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Increased Serum Leptin Concentrations in Patients with Chronic Stable Angina Pectoris and ST-Elevated Myocardial Infarction

Departments of Biochemistry and Clinical Biochemistry, Celal Bayar University, Faculty of Medicine, Manisa, Turkey, fatma.taneli{at}bayar.edu.tr

Selma Yegane, MD

Department of Infectious Diseases, Moris Íinasi International Hospital, Manisa, Turkey

Cevval Ulman, MD

Departments of Biochemistry and Clinical Biochemistry, Celal Bayar University, Faculty of Medicine, Manisa, Turkey

Hakan Tikiz, MD

Department of Cardiology, Celal Bayar University, Faculty of Medicine, Manisa, Turkey

Ali Riza Bilge, MD

Department of Cardiology, Celal Bayar University, Faculty of Medicine, Manisa, Turkey

Zeki Ari, PhD

Departments of Biochemistry and Clinical Biochemistry, Celal Bayar University, Faculty of Medicine, Manisa, Turkey

Bekir Sami Uyanik, MD

Departments of Biochemistry and Clinical Biochemistry, Celal Bayar University, Faculty of Medicine, Manisa, Turkey

Leptin is an adipocytokine that is produced mainly by adipose tissue; it is also identified in atherosclerotic lesions in human coronary atherosclerosis. However, the relation of serum leptin concentrations to ischemic heart disease (IHD) is still obscure. The aims of the present study were to investigate serum leptin concentrations in patients with ST-elevated myocardial infarction (STEMI) and with chronic stable angina pectoris (CSAP) and to evaluate the possible correlations of leptin to other atherosclerotic risk factors; including serum high sensitive C-reactive protein (Hs-CRP), serum homocysteine, and fibrinogen concentrations. For this purpose, 35 patients with CSAP, 40 with acute STEMI, and 30 control subjects with normal findings from coronary angiography were taken into the study prospectively. Serum leptin concentrations were significantly higher in patients with CSAP and STEMI compared to the control group (7.74 ±1.34 vs 6.37 ±1.85 ng/mL, p=0.021 and 8.22 ±3.13 vs 6.37 ±1.85 ng/mL, p=0.023, respectively). In addition, serum homocysteine concentrations were significantly increased in patients with CSAP (15.23 ±5.96 vs 11.40 ±2.11 µmol/L, p=0.025) and patients with STEMI (15.90 ±5.02 vs 11.40 ±2.11 µmol/L, p=0.012) compared to the control group. Serum fibrinogen concentrations were significantly increased only in the CSAP group as compared to controls (4.15 ±1.39 vs 3.45 ±1.19 g/L, p=0.025). No significant correlation was found between leptin levels and selected risk factors. In conclusion, serum leptin concentrations were significantly higher in both the CSAP and STEMI groups. However, owing to the lack of correlation between the leptin levels and selected classical coronary risk factors, it may be considered that leptin can be evaluated as one of the independent risk factors for IHD. Further randomized and controlled studies will be required to determine the pathophysiological meaning of the increased leptin levels and the central role between adipocyte function and atherosclerosis.

Angiology, Vol. 57, No. 3, 267-272 (2006)
DOI: 10.1177/000331970605700302


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