Age-related changes of regional pulse wave velocity in the descending aorta using Fourier velocity encoded M-mode.
ABSTRACT Aortic pulse wave velocity (PWV) is an independent determinant of cardiovascular risk. Although aortic stiffening with age is well documented, the interaction between aging and regional aortic PWV is still a debated question. We measured global and regional PWV in the descending aorta of 56 healthy subjects aged 25-76 years using a one-dimensional, interleaved, Fourier velocity encoded pulse sequence with cylindrical excitation. Repeatability across two magnetic resonance examinations (n = 19) and accuracy against intravascular pressure measurements (n = 4) were assessed. The global PWV was found to increase nonlinearly with age. The thoracic aorta was found to stiffen the most with age (PWV [thoracic, 20-40 years] = 4.7 ± 1.1 m/s; PWV [thoracic, 60-80 years] = 7.9 ± 1.5 m/s), followed by the mid- (PWV [mid-abdominal, 20-40 years] = 4.9 ± 1.3 m/s; PWV [mid-abdominal, 60-80 years] = 7.4 ± 1.9 m/s) and distal abdominal aorta (PWV [distal abdominal, 20-40 years] = 4.8 ± 1.4 m/s; PWV [distal abdominal, 60-80 years] = 5.7 ± 1.4 m/s). Good agreement was found between repeated magnetic resonance measurements and between magnetic resonance PWVs and the gold-standard. Fourier velocity encoded M-mode allowed to measure global and regional PWV in the descending aorta. There was a preferential stiffening of the thoracic aorta with age, which may be due to progressive fragmentation of elastin fibers in this region.
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ABSTRACT: Pulse-wave velocity (PWV) is an important index for diagnosing cardiovascular diseases. The pulse wave is volumetric change induced by heartbeat or inflowing blood, and significantly depends on the propagating path and stiffness of the artery. In this study, PWV of the propagating wave was visualized using spatial compound imaging with high temporal resolution. The frame rate was 1000 Hz, or a time interval of 1ms. Subjects were four young healthy males and one young healthy female (n = 5, age: 23.8 ± 1.17 years old), and the measurement area was the right common carotid artery. PWVs in four phases (the four phases of heart valve opening and closing) were investigated during a cardiac cycle. In phase I, the heart pulsates. In phase II, the tricuspid and mitral valves close, and the aortic and pulmonic valves open. In phase III, the tricuspid and mitral valves open, and the aortic and pulmonic valves close. In phase IV, the propagating wave is reflected. PWVs in phases II and III were easily observed. PWVs were 3.52 ± 1.11 m/s in phase I, 5.62 ± 0.30 m/s in phase II, 7.94 ± 0.85 m/s in phase III, and -4.60 ± 0.99 m/s for the reflective wave. PWV was measured using Spatial Compound Imaging with high temporal resolution, and the PWV in each phase may be used as the index for diagnosing stages of arteriosclerosis progression.Ultrasonics 01/2014; · 2.03 Impact Factor
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ABSTRACT: The objective of this study was to compare multiple methods for estimation of PWV from 4D flow MRI velocity data and to investigate if 4D flow MRI-based PWV estimation with piecewise linear regression modeling of travel-distance vs. travel time is sufficient to discern age-related regional differences in PWV.Magnetic Resonance Imaging 08/2014; · 2.06 Impact Factor
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ABSTRACT: Atherosclerosis is the leading cause of cardiovascular disease (CVD) in the Western world. In the early development of atherosclerosis, vessel walls remodel outwardly such that the vessel luminal diameter is minimally affected by early plaque development. Only in the late stages of the disease does the vessel lumen begin to narrow-leading to stenoses. As a result, angiographic techniques are not useful for diagnosing early atherosclerosis. Given the absence of stenoses in the early stages of atherosclerosis, CVD remains subclinical for decades. Thus, methods of diagnosing atherosclerosis early in the disease process are needed so that affected patients can receive the necessary interventions to prevent further disease progression. Pulse wave velocity (PWV) is a biomarker directly related to vessel stiffness that has the potential to provide information on early atherosclerotic disease burden. A number of clinical methods are available for evaluating global PWV, including applanation tonometry and ultrasound. However, these methods only provide a gross global measurement of PWV-from the carotid to femoral arteries-and may mitigate regional stiffness within the vasculature. Additionally, the distance measurements used in the PWV calculation with these methods can be highly inaccurate. Faster and more robust magnetic resonance imaging (MRI) sequences have facilitated increased interest in MRI-based PWV measurements. This review provides an overview of the state-of-the-art in MRI-based PWV measurements. In addition, both gold standard and clinical standard methods of computing PWV are discussed.Cardiovascular diagnosis and therapy. 04/2014; 4(2):193-206.
