Pulse wave velocity (PWV) is the velocity at which the blood pressure pulse propagates through the circulatory system, usually an artery or a combined length of arteries.
[2][3][4] cfPWV is reproducible,[5] and predicts future cardiovascular events and all-cause mortality independent of conventional cardiovascular risk factors.
[8] The theory of the velocity of the transmission of the pulse through the circulation dates back to 1808 with the work of Thomas Young.
[9] The relationship between pulse wave velocity (PWV) and arterial wall stiffness can be derived from Newton's second law of motion (
For an incompressible fluid (blood) in a compressible (elastic) tube (e.g. an artery):[11]
This is the equation derived by Otto Frank,[12] and John Crighton Bramwell and Archibald Hill.
The Moens–Korteweg equation: characterises PWV in terms of the incremental elastic modulus
It was derived independently by Adriaan Isebree Moens and Diederik Korteweg and is equivalent to the Frank / Bramwell Hill equation:[11]: 64 These equations assume that: Since the wall thickness, radius and incremental elastic modulus vary from blood vessel to blood vessel, PWV will also vary between vessels.
[11] Most measurements of PWV represent an average velocity over a path length consisting of several vessels (e.g. from the carotid to the femoral artery).
[14] PWV intrinsically varies with blood pressure.
Some general approaches are: PWV, by definition, is the distance traveled (
, in practice this approach is complicated by the existence of reflected waves.
[11] It is widely assumed that reflections are minimal during late diastole and early systole.
[11] With this assumption, PWV can be measured using the `foot' of the pressure waveform as a fiducial marker from invasive or non-invasive measurements; the transit time corresponds to the delay in arrival of the foot between two locations a known distance apart.
Locating the foot of the pressure waveform can be problematic.
[17] This is based on the method described by Bramwell & Hill[18] who proposed modifications to the Moens-Kortweg equation.
Quoting directly, these modifications were: "A small rise
This permits calculation of local PWV in terms of
, as detailed above, and provides an alternative method of measuring PWV, if pressure and arterial dimensions are measured, for example by ultrasound[19][20] or magnetic resonance imaging (MRI).
[21] The Water hammer equation expressed either in terms of pressure and flow velocity,[22] pressure and volumetric flow, or characteristic impedance[23] can be used to calculate local PWV:
This approach is only valid when wave reflections are absent or minimal, this is assumed to be the case in early systole.
[24] A related method to the pressure-flow velocity method uses vessel diameter and flow velocity to determine local PWV.
gives a 'lnDU-loop', and the linear portion during early systole, when reflected waves are assumed to be minimal, can be used to calculate PWV.
Clinically, PWV can be measured in several ways and in different locations.
The 'gold standard' for arterial stiffness assessment in clinical practice is cfPWV,[3][4] and validation guidelines have been proposed.
[26] Other measures such as brachial-ankle PWV and cardio-ankle vascular index (CAVI) are also popular.
[27] For cfPWV, it is recommended that the arrival time of the pulse wave measured simultaneously at both locations, and the distance travelled by the pulse wave calculated as 80% of the direct distance between the common carotid artery in the neck and the femoral artery in the groin.
[3] Numerous devices exist to measure cfPWV;[28][29] some techniques include: Newer devices that employ an arm cuff,[30] fingertip sensors[31] or special weighing scales[32] have been described, but their clinical utility remains to be fully established.
Current guidelines by the European Society of Hypertension state that a measured PWV larger than 10 m/s can be considered an independent marker of end-organ damage.
[15] A high pulse wave velocity (PWV) has also been associated with poor lung function.