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Arterial calcification: A new perspective?
1Department of Public Health and Clinical Medicine, Umeå University, Heart Centre, Umea, Sweden.
Insights
Arterial calcification may be a protective immune response to endothelial injury, not a disease progression. Treating the causes of endothelial injury, rather than calcification itself, is proposed.
Area of Science:
- Cardiovascular Research
- Nephrology
- Immunology
Background:
- Arterial calcification is prevalent in atherosclerosis, chronic kidney disease (CKD), and diabetes.
- Current understanding views calcification as a pathological progression, with no effective regression treatments; lipid-lowering therapies may exacerbate it.
- Existing research links calcification to biomarkers but lacks a unifying mechanism for its diverse associations with cardiovascular events.
Purpose of the Study:
- To challenge the conventional view of arterial calcification as a pathological process.
- To propose a novel hypothesis for the pathogenesis of arterial calcification.
- To suggest a new therapeutic strategy focusing on endothelial injury.
Main Methods:
- Review of existing literature on arterial calcification, atherosclerosis, CKD, and diabetes.
- Analysis of associations between calcification, biomarkers, and cardiovascular events.
- Formulation of a new hypothesis based on immunological principles.
Main Results:
- Arterial calcification is observed across various conditions and is not consistently causal in cardiovascular events.
- Calcification's presence or absence can predict plaque rupture, suggesting a complex, non-pathological role.
- Lipid-lowering therapies do not regress calcification and may worsen it, contradicting a purely pathological model.
Conclusions:
- Arterial calcification is hypothesized to be an immune response to endothelial injury, acting as a defense mechanism.
- This immune response hypothesis explains calcification's protective role against plaque rupture and its unresponsiveness to lipid-lowering agents.
- Future research and treatment should focus on preventing and treating endothelial injury, not arterial calcification itself.
Abstract:
Arterial calcification is commonly seen in atherosclerosis, chronic kidney disease (CKD) and diabetes and has long been considered a natural progression of atherosclerosis. Yet it is a systemic condition, occurring in a wide and diverse range of disease states and no medical treatment for cardiovascular disease has yet found a way to regress it; on the contrary, lipid-lowering therapy may worsen its progression. Although numerous studies have found associations between calcification and biomarkers, none has yet found a unifying mechanism that explains the calcification found in atherosclerosis, CKD or diabetes and many of the biomarkers are equally associated with atheroma development and cardiovascular events. Furthermore, both presence and absence of coronary artery calcification appear predictive of plaque rupture and cardiovascular events, indicating that the association is not causal. This suggests that we are no further forward in understanding the true nature of arterial calcification or its pathogenesis, other than noting that it is 'multifactorial'. This is because most researchers view arterial calcification as a progressive pathological condition which must be treated. Instead, we hypothesise that calcification develops as an immune response to endothelial injury, such as shear stress or oxidative stress in diabetics, and is consequently part of the body's natural defences. This would explain why it has been found to be protective of plaque rupture and why it is unresponsive to lipid-lowering agents. We propose that instead of attempting to treat arterial calcification, we should instead be attempting to prevent or treat all causes of endothelial injury.
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