Clinical course of ST elevation myocardial infarction and blood leptin levels

Recently, researchers have been increasingly interested in the association between the incidence of cardiovascular events (such as myocardial infarction, MI) and leptin – an adipocyte-produced hormone, which normally is involved in the body mass regulation.

Aim. To assess the role of leptin in the clinical course of acute myocardial infarction with ST segment elevation (STEMI) on ECG.

Material and methods. The study included 89 men aged 23–77 years. All patients underwent coronary angiography (CAG) in the first 12 hours of STEMI. Based on the CAG findings, 80 patients underwent percutaneous coronary interventions (PCI). All participants were divided into two groups, based on the plasma levels of leptin.

Group 1 (n=42) had elevated leptin levels (>5,63 ng/ml), while Group 2 (n=47) had normal leptin levels (<5,63 ng/ml).

Results. In MI patients, leptin concentration was a predictor of the in-hospital diagnosis of Type 2 diabetes mellitus (DM-2). The plasma leptin concentration in the first 24 hours of MI was associated with the levels of interleukin-1-beta, potassium, creatinine, triglycerides, haemoglobin, body mass index, and left ventricular enddiastolic dimension.

Conclusion. Leptin levels in the acute phase of STEMI could be used for the prediction of MI complications and DM-2.

1. Dubey L., Zeng H., Hashmi S et al. Association of plasma leptin levels and complexity of the culprit lesion in patients with unstable angina. Int J Cardiol, 2008; 126 (2):183–9.

2. Krasnodebski P., Bak M. I., Opolski G., Karnafel W. et al. Leptin in acute myocardial infarction and period of convalescence in patients with type 2 diabetes mellitus. Kardiol Pol, 2010; 68 (6):648–53.

3. Ku I. A., Farzaneh-Far R., Vittinghoff E. et al. Association of low leptin with cardiovascular events and mortality in patients with stable coronary artery disease: the Heart and Soul Study. Atherosclerosis, 2011; 217 (2):503–8.

4. Mattu H. S., Randeva H. S. et al. Role of adipokines in cardiovascular disease. J Endocrinol, 2013; 216 (1): T17–36.

5. Simonds S. E., Cowley M. A. et al. Hypertension in obesity: is leptin the culprit? Trends Neurosci, 2013; 36 (2):121–32.

6. Taneli F., Yegane S., Ulman C. et al. Increased serum leptin concentrations in patients with chronic stable angina pectoris and ST-elevated myocardial infarction. Angiology, 2006; 57 (3):267–72.

7. Amasyali B., Kose S., Kursaklioglu H. et al. Leptin in acute coronary syndromes: has the time come for its use in risk stratification? Int J Cardiol, 2008; 130 (2):264–5.

8. Bigalke B., Stellos K., Geisler T. et al. High plasma levels of adipocytokines are associated with platelet activation in patients with coronary artery disease. Platelets, 2010; 21 (1):11–9.

9. Dubey L., Zeng H. S., Wang H. J. et al. Potential role of adipocytokine leptin in acute coronary syndrome. Asian Cardiovasc Thorac Ann, 2008; 16 (2):124–8.

10. Piestrzeniewicz K., Luczak K., Komorowski J. et al. The relationship between leptin and obesity and cardiovascular risk factors in men with acute myocardial infarction. Cardiol J, 2007; 14 (3):252–9.

11. Sierra-Johnson J., Romero-Corral A., Lopez-Jimenez F. et al. Relation of Increased Leptin Concentrations to History of Myocardial Infarction and Stroke in the United States Population. Am. J. Cardiol, 2007; 100:234–9.

12. Amasyali B., Aytemir K., Kose S. et al. Admission plasma leptin level strongly correlates with the success of thrombolytic therapy in patients with acute myocardial infarction. Angiology, 2007; 57 (6):671–80.

13. Hasan-Ali H., Abd El-Mottaleb N. A., Hamed H. B. et al. Serum adiponectin and leptin as predictors of the presence and degree of coronary atherosclerosis. Coron Artery Dis, 2011; 22 (4):264–9.

14. Khafaji H. A., Bener A. B., Rizk N. M., Al Suwaidi J. Elevated serum leptin in patients with acute myocardial infarction; correlation with coronaryangiographic and echocardiographic finding. BMC Res Notes, 2012; 5:262.

15. Abe Y., Ono K., Kawamura T. et al. Leptin induces elongation of cardiac myocytes and causes eccentric left ventricular dilatation with compensation. Am J Physiol Heart Circ Physiol, 2007; 292 (5): H2387–96.