Published online before print December 10, 2007, doi: 10.1161/HYPERTENSIONAHA.107.101196
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Hypertension. 2008;51:33.)
© 2008 American Heart Association, Inc.
Editorial Commentaries |
Pathogenesis of Elevated Peripheral Pulse Pressure
Some Reflections and Thinking Forward
From the National Heart, Lung, and Blood Institute’s Framingham Heart Study; the Cardiology Section, and the Department of Preventive Medicine and Epidemiology, Boston University School of Medicine, Boston, Mass.
Correspondence to Ramachandran S. Vasan, MD, FACC, Framingham Heart Study, 73 Mount Wayte Avenue, Suite 2, Framingham, MA 01702-5803. E-mail vasan@bu.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
 |
Introduction |
|---|
"Ashes to ashes, dust to dust, if the cancer don’t get us, the arteriosclerosis must"— —Richard Gordon in The Alarming History of Medicine, 1993
Substantial evidence suggests that arterial remodeling evolves over a life course under the conjoint influence of genes, environmental factors (including vascular risk factors), and lifestyle characteristics (such as diet and physical activity).1 Such arterial remodeling involves multiple vascular territories and is panarterial, ie, it involves all layers of the arterial wall.1 More recently, considerable attention has focused on the physiological aspects of propagation of blood within the aorta, and several important concepts have evolved. First, the aorta is no longer regarded as just a passive conduit that transports blood to the vital organs. Rather, it is a complex organ that remodels in dynamic fashion in response to biomechanical stresses that accumulate over the life course.1 The different segments of the aorta vary in their relations to risk factors, underscoring the heterogeneity in remodeling characteristics across the arterial tree.2 Second, age-associated changes in the aortic wall include fragmentation of the elastin fibers, increased synthesis of collagen, and calcification. The molecular epidemiology of these vascular remodeling changes have been well characterized, and are complex, being mediated via the interaction of vascular smooth muscle cells, integrins, metalloproteinases, endothelial function, and the renin-angiotensin axis, inflammation, and other pathways.1 Third, vascular flow propagation is the combination of steady flow (mean arterial pressure) and pulsatile (pulse pressure) components. The proximal (central) aorta stiffens with age, and these changes are associated with
Related Article:
Hypertension 2008 51: 105-111.
This article has been cited by other articles:
 |
|
 |
|
  M. Namasivayam, B. J. McDonnell, C. M. McEniery, M. F. O'Rourke, and on behalf of the Anglo-Cardiff Collaborative Trial Does Wave Reflection Dominate Age-Related Change in Aortic Blood Pressure Across the Human Life Span? Hypertension, June 1, 2009; 53(6): 979 - 985. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Ingelsson, M. J. Pencina, D. Levy, J. Aragam, G. F. Mitchell, E. J. Benjamin, and R. S. Vasan Aortic Root Diameter and Longitudinal Blood Pressure Tracking Hypertension, September 1, 2008; 52(3): 473 - 477. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Richart, T. Kouznetsova, H. Struijker-Boudier, and J. A. Staessen Wave Reflection in Systolic Hypertension: Smaller Stature, Shorter Aorta: Higher Pulse Pressure? Hypertension, May 1, 2008; 51(5): e37 - e37. [Full Text] [PDF]
|
|
|
|
|
|
G. F. Mitchell, P. R. Conlin, M. E. Dunlap, Y. Lacourciere, J. M. O. Arnold, R. I. Ogilvie, J. Neutel, J. L. Izzo Jr, and M. A. Pfeffer Response to Wave Reflection in Systolic Hypertension: Smaller Stature, Shorter Aorta: Higher Pulse Pressure? and Questions Regarding the Aortic Measurements of Mitchell et al Hypertension, May 1, 2008; 51(5): e39 - e40. [Full Text] [PDF]
|
|