Evaluation of Vascular Endothelial Growth Factor Levels and Serum Angiotensin‐Converting Enzyme Activity in Hyperlipidemia and Coronary Artery Disease
Authors: Turan Taylan , Biyikoglu Funda , Duru Erdal , Gonenc Aymelek 
Published: November 2023

Half of all deaths in the developed world and a quarter of deaths in the developing world are on account of cardiovascular diseases. Coronary Artery Disease (CAD) continues to be the most common type of cardiovascular diseases and the major cause of death in both genders. Hyperlipidemia and endothelial dysfunction often precedes the occurrence of CAD. CAD most commonly originate from atherosclerotic occlusion of the coronary arteries. Vascular endothelial growth factors (VEGF) are primary angiogenic molecules controlling vascular homeostasis, vascular growth and function. It plays a cardinal role in the development of collateral vessels and angiogenesis. Angiotensin‐Converting Enzyme (ACE) is widely distributed on the luminal surface of the vascular endothelium. It catalyzes the proteolytic cleavage of angiotensin I to angiotensin II (ANG II) and has bradykinin degrading activity means that it participates in the control of vascular resistance. ANG II also takes a role in angiogenesis, vascular remodeling. Therefore ACE and VEGF are of great importance in pathogenesis of atherogenesis, particularly CAD. From this viewpoint we decided to investigate of changes in serum VEGF and ACE levels in CAD and Hyperlipidemia.

In the present study, the serum levels of VEGF‐A and ACE from the patients with CAD (N=30) and hyperlipidemia (N=30) and normal controls (N=30) were measured by enzyme‐linked immunosorbent assay (ELISA) kits (e‐Bioscience, Eastbiopharm, respectively).

No significant differences were found between serum levels of ACE in three groups (p>0.05). Serum VEGF levels were decreased significantly in hyperlipidemic patients as compared to healthy controls (p<0.05), while there was no significant differences between CAD patients and control groups (p>0.05).

In conclusion, our study revealed that ACE activity was not changed significantly among the groups. A more accurate assessment require further investigation using a larger sample size. There are conflicting results regarding VEGF in cardiovascular diseases. Increased VEGF levels were found in various studies. Nakajima et al. evaluated the relationship between plasma VEGF level and multivessel coronary artery disease in 73 patients and 70 healthy controls. They developed a hypothesis that plasma VEGF level may be associated with coronary artery disease and other cardiovascular risk factors and found out VEGF levels were elevated in patients with multivessel disease. Hojo et al. suggest that the extent of myocardial damage contributes to the elevation of serum VEGF levels in acute myocardial infarction. Trapé and his colleagues show that patients with hyperlipidemia have higher serum VEGF levels than individuals with normal lipid levels. On the other hand, Arakawa et al. reported that a significant decrease in serum VEGF concentration in patients with Congestive Heart Failure (CHF) compared to control subjects. Previously, Kraus et al. and Cheng et al. also reported that VEGF concentrations in skeletal muscle and in the pleural fluid in patients with CHF were reduced significantly, respectively. We found that VEGF levels were decreased significantly in hyperlipidemia (p<0.05). The decreased circulating VEGF concentrations may be caused by the receptors, which are expressed predominantly in hyperlipidemia. However, serum VEGF in CAD groups were not different from controls (p>0.05). Further studies are needed to clarify the relation between VEGF and CHF.