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Serum level of lipoprotein (a) is inversely associated with the development of coronary collateral circulation
Dursun Aras1, Bilal Geyik, Serkan Topaloglu
1Department of Cardiology, Türkiye Yüksek Ihtisas Hospital, Ankara, Turkey. sevgidursun06@yahoo.com
Insights
High levels of lipoprotein (a) negatively impact the formation of coronary collateral vessels. This may be due to reduced vascular endothelial cell growth factor, affecting collateral development in patients with coronary artery disease.
Area of Science:
- Cardiovascular Research
- Vascular Biology
- Lipid Metabolism
Background:
- Coronary collateral circulation is crucial for myocardial perfusion in obstructive coronary artery disease.
- Lipoprotein (a) [Lp(a)] is an independent risk factor for atherosclerotic cardiovascular disease.
- The role of Lp(a) in modulating coronary collateral growth remains incompletely understood.
Purpose of the Study:
- To investigate the association between serum lipoprotein (a) levels and the extent of coronary collateral circulation.
- To determine if lipoprotein (a) influences vascular endothelial cell growth factor (VEGF) levels.
Main Methods:
- Sixty patients with angiographically confirmed total coronary artery occlusion were analyzed.
- Collateral development was graded using Rentrop's classification (0-3).
- Serum Lp(a) and VEGF levels were quantified using enzyme-linked immunosorbent assay.
Main Results:
- Patients with poorly developed collaterals (grades 0-1) exhibited significantly higher Lp(a) and lower VEGF levels compared to those with well-developed collaterals (grades 2-3).
- A significant negative correlation was found between Lp(a) and VEGF levels (r=-0.708, P<0.0001).
- Multivariate analysis indicated that high Lp(a) levels were associated with impaired collateral development, while angina duration positively influenced it.
Conclusions:
- Elevated serum lipoprotein (a) levels are detrimental to the formation of coronary collateral vessels in humans.
- Reduced VEGF production or bioactivity secondary to high Lp(a) may underlie the impaired collateralization observed in hyperlipoproteinemia (a).
- These findings highlight a potential mechanism linking Lp(a) to adverse coronary collateralization and suggest therapeutic targets for improving collateral function.
Background:
This study sought to determine the relationship between serum lipoprotein (a) levels and angiographically visible coronary collateral circulation and to evaluate whether lipoprotein (a) exerts any effect on vascular endothelial cell growth factor.
Methods:
The study population included 60 patients (39 men, mean age 59+/-13 years) with angiographically documented total occlusion in one of the major coronary arteries. Development of collaterals was classified by Rentrop's method. Patients were defined as having poorly developed collaterals for grades 0 and 1 (group 1), or well-developed collaterals for grades 2 and 3 (group 2). Serum lipoprotein (a) and vascular endothelial cell growth factor levels were determined by enzyme-linked immunosorbent assay.
Results:
In group 1, lipoprotein (a) levels were significantly higher and vascular endothelial cell growth factor levels were significantly lower than in group 2 (34+/-19 vs. 20+/-12 mg/dl, P<0.001, and 2.5+/-0.7 vs. 3.4+/-0.8 ng/dl, P<0.001, respectively). Poorly developed collaterals were significantly more frequent in patients with lipoprotein (a) levels >or=30 mg/dl than in patients with levels <30 mg/dl (72 vs. 37%, P=0.008). A strong negative correlation was observed between lipoprotein (a) and vascular endothelial cell growth, factor (r=-0.708, P<0.0001). Multivariate analysis revealed that a high level of lipoprotein (a) negatively affected the development of collaterals, whereas the duration of angina had a positive effect.
Conclusion:
This study demonstrated for the first time that the high level of lipoprotein (a) negatively affects the formation of coronary collateral vessels in human beings. Reduced production or bioactivity of vascular endothelial cell growth factor caused by high levels of lipoprotein (a) may be the possible responsible mechanisms of hyperlipoprotein (a)-related poor collateral formation.
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