Circulating levels of erythropoietin and its relation to arterial stiffness in patients with hypertension


GEDİKLİ Ö., Kiris A., KARAHAN C.

INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE, cilt.6, sa.8, ss.706-711, 2013 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 6 Sayı: 8
  • Basım Tarihi: 2013
  • Dergi Adı: INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.706-711
  • Karadeniz Teknik Üniversitesi Adresli: Evet

Özet

Background: Emerging experimental and clinical data indicates that erythropoietin (EPO) have significant roles in the cardiovascular system. But the relationship between endogenous EPO levels and arterial stiffness remains unknown. We investigated the EPO levels in relation to arterial stiffness parameters in patients with never treated newly diagnosed hypertension (HT). Methods: We studied 42 (47.8 +/- 10 years) never treated HT patients and age and gender-matched 40 (47 +/- 8.6 years) normotensive individuals. Serum EPO levels were determined in all subjects using the chemiluminescence immunoassay kit. We evaluated heart rate-corrected augmentation index (AIx@75), a marker of wave reflections and aortic pulse wave velocity (PWV) as indices of elastic-type aortic stiffness using applanation tonometry (Sphygmocor). Results: The levels of EPO were not significantly different in hypertensive patients and the controls (10.6 +/- 5 vs. 11.6 +/- 9, mIU/mL, p = 0.5). Aortic PWV (10.3 +/- 2.3 vs. 8.7 +/- 1.6 m/s, p = 0.0001) and AIx@75 (22.7 +/- 10 vs. 15 +/- 11, %, p = 0.002) were significantly higher in hypertensive patients than the controls. EPO levels were not correlated with brachial and central pressures. Also EPO level was not significantly correlated with AIx@75 (r = -0.15, p = 0.17) and aortic PWV (r = -0.16, p = 0.13). Conclusion: Results from this study indicate that endogenous EPO levels may not be a factor in development of increased arterial stiffness.