Effect of sedation on soluble P-selectin levels, coagulation and myocardial damage following a coronary intervention

Yazici M., Demircan S., Aygul E., Sahin M., Albayrak F., Aksakal E., ...Daha Fazla

INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, cilt.60, sa.5, ss.526-532, 2006 (SCI-Expanded, Scopus) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 60 Sayı: 5
  • Basım Tarihi: 2006
  • Doi Numarası: 10.1111/j.1368-5031.2006.00834.x
  • Dergi Adı: INTERNATIONAL JOURNAL OF CLINICAL PRACTICE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.526-532
  • Anahtar Kelimeler: coronary stent, soluble P-selectin, sedation, platelet, coagulation, ADHESION MOLECULES, UNSTABLE ANGINA, IN-VIVO, MIDAZOLAM, PLATELET, ANGIOPLASTY, ACTIVATION, FIBRINOGEN, INFARCTION, FENTANYL
  • Ondokuz Mayıs Üniversitesi Adresli: Evet

Özet

This study was aimed to investigate the effect of sedation on plasma soluble P-selectin (sP-selectin) levels and initiation phase of coagulation following coronary intervention. A total of 58 patients with unstable angina were randomised into two groups of sedated (n = 29) and nonsedated (n = 29) patients. sP-Selectin, adrenaline, noradrenaline, von Willebrand factor (vWF), fibrinogen, platelet and troponin-I levels were measured before the intervention and at 30 min and 24 h after the intervention. In the sedated group, adrenaline, noradrenaline, sP-selectin and fibrinogen levels remained stable 30 min after the intervention (p > 0.05), whereas vWF level increased (p < 0.05). In the nonsedated group, 30-min sP-selectin (p < 0.001), adrenaline (p < 0.05), noradrenaline (p = 0.012), vWF (p < 0.001) and fibrinogen (p < 0.001) levels were found to be increased. Also, 24-h sP-selectin, vWF and fibrinogen levels for both groups showed significant increases when compared with the values both 30 h before (p < 0.001) and 30 min after the intervention (p < 0.001). Sedation before interventions reduces sP-selectin levels, initial phase of coagulation and, consequently, myocardial damage.