Published online before print August 28, 2006, doi: 10.1161/01.HYP.0000238325.41764.41
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(Hypertension. 2006;48:543.)
© 2006 American Heart Association, Inc.
Editorial Commentaries |
Triangulating the Peaks of Arterial Pressure
From Cardiovascular Engineering, Inc, Waltham, Mass.
Correspondence to Gary F. Mitchell, Cardiovascular Engineering, Inc, University Office Park, Building 2, 51 Sawyer Rd, Suite 100, Waltham, MA 02453. E-mail GaryFMitchell@mindspring.com
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Increased arterial stiffness and excessive pressure pulsatility have emerged as important risk factors for a number of common disorders of aging, including cardiovascular disease, stroke, cognitive impairment, and renal disease. The triple-threat combination of robust associations between arterial stiffness and the foregoing disorders, a marked increase in arterial stiffness with advancing age and the graying of our society, has led to intensive efforts to identify mechanisms that contribute to arterial stiffening and widening pulse pressure to define interventions to prevent or reverse stiffness and potentially reduce the substantial burden of related disease.
Wave reflections complicate the task of evaluating arterial hemodynamics and play an unclear role in the foregoing diseases. When the heart ejects, ventricular outflow interacts with characteristic impedance of the proximal aorta to produce the forward pressure wave, which travels down the normally compliant aorta at a finite pulse wave velocity (PWV). When the forward wave encounters impedance mismatch, such as a branch point or a change in diameter or wall properties, a partial reflection occurs. Innumerable reflections arising from locations distributed throughout the arterial tree summate into a remarkably discrete reflected pressure wave with amplitude 
40% of the incident wave. The summated reflected wave returns to the central aorta in midsystole, creating an inflection point and secondary late systolic pressure rise that often augments central aortic systolic and pulse pressure.1 Variable timing of this retrograde-traveling reflected wave creates regional inequalities in systolic and pulse pressure and, therefore, complicates interpretation of single point pressure measurements, such as standard
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