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Cardiovascular risk factors and collateral artery formation
D de Groot1, G Pasterkamp, I E Hoefer
1Laboratory of Experimental Cardiology, UMC Utrecht, the Netherlands.
Insights
Cardiovascular risk factors impact collateral artery growth, affecting blood flow recovery in atherosclerosis. Understanding these influences is crucial for managing cardiovascular disease and improving patient outcomes.
Area of Science:
- Cardiovascular biology
- Vascular remodeling
- Atherosclerosis research
Background:
- Arterial lumen narrowing in atherosclerosis causes significant morbidity and mortality.
- Collateral artery formation (arteriogenesis) is a compensatory mechanism bypassing arterial obstructions.
- Hemodynamic forces, cytokines, and leucocyte invasion are key to arteriogenesis.
Purpose of the Study:
- To review the influence of cardiovascular risk factors on collateral vessel development.
- To examine the effects of cardiovascular medications on arteriogenesis.
- To understand variations in collateralization among patients with atherosclerotic disease.
Main Methods:
- Review of experimental and clinical studies on arteriogenesis.
- Analysis of the role of hemodynamic forces (shear stress, wall stress) in collateral growth.
- Investigation of cytokine expression and leucocyte involvement in collateral formation.
Main Results:
- Cardiovascular risk factors (hypertension, hypercholesterolemia, diabetes) directly and indirectly affect collateral artery growth.
- Inadequate collateralization due to risk factors increases cardiovascular event risk.
- Cardiovascular medications may influence collateral artery development, either positively or negatively.
Conclusions:
- Cardiovascular risk factors significantly modulate the effectiveness of collateral circulation in atherosclerosis.
- Patient outcomes in atherosclerotic disease are influenced by the interplay between risk factors, collateralization, and medication.
- Further research is needed to optimize therapeutic strategies targeting arteriogenesis in cardiovascular disease.
Abstract:
Arterial lumen narrowing and vascular occlusion is the actual cause of morbidity and mortality in atherosclerotic disease. Collateral artery formation (arteriogenesis) refers to an active remodelling of non-functional vascular anastomoses to functional collateral arteries, capable to bypass the site of obstruction and preserve the tissue that is jeopardized by ischaemia. Hemodynamic forces such as shear stress and wall stress play a pivotal role in collateral artery formation, accompanied by the expression of various cytokines and invasion of circulating leucocytes. Arteriogenesis hence represents an important compensatory mechanism for atherosclerotic vessel occlusion. As arteriogenesis mostly occurs when lumen narrowing by atherosclerotic plaques takes place, presence of cardiovascular risk factors (e.g. hypertension, hypercholesterolaemia and diabetes) is highly likely. Risk factors for atherosclerotic disease affect collateral artery growth directly and indirectly by altering hemodynamic forces or influencing cellular function and proliferation. Adequate collateralization varies significantly among atherosclerotic patients, some profit from the presence of extensive collateral networks, whereas others do not. Cardiovascular risk factors could increase the risk of adverse cardiovascular events in certain patients because of the reduced protection through an alternative vascular network. Likewise, drugs primarily thought to control cardiovascular risk factors might contribute or counteract collateral artery growth. This review summarizes current knowledge on the influence of cardiovascular risk factors and the effects of cardiovascular medication on the development of collateral vessels in experimental and clinical studies.
