Intrinsic velocity propagation of myocardial stretch (iVP)
Left ventricular inflow through the mitral valve during systole and
diastole has been well described and evaluated by cardiac ultrasound
after a very comprehensive functional study, but in addition to inflow,
we can also perform corresponding functional studies from the point of
view of myocardial motion. Apart from the functional evaluation of the
velocity of annular and ventricular wall motion using tissue Doppler
techniques, the perspective of the intrinsic wave transmission of the
myocardium has become a new research hotspot.
These waves may have a mechanism
similar to pulse wave propagation in arteries. An earlier study
described a sequential onset of circumferential lengthening in different
parts of the LV, which is suggestive of a wave propagating from LV base
to apex.(54) Based on this, a
hypothesis has been proposed that the ventricular filling that begins
after atrial contraction stretches the base of the left ventricle,
producing a wave that propagates apically with a velocity proportional
to the elasticity of the myocardial wall (Figure 2C). In 2014, Pislaru
C, et al.(55) found in basic animal experiments that the main factors
determining myocardial longitudinal stretch wave propagation were LV
myocardial stiffness and left ventricular geometry and pressure
(r2 model=0.83, p<0.0001), and the stiffer
the myocardium, the faster the intrinsic propagation of the
myocardium(Vp was higher at reperfusion compared to baseline: 2.6 ± 1.3
vs. 1.3 ± 0.4 m/s, p = 0.005). Thereafter, several studies investigated
the alterations of iVP in different populations. Strachinaru M et al.
(56)and Zhang J et al.(57) found that iVP was significantly higher in
patients with hypertrophic cardiomyopathy (1.8±0.3m/s vs.1.6±0.3m/s,
P=0.14) and hypertension (1.53±0.39 m/s vs 1.40±0.19 m/s, p=0.031)
compared to normal healthy controls. Similar findings were also found in
patients with aortic Stenosis and mitral regurgitation(58) (AS 2.2±0.7
m/sec vs MR 1.6±0.5 m/sec vs control subjects 1.4±0.2 m/sec,
P<0.0001). These studies, side-by-side, hint at changes in LV
myocardial stiffness and may be a predictor of poor prognosis. Pislaru
C,et al. (58) showed a lower survival free of major adverse cardiac
events in patients with high iVP in their study of patients with aortic
stenosis and mitral regurgitation (P = 0.002). It is worth noting that
iVP also increased in patients with normal left ventricular systolic
function (LVEF and GLS), suggesting that increased LV myocardial
stiffness may precede systolic dysfunction. This provides a direction
for early identification of HFpEF. Measuring the changes of myocardial
elasticity is helpful to evaluate the changes of cardiac structure and
function caused by the changes of LV myocardial stiffness. However, the
iVP still has its limitations: first, there is no gold standard (cardiac
catheterization) validation both in animal and clinical studies.
Secondly, the heart is not a circular tube and its motion is torsional,
which contradicts the original intention of the Moens-Korteweg theory,
which postulates that the structure is a cylindrical tube, wall is
homogenous and thin compared to radius, thickness is constant, and there
are no reflections.Third, because of the extremely high frame rate
required, this parameter may not be suitable in patients with enlarged
chambers.