Age-related changes of regional pulse wave velocity in the descending aorta using Fourier velocity encoded MR M-mode
V. Taviani1, S. S. Hickson2, C. J. Hardy3, A. J. Patterson1, C. M. McEniery2, I. B. Wilkinson2, J. H. Gillard1, and M. J. Graves1
1Department of Radiology, University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom, 2Clinical Pharmacology Unit, University of Cambridge,
Addenbrooke's Hospital, Cambridge, United Kingdom, 3GE Global Research, Niskayuna, New York, United States
Central arteries, like the aorta, play a crucial role in buffering and attenuating the pulsatile nature of blood flow. Aging is the most important process involved in altering
arterial compliance. Over time, stiffening of the aorta reduces its buffering function, with adverse consequences on the left ventricle  and more peripheral arteries .
Although aortic stiffening with age has been extensively documented , the interplay between aging and regional arterial compliance is still a debated question, with
major implications for therapeutic interventions.
Previous MR studies have addressed the problem of quantifying regional arterial compliance either by direct measurement of arterial distensibility  or by pulse wave
velocity (PWV) measurement using cine phase contrast (CPC) with through-plane velocity encoding . Direct measurements of arterial distensibility are limited by the
fact that local pulse pressure is difficult to evaluate. The accuracy of PWV measurements by PC with through-plane velocity encoding can be degraded when short
arterial segments are considered. Fourier velocity encoded (FVE) M-mode can produce time-velocity profiles with high temporal and spatial resolution along a
relatively straight arterial segment . The aim of this work was to measure regional PWV in the descending aorta using FVE M-mode in a large cohort of healthy
subjects and to investigate the interplay between regional aortic stiffening and age.
Fifty-six healthy subjects (age range: 25-76 years, mean age: 53.1 years) participated in the study after providing written informed consent. All subjects were
normotensive and free from cardiovascular disease and medication. Images were acquired on a 1.5T whole-body imaging system (Signa HDx, GE Healthcare,
Waukesha, WI) using an 8-channel abdo-torso phased-array surface coil.
An ECG-triggered, oblique-sagittal double inversion recovery prepared fast spin-echo (FSE) sequence was used to localize the descending aorta (Figure 1a). The FVE
M-mode sequence consisted of a cylindrical excitation pulse, followed by a bipolar velocity-encoding gradient and a readout gradient applied along the axis of the
cylinder (pencil) . The sequence was gated to the cardiac R-wave and executed 32 times per heart cycle with the bipolar gradient amplitude stepped to a new value on
each new trigger. To increase the effective temporal resolution to 3.5ms, four interleaves were acquired, with the ECG trigger delay incremented by 3.5ms each time,
resulting in 128 time frames covering the first 450ms of the cardiac cycle. Thirty-two velocity-encoding steps were used, yielding a true velocity resolution of 9.4cm/s,
which resulted in aliasing of velocities greater than 150cm/s. A 24cm readout field of view (matrix size = 256×32) and a 2cm diameter cylindrical excitation pulse were
prescribed. Cylindrical excitation was achieved through an 8-cycle spiral trajectory which resulted in an inner aliasing ring diameter of 28.5cm.
