Non ST-segment elevation myocardial infarction in patient with essential thrombocythemia

Alioğlu, Emin; Tüzün, Nurullah; Şahin, Fahri; Kosova, Buket; Saygı, Serkan; Tengiz, İstemihan; Türk, Uğur Önsel; Özsan, Nazan; Ercan, Ertuğrul

doi:10.1186/1477-9560-7-1

Cited by 12 publications

(10 citation statements)

References 25 publications

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“…14 Therefore, it may be thought that, in patients with ET, antithrombotic therapy could prevent acute coronary syndrome (ACS) generated by primary platelet rich thrombus, and blocking the GP IIb/IIIa receptors could break the continuing chain of aggregation and activation. 15 Clinical improvement following tirofiban treatment, noticed without any complication, was observed in this case.…”

Section: Discussionsupporting

confidence: 63%

Non-ST-segment Elevation Myocardial Infarction in a Patient With Essential Thrombocythemia Treated With Glycoprotein IIb/IIIa Inhibitor

Zhang

Wan

Liu

et al. 2010

Clin Appl Thromb Hemost

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Essential thrombocythemia (ET) can cause systemic vascular thrombosis but rarely cause obstruction of coronary arteries or acute myocardial infarction (MI). Treatment of acute MI in patients with ET may be a problem due to the important role of platelets in the pathogenesis of infarction. In this report, a 63-year-old man presented with acute chest pain and a greatly increased platelet count. The patient was successfully treated with intravenous tirofiban, a glycoprotein IIb/IIIa receptor blocker. Essential thrombocythemia was diagnosed based on bone marrow findings, clinical presentation, and laboratory analysis. Thrombocythemia had been controlled with hydroxyurea.

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Section: Discussionsupporting

confidence: 63%

Non-ST-segment Elevation Myocardial Infarction in a Patient With Essential Thrombocythemia Treated With Glycoprotein IIb/IIIa Inhibitor

Zhang

Wan

Liu

et al. 2010

Clin Appl Thromb Hemost

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“…This, in turn, activates the coagulation system, increases platelet aggregation and constricts vessels. Acute myocardial infarction and pulmonary embolism have been described in young patients with severe hyperhomocysteinemia secondary to PA. 66 , 67 …”

Section: Clinical Manifestationsmentioning

confidence: 99%

Autoimmune atrophic gastritis: current perspectives

Minalyan¹,

Benhammou²,

Artashesyan³

et al. 2017

CEG

108

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At present there is no universally accepted classification for gastritis. The first successful classification (The Sydney System) that is still commonly used by medical professionals was first introduced by Misiewicz et al in Sydney in 1990. In fact, it was the first detailed classification after the discovery of Helicobacter pylori by Warren and Marshall in 1982. In 1994, the Updated Sydney System was proposed during the International Workshop on the Histopathology of Gastritis followed by the publication in The American Journal of Surgical Pathology by Dixon et al. Using the new classification, distinction between atrophic and nonatrophic gastritis was revised, and the visual scale grading was incorporated. According to the Updated Sydney System Classification, atrophic gastritis is categorized into multifocal (H. pylori, environmental factors, specific diet) and corpus-predominant (autoimmune). Since metaplasia is a key histological characteristic in patients with atrophic gastritis, it has been recommended to use the word “metaplastic” in both variants of atrophic gastritis: autoimmune metaplastic atrophic gastritis (AMAG) and environmental metaplastic atrophic gastritis. Although there are many overlaps in the course of the disease and distinction between those two entities may be challenging, the aim of this review article was to describe the etiology, epidemiology, pathogenesis, diagnosis, clinical manifestations and treatment in patients with AMAG. However, it is important to mention that H. pylori is the most common etiologic factor for the development of gastritis in the world.

