold that also contains nickel and releases sirolimus. Aspirin 19,20 and clopidogrel 21 can induce Kounis syndrome, whereas metal anions and sirolimus can also act as antigens. 22,23 Surprisingly, omalizumab may be helpful to treat clopidogrel hypersensitivity without discontinuation of thienopyridine administration in patients requiring double-antiplatelet therapy after coronary stent implantation.…”

Section: Too Many Cooks Spoil the Brothmentioning

confidence: 99%

Humanized Monoclonal Antibodies Against IgE Antibodies as Therapy for IgE-Mediated Coronary Syndromes: Are We There Yet?

Kounis

Koniari²,

Tsigkas

et al. 2020

Canadian Journal of Cardiology

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See article by Liu et al., pages 966.e5-966.e6 of this issue. Immunoglobulin E (IgE) antibodies are synthesized and released by B lymphocytes as a result of a complex interplay between genes, cytokines, and environmental antigen exposure. IgE antibodies participate in atopic diseases and systemic anaphylaxis, constituting components of a protein network implicated in signalling response to antigens and allergens. 1 IgEs are very short lived in plasma (w 1 day), but receptorbound IgE can remain fixed to cells in tissues for weeks or months. Their biologic activity is mainly dependent on binding to specific fragment crystallisable region (FcR) receptors high-affinity FCεRI and FCgRI and low-affinity FCεRII and FCgRII situated on the surface, mainly of mast cells, but also of basophils, eosinophils, monocytes, and epithelial and dendritic cells. 2 The IgE binding to FcR increases cell survival and causes up-regulation of the above receptors. Interactions mediated by IgEs bound on mast cells with corresponding antigens/allergens on the surface of mast cells leads to mast cell degranulation and release of a variety of preformed and newly formed substances acting as mediators. Degranulation and mediator release occur when IgE antibodies bridged with antigens/allergens reach the critical number of 2000, forming 1000 bridges for a maximum of w 500,000-1,000,000 IgE antibodies on the cell surface! 3 Mediator release can induce coronary artery spasm, independently from the existence of underlying atherosclerotic disease, manifesting as Kounis type I syndrome (Table 1) and myocardial infarction with nonobstructive coronary arteries (MINOCA). 4 The mediators might contribute to the critical progression, erosion, and rupture of atherosclerotic plaque, inducing thrombotic complications resulting from platelet activation and fibrinolytic system impairment, and further

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Kounis syndrome induced by oral intake of aspirin: case report and literature review

Cited by 16 publications

References 17 publications

Impact of aspirin use on clinical outcomes in patients with vasospastic angina: a systematic review and meta-analysis

Impact of aspirin use on clinical outcomes in patients with vasospastic angina: a systematic review and meta-analysis

Kounis Syndrome—not a Single-organ Arterial Disorder but a Multisystem and Multidisciplinary Disease

Humanized Monoclonal Antibodies Against IgE Antibodies as Therapy for IgE-Mediated Coronary Syndromes: Are We There Yet?

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