The Epicardial movement index (EMI) and Diastolic wall strain (DWS)
Researchers hypothesized that the evaluation of epicardial movement during diastole is helpful for the noninvasive assessment of LV wall distensibility following the linear elastic theory(38). Based on the laws of physics, when applying an active external force on the surface of an object, the difference between the movement of the surface and the outside should be equal to the change in the deformation of the object. In soft tissue, the effect of surface movement on the outside is small when the ventricular wall is thinning, and in hard tissue, the opposite result occurs because of less change in the wall thickness. It is assumed that the deformation of the ventricular wall under pressure also follows this principle, which is obtained with the following indices: epicardial movement index (EMI) = (endocardial movement during diastole - epicardial movement during diastole)/(wall thickness at the beginning of diastole × epicardial movement during diastole). Because the movement of the epicardium during diastole is small, to better fit the clinical application, the researchers simplified EMI to obtain the diastolic wall strain (DWS): DWS = (LV posterior wall thickness at end-systole - LV posterior wall thickness at end-diastole) / (LV posterior wall thickness at end-systole) (Figure 2B). In animal model studies, Yasushi Sakata’s team(38) not only proved that DWS can replace EMI, but also that there is an inverse correlation between EMI or DWS and the LV myocardial stiffness constant (r = -0.40, r = -0.47, P<0.05, respectively). Preload alteration did not affect EMI or DWS (before 0.48 ± 0.04 vs. after 0.55 ± 0.03 [1/mm], P = 0.18) or DWS (before 0.45 ± 0.02 vs. after 0.48 ± 0.02, P=0.39).
Thereafter, amounts of studies investigated the alterations of DWS in different populations. Both Sakata et al.(38) (0.26 ± 0.02 vs. 0.35 ± 0.02, P<0.05) and Ohtani et al. (39) (0.33 ± 0.08 vs. 0.40 ± 0.07, P<0.001) found DWS was significantly lower in patients with HFpEF compared to healthy controls. Similar findings were also found in patients with paroxysmal atrial fibrillation and structurally normal hearts (40) (0.35 ± 0.07 vs. 0.41 ± 0.06, P<0.001), in adult survivors of childhood leukemias with HFpEF(41) (0.28 ±0.07 vs 0.33 ± 0.07, P<0.001), in patients with repaired tetralogy of fallot (42) (0.38 ±0.10 vs 0.47 ±0.08, P<0.001), in adolescents and young adults after arterial switch operation for transposition of the great arteries(43) (0.30 ±0.09 vs 0.41 ±0.08, P<0.001) as well as in pediatric patients with end stage kidney disease (44) (dialysed group vs transplanted group vs healthy controls: 0.37 ±0.07 vs 0.35 ± 0.05 vs 0.47 ± 0.08, P<0.001).
The decrease in DWS in multiple disease populations is another reminder that LV myocardial stiffness is quietly changing in these patient groups, and may be a precursor to certain adverse events. In a study of patients with paroxysmal atrial fibrillation and structurally normal hearts, Uetake S et al. (40) found that a low DWS (< 0.38) was the strongest indicator of AF prevalence (OR: 1.22, 95% CI: 1.14-1.31 per 0.01 decrease, P<0.001). In 2017, Choij et al.(45) found that patients with stable angina who underwent revascularization had a significantly lower DWS than those who did not (0.26 ±0.08 vs 0.38 ± 0.09, P<0.001) and decreased DWS was associated with coronary revascularization (OR: 0.920, 95% CI 0.862–0.981, P=0.011). Immediately thereafter, Amano M et al.(46) found that DWS was an independent predictor of prognosis in the diagnosis of patients with AL amyloidosis with cardiac involvement during follow-up of patients, and DWS was significantly lower in patients with poor prognosis (all-cause death and cardiac death: HR 0.93 [95% CI 0.88- 0.99], P<.02). The same predictive value of DWS was shown by Obasare E et al.(47) in a retrospective study of patients with severe aortic stenosis, where DWS could predict mortality independently of conventional clinical and echocardiographic parameters (HR 2.5 [95% CI 1.02- 5.90], P<.05). In 2020, Kishima H et al.(48) a retrospective study of patients with PMI study showed that DWS was independently associated with AHREs (HR 0.223, 95% CI 0.137–0.357, P<0.0001), and patients with reduced DWS (<0.33) had a higher risk of incidences of AHREs.
For the patients with preserved ejection fraction, Ohtani et al. (39) in 2012 found that HFpEF patients with DWS ≤ 0.33 had a higher rate of death or HF hospitalization than those with DWS > 0.33, even after adjustment for age, sex, log B-type natriuretic peptide, LV geometry and log E/e’. Similarly, Kamimura D et al.(49) in 2017 found DWS to be significantly associated with HF symptoms in patients with AS with preserved ejection fraction (OR: 0.91, CI:0.86-0.96, P<0.005). Immediately thereafter, in 2018,Kamimura D et al.(50) found both continuous and categorical DWS were independently associated with incident HF after adjustment for traditional risk factors and incident coronary artery disease (HR 1.21, 95%CI 1.04–1.41 for 0.1 decrease in continuous DWS, P= 0.014; HR 1.40, 95%CI 1.05–1.87 for the smallest DWS quintile vs other combined quintiles, P = 0.022), and in 2019 a study by Tsujimoto S, et al.(51) showed low DWS (≤ 0.33) was a significant independent predictor of cardiovascular events after adjusting for cardiovascular comorbidities in a multivariable model (HR: 1.87, 95% CI 1.04–3.36, P=0.04). In addition, DWS has also a predictive value even in patients with reduced ejection fraction. In 2017, Soyama Y.et al. (52)found that the incidence rate (HF hospitalization or cardiovascular death) was higher in low DWS than high DWS HFrEF patients who were administrated chronic beta (Log-rank, p = 0.049), and showed DWS was the independent contributor to the event-free time(HR 2.66 [95% CI 1.10- 6.85], P=0.032).
Taken together, these findings suggested that DWS, a simple parameter, might be useful in assessing LV myocardial stiffness and predicting worse outcomes in various populations. However, the relationship between DWS and LV myocardial stiffness constant which is the gold standard to evaluate LV myocardial stiffness, was proved only in a basic experimental study and a correlation of only 0.4 does not ”prove” that the LV myocardial stiffness could be accurately reflected by DWS. In addition, despite the animal study from Takeda et al proved that there was a lack of correlation between DWS and LV systolic function, wall thickness at the beginning of diastole, LV chamber size, indices derived from the transmitral flow velocity curves as well as preload alteration, recent clinical studies(43, 46, 47, 50, 53) found that DWS may not be a pure measure of diastolic function since it also correlates with systolic function. Therefore, DWS may be considered as an overall marker of cardiac performance, including systolic and diastolic mechanics. Furthermore, DWS is an abbreviated term from the original equation that sought to quantify LV stiffness, the epicardial motion index (DWS)/(epicardial movement during diastole). Though the epicardial motion index is a more exact marker of LV diastolic stiffness, this formula requires direct measurement of epicardial movement, which is difficult to achieve with 2D echocardiography. The epicardial motion index may better reflect LV diastolic stiffness compared to DWS, but its difficult implementation in routine clinical practice would reduce its clinical utility. Another important point is that regional assessment of LV stiffness at the posterior wall may not reflect global LV myocardial stiffness. Therefore, the role of DWS in the evaluation of LV myocardial stiffness awaits further study.