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“…Current literature dealing with coronary patients and platelet count disorders focuses mainly on the clinical outcome and consists of case reports or a series of case reports [5,[12][13][14][15]. Laboratory measurement of platelet reactivity in such patients is challenging and underresearched [16].…”

Section: Discussionmentioning

confidence: 99%

Platelet Reactivity and Response to Aspirin and Clopidogrel in Patients with Platelet Count Disorders

Kuliczkowski

Żurawska-Płaksej

Podolak-Dawidziak

et al. 2021

Cardiology Research and Practice

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Background. Platelet reactivity and response to antiplatelet drugs, acetylsalicylic acid (ASA) and clopidogrel, in patients with thrombocytopenia and thrombocythemia can have a potentially important effect on the outcome. The effectiveness and safety of antiplatelet drugs in such patients has not been well examined. Measuring the effect of ASA and clopidogrel on platelets could help guide the therapy. Nevertheless, platelet response to antiplatelet drugs is not routinely measured in platelet count disorders and relevant evidence is scarce. Aims. The study aimed to measure platelet reactivity and response to ASA and clopidogrel in patients with platelet count disorders. Materials and Methods. This was a cross-sectional study of consecutive patients hospitalized in cardiology and hematology departments in the years 2018–2019. The study included patients with thrombocytopenia (PLT < 150 G/L) and thrombocythemia (PLT > 450 G/L) on ASA or dual antiplatelet therapy (DAPT; ASA plus clopidogrel). Controls included patients on antiplatelet drugs with normal platelet count. Platelet reactivity was measured in whole blood (Multiplate aggregometer, Roche, Switzerland) using arachidonic acid (AA), adenosine-5′-diphosphate (ADP), and thrombin receptor agonist peptide-6 (TRAP) as agonists. Platelet aggregation was expressed in arbitrary units (AU). AA-induced aggregation was used as a measure of response to ASA with a cut-off above 30 AU showing high on-treatment platelet reactivity to ASA (HTPR-A). ADP-induced aggregation measured response to clopidogrel with a cut-off above 48 AU for high on-treatment platelet reactivity to clopidogrel (HTPR-C). TRAP-induced aggregation measured baseline platelet reactivity not affected by oral antiplatelet drugs. Results. The study included 174 patients. There were 64 patients with thrombocytopenia, 30 patients with chronic thrombocythemia, and 80 controls. All patients were on 75 mg of ASA and 32% of them additionally on 75 mg of clopidogrel due to a history of recent coronary artery angioplasty. AA- and ADP-induced aggregation was comparable between thrombocytopenic patients and controls (median (IQR) 19 (7–28) vs. 23 (15–38) for AA AU and 32 (16–44) vs. 50 (32–71) for ADP AU, respectively), while it was significantly higher in thrombocythemic patients (median (IQR) 80 (79–118) for AA AU and 124 (89–139) for ADP AU). TRAP-induced aggregation showed significantly lowest aggregation in thrombocytopenic (median (IQR) 41 (34–60) for TRAP AU) and highest in thrombocythemic patients (median (IQR) 137 (120–180) for TRAP AU). HTPR-A was frequent in thrombocythemic patients in comparison with thrombocytopenic patients and controls (60% vs. 4% vs. 15%, respectively; p < 0.0002 ). HTPR-C was highly common in thrombocythemic patients and least common in thrombocytopenic ones in comparison with controls (80% vs. 8% vs. 40%, respectively; p < 0.001 ). Conclusion. Chronic thrombocytopenia does not significantly affect platelet reactivity and response to ASA and clopidogrel in comparison with controls. Thrombocytosis significantly increases platelet reactivity and attenuates response to both ASA and clopidogrel.

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Non ST-segment elevation myocardial infarction in patient with essential thrombocythemia

Cited by 12 publications

References 25 publications

Non-ST-segment Elevation Myocardial Infarction in a Patient With Essential Thrombocythemia Treated With Glycoprotein IIb/IIIa Inhibitor

Non-ST-segment Elevation Myocardial Infarction in a Patient With Essential Thrombocythemia Treated With Glycoprotein IIb/IIIa Inhibitor

Autoimmune atrophic gastritis: current perspectives

Platelet Reactivity and Response to Aspirin and Clopidogrel in Patients with Platelet Count Disorders

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