Non-triggered quantification of central and peripheral pulse-wave velocity
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RESEARCH
Open Access
Non-triggered quantification of central and peripheral pulse-wave velocity Michael C Langham, Cheng Li and Felix W Wehrli*
Abstract Purpose: Stiffening of the arteries results in increased pulse-wave velocity (PWV), the propagation velocity of the blood. Elevated aortic PWV has been shown to correlate with aging and atherosclerotic alterations. We extended a previous non-triggered projection-based cardiovascular MR method and demonstrate its feasibility by mapping the PWV of the aortic arch, thoraco-abdominal aorta and iliofemoral arteries in a cohort of healthy adults. Materials and Methods: The proposed method “simultaneously” excites and collects a series of velocity-encoded projections at two arterial segments to estimate the wave-front velocity, which inherently probes the highfrequency component of the dynamic vessel wall modulus in response to oscillatory pressure waves. The regional PWVs were quantified in a small pilot study in healthy subjects (N = 10, age range 23 to 68 yrs) at 3T. Results: The projection-based method successfully time-resolved regional PWVs for 8-10 cardiac cycles without gating and demonstrated the feasibility of monitoring beat-to-beat changes in PWV resulting from heart rate irregularities. For dul-slice excitation the aliasing was negligible and did not interfere with PWV quantification. The aortic arch and thoracoabdominal aorta PWV were positively correlated with age (p < 0.05), consistent with previous reports. On the other hand, the PWV of the iliofemoral arteries showed decreasing trend with age, which has been associated with the weakening of muscular arteries, a natural aging process. Conclusion: The PWV map of the arterial tree from ascending aorta to femoral arteries may provide additional insight into pathophysiology of vascular aging and atherosclerosis.
Background In elastic arteries, e.g. aorta and carotid arteries, the repeated mechanical loading fragments and degrades elastin and is replaced by much stiffer collagen giving rise to decreased wall distensibility [1]. Aortic stiffness can be assessed via quantification of pulse-wave velocity (PWV), which is defined as the rate at which blood motion is transmitted. It is typically quantified by measuring the time delay of the systolic pressure wave at some downstream location, using pressure transducers [2,3] or Doppler US [4] placed at the two locations (typically carotid and common femoral arteries). The method has significant limitations in that the actual path length of the wave is not known. Further, arterial tortuosity increases with age and can vary from subject to subject [5]. By contrast, cardiovascular magnetic resonance (CMR) allows an accurate measurement of the * Correspondence: [email protected] Department of Radiology, University of Pennsylvania Medical Center, 3400 Spruced Street, Philadelphia, (19104), USA
path length and provides regional differences in aortic stiffness [6-9]. Cardiac-gated phase contrast CMR in the sagittal plane [8,10], “pencil beam” excitation [11,12]
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