Necip ERMİŞ, Erdal AKTÜRK, İsa SİNCER, Ramazan ÖZDEMİR, Şengül ÇEHRELİ

Yavaş Koroner Akımlı Hastalarda Dipridamol’ün Akım Aracılı Dilatasyon Üzerine Etkisi

Amaç: Yavaş koroner akım (YKA), anjiyografik olarak belirgin koroner arter hastalığı yokluğunda, Thrombolysis in Myocardial Infarction (TIMI)-2 akımın izlendiği farklı bir anjiyografik bulgu olup patofizyolojisi ile ilgili olarak endotel ve mikrovasküler disfonksiyon üzerinde durulmaktadır. Önceki çalışmalarda oral başlanan dipridamolün anjiyografik olarak YKA'ı düzelttiği gösterilmiştir. Bu çalışmanın amacı;fizyopatolojisinde endotel disfonksiyonunun düşünüldüğü YKA'da, dipridamolün endotel fonksiyonları üzerine olan etkisini değerlendirmektir. Gereç ve yöntem: Çalışmaya anjiyografik olarak bir veya daha fazla koroner arterinde yavaş akımın tespit edildiği, 28 hasta (ortalama yaşları 50 ± 8.0 olan 22 erkek 6 kadın) alındı. Çalışmaya katılan hastalarda endotel fonksiyonlarını etkileyebilecek olan ilaçlar 15 gün öncesinden kesildi. 15. gün sonunda bazal brakiyal arter Doppler incelemesi yapıldıktan sonra hastalara 1 ay süre ile 75 mg dipridamol günde 3 defa verildi ve 1. ay sonunda brakiyal arter Doppler incelemesi tekrarlandı. Bulgular: Hastaların dipridamol öncesi ve sonrası değerleri karşılaştırıldığında bazal akım aracılı vazodilatasyon (AAD) % değerine göre dipridamol sonrası bakılan % AAD değerinde anlamlı artış izlendi (AAD dipridamol öncesi: %2.7±1.9, AAD dipridamol sonrası: %3.1±1.8, p=0.001). Nitrogliserin (NTG), yani endotel bağımsız dilatasyonda dipridamol öncesi ve sonrası açısından farklılık tespit edilmedi (NTG dipiridamol öncesi: %13.1±3.3, NTG dipiridamol sonrası: %13.0±3.0, p=0.9). Ortalama düzeltilmiş TIMI frame sayısının bazal AAD yüzdesi ile güçlü fakat ters bir ilişki gösterdiği belirlendi. (r=-0.26, p<0.05) Sonuç: YKA'lı hastalarda dipridamol, endotel disfonksiyonuna bağlı olarak gelişen bozulmuş AAD üzerine olumlu etki gösterir. Anahtar kelimeler: Yavaş Koroner Akım, Akım Aracılı Vazodilatasyon, Endotel Disfonksiyonu

Anahtar Kelimeler:

Yavaş Koroner Akım, Akım Aracılı Vazodilatasyon, Endotel Disfonksiyonu

The Effect of Diprydamole on Flow-Mediated Dilatation in Patients with Slow Coronary Flow

Aim: The slow coronary flow (SCF), a distinct angiographic finding characterized by presence of Thrombolysis in Myocardial Infarction (TIMI) –2 flow in the absence of coronary disease, pathophysiologically related to endothelial and microvascular dysfunction. Previous studies, it has been shown that oral diprydamole could correct the SCF angiographically. The aim of this study is to evaluate the effect of diprydamole on endothelial functions tested from the forearm, SCF which is physiopathologically related to endothelial dysfunction. Material and methods: 28 patients (22 male, 6 female, mean age 50±8.0) with angiographically-proven slow coronary flow at one or more coronary arterieswere included in study. All drugs that may interact with endothelial functions were stopped 15 days before the study. At the end of 15 days, baseline brachial artery Doppler examinations were performed and diprydamole 75 mg tid. was given to all patients during the nex tone month, and at the end of one month, brachial artery Doppler examinations were reperformed. Results: When the results of the patients before and after use of diprydamole were compared, it was observed that post-diprydamole flow mediated vasodilatation (FMD) value was significantly higher than the basal FMD value (FMD-prediprydamole: 2.7%±1.9, FMD-postdiprydamole: 3.1%±1.8, p=0.001). Nitroglyserine (NTG), thus shows endothelium-independent vasodilatation, showed no significant difference in prediprydamole and postdiprydamole period (NTG-prediprydamole: 13.1%±3.3, NTG-postdiprydamole: 13.0%±3.0, p=0.9). It was also noted that mean corrected TIMI frame count showed strong but inverse relationship with baseline FMD percent (r=-0.26, p<0.05). Conclusion: In patients with SCF, diprydamole improves FMD related to endothelial dysfunction. Key words: Slow Coronary Flow, Flow-Mediated Vasodilatation, Endothelial Dysfunction

Keywords:

Slow Coronary Flow, Flow-Mediated Vasodilatation, Endothelial Dysfunction,

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