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ST elevasyonlu ve ST elevasyonsuz miyokard infarktüsünde ortalama trombosit hacmi

Mean platelet volume in ST elevation and non-ST elevation myocardial infarction

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Abstract (2. Language): 
Platelet activation is thought to play a key pathogenetic mechanism in acute coronary syndromes. We investigated the mean platelet volume and platelet count in patients with both ST elevation myocardial infarction and non-ST elevation myocardial infarction. Fifty two patients with non-ST elevation myocardial infarction and 56 patients with ST elevation myocardial infarction were enrolled in the study. Age- and gender-matched 50 healthy subjects constituted the control group. Venous blood samples for whole blood analysis were drawn on admission and analyzed by an autoanalyser. The difference in mean platelet volume was statistically significant in ST elevation myocardial infarction and non-ST elevation myocardial infarction patients, which was 8.7±1 and 7.9±0.7 fl (p<0.01), respectively. However, the difference in mean platelet volume between non-ST elevation myocardial infarction and control group was not significant (7.9±0.7 and 8.1±0.7 fl; p=0.52, respectively). Moreover, platelet counts of both ST elevation myocardial infarction and non-ST elevation myocardial infarction groups were significantly lower than the controls. Platelet counts in the ST elevation myocardial infarction and non-ST elevation myocardial infarction patients did not show any statistically significant difference. The underlying mechanism should be investigated in further studies, which may shed light on developing new therapeutic strategies for this particular acute coronary syndrome
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Abstract (Original Language): 
Akut koroner sendromların fizyopatolojik mekanizmasında trombosit aktivasyonunun anahtar rol oynadığı düşünülmektedir. Çalışmamızda ST elevasyonlu miyokard infaktüsü ve ST elevasyonsuz miyokard infarktüsü olgularında ortalama trombosit hacmi ve trombosit sayılarını araştırdık. ST elevasyonsuz miyokard infarktüslü 52 hasta ve ST elevasyonlu miyokard infaktüslü 56 hasta çalışmaya dahil edildi. Yaş ve cinsiyet uyumlu 50 sağlıklı olgu kontrol grubunu oluşturdu. Hastaların ilk kabullerinde venöz kan örnekleri alınarak otoanalizörde tam kan sayımları yapıldı. Ortalama trombosit hacmi ST elevasyonlu ve ST elevasyonsuz miyokard infarktüslü olgularda istatistiksel olarak anlamlı olacak şekilde (sırasıyla 8.7±1 ve 7.9±0.7 fl (p<0.01)) farklıydı. Ancak ST elevasyonsuz miyokard infarktüslü ve kontrol grubu olgular arasında ortalama trombosit hacmi açısından istatistiksel olarak anlamlı farklılık yoktu (sırasıyla 7.9±0.7 ve 8.1±0.7 fl; p=0.52). Bunun yanı sıra trombosit sayısı hem ST elevasyonlu, hem de ST elevasyonsuz miyokard infarktüslü olgularda kontrol grubuna göre daha düşüktü. ST elevasyonlu ve ST elevasyonsuz miyokard infarktüslü olgular arasında trombosit sayısı açısından istatistiksel olarak anlamlı farklılık yoktu. Akut koroner sendromların bu özel grubunda yeni tedavi stratejilerine yön verebilecek ve altta yatan mekanizmaların aydınlatılması için ileri çalışmalara ihtiyaç vardır
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