FVE M-mode images (Figure 1b) were reformatted to yield Doppler-like time-velocity images (Figure 1c) along the length of the pencil . An automatic line detector
was used to extract the velocity profile as a function of time from each of the time-velocity images. The velocity profiles extracted from the time-velocity images at
different spatial positions were visualized as a velocity surface, each point of which represented velocity at a given time and position. Bilinear interpolation and the
gradient-based regularization technique, implemented in the Matlab (The Mathworks, Inc., Natick, MA) function gridfit , were used to smooth the obtained velocity
surface, with the smoothing parameter chosen for each subject on the basis of visual comparison with the original data points. The foot of the velocity wave was defined
at each spatial location as the intersection between a line fitted to the early systolic upslope (10% to 40% of peak velocity) and the zero velocity line.
Four planes, orthogonal to the descending aorta, were defined on the FSE scout image: 1) 2cm distal to the aortic valve; 2) at the level of the diaphragm; 3) midway
between location 2) and a location 3cm proximal to the aortic bifurcation; 4) 3cm above the aortic bifurcation (Figure 1a). PWV was computed over the entire length of
the pencil and for the three segments delimited by these planes, by linear regression of the foot of the wave at each position along the vessel as a function of the
corresponding location along the aorta (Figure 1d). Repeatability of segmental PWV was evaluated on a smaller cohort of 10 volunteers over two visits, a week apart.
Repeated regional PWVs were in good agreement (mean difference=0.19±0.82cm/s). A significant nonlinear relationship between overall PWV and age was found (2nd
order polynomial regression: r2=0.73, p<0.001) (Figure 2), confirming previous results . Overall PWV was found to decrease along the aorta (PWV1=6.4±2.1m/s;
PWV2=6.0±1.9m/s; PWV3=5.2±1.5m/s), with PWV3 significantly lower than both PWV1 and PWV2 (p<0.05). Two-way ANOVA showed a significant interplay
between age and position (p<0.01) (Figure 3). The distal thoracic aorta was found to stiffen the most with age (Seg1, PWV1(20-40ys)=4.7±1.1m/s; PWV1(60-
80ys)=7.9±1.5m/s), followed by the proximal (Seg2, PWV1(20-40ys)=4.9±1.3m/s; PWV1(60-80ys)=7.4±1.9m/s) and distal abdominal aorta (Seg3, PWV1(20-
Although peripheral arteries have been found to be stiffer than central arteries , the existing data concerning the descending part of the aorta are contradictory,
probably due to the small sample size and the different techniques used. Our results are in agreement with the two major MR studies conducted to date [4,5] and support
the well-known hypothesis of age-related degradation of elastin , mainly found in the thoracic aorta, as the major determinant of vascular stiffening.
In conclusion, we used the high spatial and temporal resolutions achievable with FVE M-mode to evaluate regional PWV in a large cohort of healthy subjects. We
found a nonlinear relationship between overall PWV and age and a preferential stiffening of the thoracic aorta with age.
Position along the vessel
Position of the foot of the wave
203040 506070 80
PWV [m/s] = 0.002·Age [ys]2 - 0.11·Age [ys] + 5.94
20-40ys 40-60ys 60-80ys
Figure 1 Figure 2 Figure 3
 Kingwell BA, et al. Adv. Cardiol. 2007; 44:125-38.  Agabiti-Rosei E, et al. Adv. Cardiol. 2007; 44:173-86.  McEniery CM, et al. JACC 2005; 46(9):1753-60.
 Nelson AJ, et al. J Hypertens. 2009; 27(3):535-42.  Rogers WJ, et al. JACC 2001; 38(4):1123-9.  Hardy CJ, et al. MRM 1996; 35(6):814-9.  Hardy CJ, et al.
ISMRM08.  FileEx: 8998.  Mitchell GF, et al. Hypertension 2004; 43:1239-45.  Izzo JL, et al. Adv. Cardiol. 2007; 44: 19-34.