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Published on: May 3, 2018
Central artery stiffness and thoracic aortopathy
J D Humphrey1,2, G Tellides3,2
1Department of Biomedical Engineering, Yale University , New Haven, Connecticut.
Insights
Thoracic aortopathy, including aneurysms and dissections, is linked to hypertension and aging. Understanding mechanical stress on the aorta is crucial for developing new treatments for these dangerous conditions.
Area of Science:
- Cardiovascular Medicine
- Biomedical Engineering
- Genetics
Background:
- Thoracic aortopathy, encompassing aneurysms, dissections, and ruptures, is a major cause of illness and death.
- Hypertension and aging are key risk factors, increasing mechanical stress and structural weakness in the aorta.
- Genetic mutations affecting mechanosensing and extracellular matrix regulation are implicated in thoracic aortopathy.
Purpose of the Study:
- To review the impact of central artery stiffening on thoracic aortic biomechanics and hemodynamics.
- To discuss the role of mechanical factors in various thoracic aortopathies, using Marfan syndrome as an example.
- To emphasize the need for biomechanical phenotyping and the utility of mouse models in understanding disease mechanisms.
Main Methods:
- Review of existing literature on thoracic aortopathy, hypertension, aging, and genetics.
- Discussion of hemodynamic principles, including central artery stiffening and pulse pressure.
- Consideration of biomechanical phenotyping and animal models for disease research.
Main Results:
- Central artery stiffening increases pulse pressure, exacerbating mechanical stress on the proximal thoracic aorta.
- Dysfunctional mechanosensing and extracellular matrix regulation contribute to thoracic aortopathy.
- Current non-surgical treatments focus on reducing mechanical load, such as antihypertensive medications.
Conclusions:
- Central artery stiffening plays a critical role in thoracic aortopathy, similar to its known role in other end-organ diseases.
- Biomechanical phenotyping of the aorta is essential for a comprehensive understanding of thoracic aortopathy.
- Further research using mouse models can elucidate molecular and mechanical mechanisms underlying these conditions.
Abstract:
Thoracic aortopathy, especially aneurysm, dissection, and rupture, is responsible for significant morbidity and mortality. Uncontrolled hypertension and aging are primary risk factors for such conditions, and they contribute to an increase in the mechanical stress on the wall and an increase in its structural vulnerability, respectively. Select genetic mutations also predispose to these lethal conditions, and the collection of known mutations suggests that dysfunctional mechanosensing and mechanoregulation of the extracellular matrix may contribute to pathogenesis and disease progression. In the absence of a well-accepted pharmacotherapy, nonsurgical treatments tend to focus on reducing the mechanical loading on the aorta, particularly via the use of antihypertensive medications and recommendations to avoid strenuous exercises such as weight lifting. In this brief review, we discuss the important effects of central artery stiffening on global hemodynamics and, in particular, on the increase in pulse pressure that acts on the proximal thoracic aorta. We consider Marfan syndrome as an illustrative aortopathy but discuss other conditions leading to thoracic aortic aneurysm and dissection. We highlight the importance of phenotyping the aorta biomechanically, not just clinically, and emphasize the utility of mouse models in elucidating molecular and mechanical mechanisms of disease. Notwithstanding the widely recognized role of central artery stiffening in driving end-organ disease, we suggest that there is similarly a need to consider its key role in thoracic aortopathy.
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