Recurrent Coronary Artery Disease Due to Acetylsalicylic Acid Resistance May Be Related to COX-1 and COX-2 Mutations Asetilsalisilik Asit Direnci Nedeni ile Oluşan Rekürren Koroner Arter Hastalığı, COX-1 ve COX-2 Mutasyonları ile İlişkili Olabilir
Medical Journal of Bakirkoy, cilt.18, sa.1, ss.46-51, 2022 (ESCI, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 18 Sayı: 1
- Basım Tarihi: 2022
- Doi Numarası: 10.4274/bmj.galenos.2022.2021.10-20
- Dergi Adı: Medical Journal of Bakirkoy
- Derginin Tarandığı İndeksler: Emerging Sources Citation Index (ESCI), Scopus, Academic Search Premier, CINAHL, EMBASE
- Sayfa Sayıları: ss.46-51
- Anahtar Kelimeler: ASA resistance, recurrent CAD, COX-1, COX-2
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
Objective: Acetylsalicylic acid (ASA) is a commonly used antiplatelet drug for the treatment of coronary artery disease (CAD). However, in some patients recurrent CAD occurs due to ASA resistance (AR). This condition may be related to some genetic factors. Therefore, this study aims to investigate the effects of cyclooxygenase (COX)-1 and COX-2 mutations on recurrent CAD due to AR. Methods: Hundred CAD patients taking 100 mg ASA daily for 2 years were enrolled to the study. The patients were divided into two groups according to their recurrent CAD status. Forty-eight patients with recurrent CAD due to AR and 52 patients without recurrent CAD were selected to ASA resistant (AR+) and ASA non-resistant (AR-) group, respectively. AR was confirmed by platelet aggregation testing. Risk factors related to recurrent CAD were also obtained. After DNA was isolated from peripheral blood, rs1330344 variation in COX-1 and rs20417 variation in COX-2 were determined using real-time polymerase chain reaction. Results were evaluated statistically. Results: COX-1 and COX-2 mutations were mostly detected in the AR+ group however these data were not found statistically significant. Nevertheless, C allele of COX-2 was found statistically high in the AR+ group (67.9%) (p=0.023). Additionally statistically significant associations were found between high total cholesterol and low density lipoprotein cholesterol levels with the GC genotype of COX-2. Conclusion: It was suggested a relation between COX-2 mutations and recurrent CAD due to AR. Similar studies with a large population must explain the mechanisms governing the association of COX-1 and COX-2 genotypes and response to ASA in recurrent CAD patients.