Nil ÖZYÜNCÜ, Eralp TUTAR, Kerim ESENBOĞA, Hüseyin NAZMAN, Cemre TEKİN, Turkan SEDA TAN

Akut Miyokard İnfarktüsü Alt Tipleri Arasında Başvuru Esnasında Ölçülen Ortalama Trombosit Hacminin Karşılaştırılması

Amaç: Akut miyokard infarktüsü (MI) patofizyolojisinde aktive trombositlerin sebep olduğu trombus ve buna bağlı azalan kan akımı ile bozulanmiyokard beslenmesi yatmaktadır. Ortalama trombosit hacmi (OTH), artan trombosit aktivitesi ve yıkımıyla artmaktadır. Çalışmalarda akut MIhastalarında bu parametrenin arttığı ve yüksek değerlerin kötü prognoz ile ilişkili olduğu gösterilmiştir. Literatürde ST elevasyonu olan ve olmayanMI hastalarının trombosit aktivitesi açısından kıyaslandığı çok az çalışma mevcuttur. Çalışmamızda bu iki akut MI alt tipini ortalama trombosit hacmiaçısından kıyaslamayı planladık.Gereç ve Yöntem: Koroner yoğun bakımımıza akut MI ile kabul edilmiş ve izlenmiş hasta verileri retrospektif olarak tarandı. Başvuru anında alınankanlardan, tam kan sayımı tetkiki içerisinde OTH analizi otomatik olarak yapıldı. Hastalar ST elevasyonu olan MI ve ST elevasyonu olmayan MI olarakiki grupta kıyaslandı.Bulgular: Sonuç olarak uygunluk kriterlerine uyan 356 hasta çalışmamıza dahil edildi (203 hasta ST elevasyonu olmayan MI, 153 hasta ST elevasyonuolan MI). Ortalama hasta yaşı 63 olup hastaların %29’u kadın idi. ST elevasyonu olmayan MI’da ortalama trombosit hacmi diğer MI tipine kıyaslabelirgin olarak daha yüksek bulundu (10,5±1,2 vs 10,1±1,2, p=0,001).Sonuç: ST elevasyonu olan ve olmayan MI hastalarının trombosit aktiviteleri hakkında öngördürücü OTH’nin kıyaslandığı çalışmamızda, ST elevasyonuolmayan MI geçiren hastalarda OTH’nin anlamlı olarak daha yüksek olduğu sonucuna ulaştık. Altta yatan kronik ateroskleroz, komorbiditelerve patofizyolojide muhtemel daha merkezde rol alan aktive trombositler ile ST elevasyonu olmayan MI’daki bu sonuçları açıklayabilir.Bu hastagrubuna, ST elevasyonu olan MI kadar önem verilerek acil ve kılavuzlara uygun antiagregan tedavinin erkenden başlanmasını vurgulaması açısındansonuçlarımızın önemli olduğunu düşünmekteyiz.

Comparison of Mean Platelet Volume at Admission in Subtypes of Acute Myocardial Infarction

Objectives: Thrombus by the activated platelets and reduced blood flow of myocardium as a result of the thrombus lies under the pathophysiology of acute myocardial infarction (MI). Mean platelet volume (MPV) is known to increase by the activation and rapid turnover of the platelets. This parameter has been shown to increase in acute MI and high levels are associated with poor prognosis. Trials comparing the MPV in ST elevated and non-ST elevated myocardial infarction (MI) patients are so rare in the literature. We aimed to search for the difference in MPV in these 2 types of acute MI. Materials and Methods: We retrospectively searched for the patients followed up because of acute MI in our coronary intensive care unit. MPV was routinely worked up from the admission complete blood count analysis. Patients were compared in two groups as ST elevation MI and non-ST elevation MI. Results: As a result, 356 elligible patients were included in our trial (203 were non-ST elevation patients, 153 were ST elevation patients). Mean patient age was 63 and 29% were female. MPV in non-ST elevation group was significantly higher than ST elevation MI group (10.5±1.2 vs 10.1±1.2, p=0.001). Conclusion: We concluded that MPV, a parameter of platelet reactivity, was significantly higher in patients with non-ST elevated MI. Chronic underlying atherosclerosis, comorbidities and activated platelets probably playing more central role in pathophysiology of this acute MI type may explain these results. In non-ST elevation MI, urgent and appropriate antiaggregant therapy, as explained in the guidelines is as important as it is in ST elevated MI, we believe our results may be important for reminding this issue.

