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.