Koroner arter hastalığının klinik ve anjiyografik görünümü ile trombosit sayısı ve volümünün ilişkisi
Akut koroner sendromlar (AKS)'ın gelişmesinde esas olay aterosklerotik plağın koroner damarda kısmi veya tam tıkaç oluşturmasıdır. Trombosit aktivasyonu AKS'ın patogenezinde önemli bir role sahiptir. Trombositler büyüklük, yoğunluk ve reaktivitelerine göre farklılıklar gösterirler. Büyük trombositlerin hemostatik olarak daha aktif olduğu ve AKS'lu hastalarda trombosit hacminin arttığı ileri sürülmüştür. Klinik olarak nonkardiyak göğüs ağrısı (n=74), stabil angina pektoris (n=96), anstabil angina pektoris (n=156) ve akut miyokard infarktüslü (n=70) toplam 396 kalp hastası çalışmaya alındı. Bu hastaların 377'sine koroner anjiyografi yapıldı ve anjiyo sonuçlarına göre hastalar normal (n=81), tek damar hastalığı (n=100), iki damar hastalığı (n=102) ve üç damar hastalığı (n=94) olarak gruplandırıldı. Bu hastalarda ortalama trombosit hacimleri (OTH) ve trombosit sayıları ölçüldü. Anstabil anginalı hastalarda OTH diğer klinik durumdaki hastalara göre anlamlı olarak yüksek bulundu (p=0.041). Normal koroner anjiyogramlı hastalarla koroner arter hastalığı saptananlar arasında OTH anlamlı farklılık göstermedi. Grupların trombosit sayıları arasında anlamlı fark bulunmadı. Bu bulgulara göre, rutin laboratuar işleminde OTH'nin değerlendirilmesi anstabil koroner kalp hastalığının bir göstergesi olarak kullanılabilir, ancak akut miyokard infarktüsünde yararlı bulunmamıştır.
The relation of mean platelet volume and count with the clinical and angiographic presentation of coronary artery disease
Rupture of an atherosclerotic plaque associated with partial or complete thrombotic vessel occlusion is fundamental to the development of acute coronary syndromes. Activated platelets play an important role in the pathogenesis of acute coronary syndromes (ACS). Platelets are heterogeneous with respect to their size, density, and reactivity. It was proposed that large platelets are more active hemostatically, and platelet size has been found to be increased in patients with ACS. We studied 396 patients defined clinically as noncoronary chest pain (n=74), stable angina pectoris (n=96), unstable angina pectoris (n=156) and acute myocardial infarction (n=70). Coronary angiography was performed to 377 patients and the patients were subdivided into those with normal coronary angiogram (n=81), single (n=100), double (n=102) and triple-vessel disease (n=94). We measured the mean platelet volume (MPV) and platelet count in these patients. Mean platelet volume in patients with unstable angina pectoris was significantly larger than the patients with other clinical presentation (p=0.041). There was no significant difference in mean platelet volume between patients with normal coronary angiogram and 1-, 2-, or 3-vessel disease. The mean platelet count was not significantly different in among the groups. Our findings suggested that, using a routine laboratory procedure; MPV might be used as a predictive marker for unstable coronary heart disease, but not for acute myocardial infarction.
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1. Prentice CRM. Platelets and atherosclerosis. Eur Heart J 1999 {Suppl A): A3-A7,
2. DeFeyter PJ. The benefits and risks of coronary intervention-balancing the equation. Clin Cardiol 1997; 20 (Suppl I): 114-121
3. Cimminiello C, Toschi V. Athcrotrombosis: the role of plalelels. Eur Heart J 1999 (Suppl A) : A8-A13.
4. Knight CJ. New insights into the pathopbysiology of acute coronary occlusion. Eur Heart J 1999 [Suppl F) : F3-F6.
5. Kristensen DS, Martin JF. Megakaryocytes and atherosclerosis. Clin Sc 1992; 82: 353-355.
6. van der l,oo B, Martin JF. A role for changes in plateleL production in the cause of acule coronary syndromes. Arterioscler Thromb Vasc Biol 1999; 19: 672-679.
7. Caameron HA. Phillips R, Ibbotson RM. et al. Platelet size in myocardial infarction. Br Med J 1983; 287: 449-451.
8. Mailin JF, Plumb J, Kilbey RS. ei al. Changes in volume and density of platelets in myocardial infarction. Br Med J 1983; 287: 456-459.
9. Pizzulli L, Yang A, Martin JF, et al. Changes in platelet size and count in anstabil angina compared to stabtl angina or non-cardiac chest pain. Eur Heart J 1998; 19: 80-84.
10. Trip MD, Cats VM, vanCapeile FK, et al. Platelet hyper-reactivity and prognosis in survivors of myocardial infarction. N Eng j Med 1990; 322: 1549-1554.
11. Halbmayer WM, Haushofer A, Radek J. Schon R. et al. Platelet size, fibrinogen and lipoprotein (a) in coronary heart disease. Coron Artery Dis 1995; 5: 397-402.
12. Smyth DW, Martin JF. Michalis L. et al. Influence of platelet size before coronary angioplasty on subsequent restenosis. Eur J Clin Invest 1993; 6: 361-367.