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1. Amraotkar AR, Song DD, Otero D, et al. Platelet Count and Mean Platelet Volume at the Time of and After Acute Myocardial Infarction. Clin Appl Thromb Hemost. 2017;23:1052-1059.
2. Park Y, Schoene N, Harris W. Mean platelet volume as an indicator of platelet activation: methodological issues. Platelets. 2002;13:301-306.
3. De Luca G, Secco GG, Verdoia M, et al. Combination between mean platelet volume and platelet distribution width to predict the prevalence and extent of coronary artery disease: results from a large cohort study. Blood Coagul Fibrinolysis. 2014;25:86-91.
4. Coban E, Ozdogan M, Yazicioglu G, et al. The mean platelet volume in patients with obesity. Int J Clin Pract. 2005;59:981-982.
5. Cho SY, You E, Lee HJ, et al. Smoking cession decreases mean platelet volume in healthy Korean populations. Clin Lab. 2014;60:1413-1416.
6. Endler G, Klimesch A, Sunder-Plassmann H, et al. Mean platelet volume is an independent risk factor for myocardial infarction but not for coronary artery disease. Br J Haematol. 2002;117:399-404.
7. Bath P, Algert C, Chapman N, et al; PROGRESS Collaborative Group. Association of mean platelet volume with risk of stroke among 3134 individuals with history of cerebrovascular disease. Stroke. 2004;35:622- 626.
8. Colkesen Y, Coskun I, Muderrisoglu H. The effect of aspirin on mean platelet volume in patients with paroxysmal atrial fibrillation. Platelets. 2013;24:263-266.
9. Huczek Z, Kochman J, Filipiak KJ, et al. Mean platelet volume on admission predicts impaired reperfusion and long-term mortality in acute myocardial infarction treated with primary percutaneous coronary intervention. J Am Coll Cardiol. 2005 19;46:284-290.
10. Wasilewski J, Desperak P, Hawranek M, et al. Prognostic implications of mean platelet volume on short- and long-term outcomes among patients with non-ST-segment elevation myocardial infarction treated with percutaneous coronary intervention: A single-center large observational study. Platelets. 2016;27:452-458.
11. Ozkan B, Uysal OK, Duran M, et al. Relationship between mean platelet volume and atherosclerosis in young patients with ST elevation myocardial infarction. Angiology. 2013;64:371-374.
12. Ulusoy RE, Yokusoglu M, Kirilmaz A. Mean platelet volume in ST elevation and non-ST elevation myocardial infarction. Gulhane Tıp Derg. 2011;53:114- 118.
13. White H, Thygesen K, Alpert JS, et al. Universal MI definition update for cardiovascular disease. Curr Cardiol Rep. 2014;16:492
14. Windecker S, Kolh P, Alfonso F, et al, Authors/Task Force members, 2014 ESC/EACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS)Developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur Heart J. 2014;35:2541-2619.
15. Nording HM, Seizer P, Langer HF. Platelets in inflammation and atherogenesis. Front Immunol. 2015;6:98.
16. Kamińska J, Koper OM, Siedlecka-Czykier E, et al. The utility of inflammation and platelet biomarkers in patients with acute coronary syndromes. Saudi J Biol Sci. 2018;25:1263-1271.
17. Pal R, Bagarhatta R, Gulati S, et al. Mean platelet volume in patients with acute coronary syndromes: a supportive diagnostic predictor. J Clin Diagn Res. 2014;8:MC01-4.
18. Karpatkin S. Heterogeneity of human platelets. VI. Correlation of platelet function with platelet volume. Blood. 1978;51:307-316.
19. Threatte GA. Usefulness of the mean platelet volume. Clin Lab Med. 1993;13:937-950.
20. Pizzulli L, Yang A, Martin JF, et al. Changes in platelet size and count in unstable angina compared to stable angina or non-cardiac chest pain. Eur Heart J. 1998;19:80-84.
21. Wan ZF, Zhou D, Xue JH, et al. Combination of mean platelet volume and the GRACE risk score better predicts future cardiovascular events in patients with acute coronary syndrome. Platelets. 2014;25:447-451.
22. van der LOO B, Martin JF. A role for changes in platelet production in the cause of acute coronary syndromes. Arterioscler Thromb Vasc Biol. 1999;19:672-679.
23. Klinik Kardiyoloji, tanı ve tedavi. Editör: Prof Dr. Kamil Adalet. İstanbul Tıp Kitabevi, 2013;sf 425-459.
24. Figueras J, Otaegui I, Marti G, et al. Area at risk and collateral circulation in a first acute myocardial infarction with occluded culprit artery. STEMI vs non-STEMI patient. Int J Cardiol. 2018;259:14-19.
25. Ndrepepa G, Fusaro M, King L, et al.Statin pretreatment and presentation patterns in patients with coronary artery disease. Cardiol J. 2013;20:52-58.
26. Libby P. Seeing and Sampling the Surface of the Atherosclerotic Plaque: Red or White Can Make Blue. Arterioscler Thromb Vasc Biol. 2016;36:2275- 2277.
27. Denlinger LN, Keeley EC.Medication Administration Delays in Non-ST Elevation Myocardial Infarction: Analysis of 1002 Patients Admitted to an Academic Medical Center. Crit Pathw Cardiol. 2018;17:73-76.