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Local pulse pressure is a major determinant of large artery remodelling
S Laurent1, A I Tropeano, A Lillo-Lelouet
1Department of Pharmacology and EMI INSERM 0107, Hôpital Européen Georges Pompidou, Paris, France. stephane.laurent@egp.ap-hop-paris.fr
Insights
Pulse pressure, not mean blood pressure, significantly impacts large artery remodeling and intima-media thickness. Reducing pulse pressure is key for regression of carotid intima-media thickness after treatment.
Area of Science:
- Cardiovascular Physiology
- Arterial Biomechanics
Background:
- Large artery stiffening increases pulse pressure, a risk factor for cardiovascular events.
- Intima-media thickness and arterial diameter changes reflect large artery remodeling.
Purpose of the Study:
- To demonstrate that pulsatile blood pressure is a more significant determinant of large artery remodeling than mean blood pressure.
- To investigate the relationship between pulse pressure and arterial structure in normotensive and hypertensive individuals.
Main Methods:
- Applanation tonometry to measure local pulse pressure.
- Intima-media thickness and internal diameter measurements of carotid and radial arteries.
- Analysis of data from normotensive individuals and patients with essential hypertension.
Main Results:
- Local pulse pressure significantly explains intima-media thickness variance in the carotid artery, but not the radial artery.
- Mean blood pressure did not contribute to intima-media thickness variance in either artery.
- Decreased carotid pulse pressure strongly correlates with the regression of carotid intima-media thickness and internal diameter after antihypertensive treatment.
Conclusions:
- Pulsatile blood pressure, specifically pulse pressure, is a primary driver of large artery remodeling.
- Pulse pressure influences intima-media thickness and arterial diameter, contributing to cardiovascular risk.
- Targeting pulse pressure may be crucial for managing large artery remodeling and preventing cardiovascular events.
Abstract:
1. The aim of the present brief review is to show that the pulsatile component of blood pressure is a stronger determinant of large artery remodelling than the steady component (i.e. mean blood pressure). 2. Pulse pressure, which is a strong determinant of cardiovascular events, including coronary heart disease and stroke, is increased when large arteries stiffen. Local pulse pressure, measured with applanation tonometry in normotensives and patients with essential hypertension, explains a significant part of the variance of intima-media thickness at the site of the carotid artery, a proximal elastic artery, whereas mean blood pressure does not contribute. Local pulse pressure has no influence on intima-media thickness at the site of the radial artery, a distal muscular artery that undergoes very little stroke change in diameter. 3. The decrease in carotid pulse pressure is also a major determinant of the regression of carotid intima-media thickness after antihypertensive treatment. Local pulse pressure can influence not only intima-media thickness, but also internal diameter. Indeed, there is a significant association between the lumen enlargement of the ascending aorta in patients with Marfan syndrome and pulse pressure. In addition, carotid pulse pressure is positively correlated with carotid internal diameter in normotensives and hypertensives, and the decrease in carotid internal diameter during long-term antihypertensive treatment is influenced by the decrease in carotid pulse pressure and not by the reduction in mean blood pressure. 4. We suggest that the effects of pulse pressure on large artery remodelling may explain part of its predictive value on cardiovascular events.