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.