Diastolic Wall Strain Research Articles

Evaluation of diastolic wall strain in patients with mitral valve regurgitation

Background: Diastolic wall strain (DWS) is a non invasive, easy, echocardiographic parameter that has been used to determine left ventricular diastolic stiffness. The relationship between left ventricle functions and diastolic wall strain is previously revealed but we don’t know if this method correlates with mitral regurgitation (MR) severity or not. In this study, we sought to determine the relationship between DWS and MR. Methods: This study included 107 subjects with primary mitral regurgitation, divided in two groups as mild-to-moderate and severe mitral regurgitation, and 54 control subjects. We calculated the DWS from the M-mode echocardiographic measurements of the LV posterior wall thickness at end-systole and end-diastole during sinus rhythm. Results: MR group had lower values of DWS than control subjects and severe MR group had the lowest ones (0.38 ± 0.06; 0.27 ± 0.07; 0.15 ± 0.035 respectively and p

Incremental value of diastolic wall strain in predicting heart failure events in patients with atrial fibrillation.

Diastolic wall strain (DWS), an echocardiographic index based on linear elasticity theory, has been identified as a predictor of heart failure (HF) in patients with sinus rhythm. However, its effectiveness in atrial fibrillation (AF) patients remains uncertain. This study aims to assess DWS as a predictor of HF in AF patients with preserved ejection fraction. We analysed a prospective database of AF patients undergoing transthoracic echocardiography. AF patients with reduced left ventricular ejection fraction (< 50%), posterior wall motion abnormality, hypertrophic cardiomyopathy, valvular heart disease, pericardial disease, congenital heart disease, or history of pacemaker/implantable cardioverter-defibrillator implantation or cardiac surgery were excluded. The study followed patients until HF development, death, or last visit. Follow-up for patients who underwent catheter ablation was censored on the date of their procedure. HF was ascertained based on the Framingham criteria. DWS was calculated using a validated formula: DWS = (PWs -PWd)/PWs, where PWs is the posterior wall thickness at end-systole and PWd is the posterior wall thickness at end-diastole. Among 411 study patients (mean age 69.6 years, 66% men), 20 (5%) was underwent catheter ablation and 57 (14%) developed HF during a mean follow-up of 82 months. Cox-proportional hazards demonstrated that low DWS (≤ 0.33) significantly predicted HF events (hazard ratio [HR] 3.28, 95% confidence interval [CI]) 1.81-5.94, P < 0.0001), independent of age (per 10 years; HR 1.99, 95% CI 1.35-2.93, P < 0.001), indexed left ventricular mass (per 10g/m2; HR 1.16, 95% CI 1.05-1.27, P < 0.01), and indexed left atrial volume (per 10 mL/m2; HR 1.14, 95% CI 1.04-1.24, P < 0.01). Additionally, global log-likelihood ratio chi-square statistics indicated that DWS incrementally predicts HF development beyond age, indexed left ventricular mass, and left atrial volume (P < 0.001).

Evaluation of left ventricular stiffness with echocardiography.

Half of patients with heart failure are presented with preserved ejection fraction (HFpEF). The pathophysiology of these patients is complex, but increased left ventricular (LV) stiffness has been proven to play a key role. However, the application of this parameter is limited due to the requirement for invasive catheterization for its measurement. With advances in ultrasound technology, significant progress has been made in the noninvasive assessment of LV chamber or myocardial stiffness using echocardiography. Therefore, this review aims to summarize the pathophysiological mechanisms, correlations with invasive LV stiffness constants, applications in different populations, as well as the limitations of echocardiography-derived indices for the assessment of both LV chamber and myocardial stiffness. Indices of LV chamber stiffness, such as the ratio of E/e' divided by left ventricular end-diastolic volume (E/e'/LVEDV), the ratio of E/SRe (early diastolic strain rates)/LVEDV, and diastolic pressure-volume quotient (DPVQ), are derived from the relationship between echocardiographic parameters of LV filling pressure (LVFP) and LV size. However, these methods are surrogate and lumped measurements, relying on E/e' or E/SRe for evaluating LVFP. The limitations of E/e' or E/SRe in the assessment of LVFP may contribute to the moderate correlation between E/e'/LVEDV or E/SRe/LVEDV and LV stiffness constants. Even the most validated measurement (DPVQ) is considered unreliable in individual patients. In comparison to E/e'/LVEDV and E/SRe/LVEDV, indices like time-velocity integral (TVI) measurements of pulmonary venous and transmitral flows may demonstrate better performance in assessing LV chamber stiffness, as evidenced by their higher correlation with LV stiffness constants. However, only one study has been conducted on the exploration and application of TVI in the literature, and the accuracy of assessing LV chamber stiffness remains to be confirmed. Regarding echocardiographic indices for LV myocardial stiffness evaluation, parameters such as epicardial movement index (EMI)/ diastolic wall strain (DWS), intrinsic velocity propagation of myocardial stretch (iVP), and shear wave imaging (SWI) have been proposed. While the alteration of DWS and its predictive value for adverse outcomes in various populations have been widely validated, it has been found that DWS may be better considered as an overall marker of cardiac function performance rather than pure myocardial stiffness. Although the effectiveness of iVP and SWI in assessing left ventricular myocardial stiffness has been demonstrated in animal models and clinical studies, both indices have their limitations. Overall, it seems that currently no echocardiography-derived indices can reliably and accurately assess LV stiffness, despite the development of several parameters. Therefore, a comprehensive evaluation of LV stiffness using all available parameters may be more accurate and enable earlier detection of alterations in LV stiffness.

Lifetime evaluation of left ventricular structure and function in male ApoE null mice after gamma and space-type radiation exposure.

The space radiation (IR) environment contains high charge and energy (HZE) nuclei emitted from galactic cosmic rays with the ability to overcome current shielding strategies, posing increased IR-induced cardiovascular disease risks for astronauts on prolonged space missions. Little is known about the effect of 5-ion simplified galactic cosmic ray simulation (simGCRsim) exposure on left ventricular (LV) function. Three-month-old, age-matched male Apolipoprotein E (ApoE) null mice were irradiated with 137Cs gamma (γ; 100, 200, and 400cGy) and simGCRsim (50, 100, 150cGy all at 500 MeV/nucleon (n)). LV function was assessed using transthoracic echocardiography at early/acute (14 and 28days) and late/degenerative (365, 440, and 660days) times post-irradiation. As early as 14 and 28-days post IR, LV systolic function was reduced in both IR groups across all doses. At 14days post-IR, 150cGy simGCRsim-IR mice had decreased diastolic wall strain (DWS), suggesting increased myocardial stiffness. This was also observed later in 100cGy γ-IR mice at 28days. At later stages, a significant decrease in LV systolic function was observed in the 400cGy γ-IR mice. Otherwise, there was no difference in the LV systolic function or structure at the remaining time points across the IR groups. We evaluated the expression of genes involved in hemodynamic stress, cardiac remodeling, inflammation, and calcium handling in LVs harvested 28days post-IR. At 28days post-IR, there is increased expression of Bnp and Ncx in both IR groups at the lowest doses, suggesting impaired function contributes to hemodynamic stress and altered calcium handling. The expression of Gals3 and β-Mhc were increased in simGCRsim and γ-IR mice respectively, suggesting there may be IR-specific cardiac remodeling. IR groups were modeled to calculate the Relative Biological Effectiveness (RBE) and Radiation Effects Ratio (RER). No lower threshold was determined using the observed dose-response curves. These findings do not exclude the possibility of the existence of a lower IR threshold or the presence of IR-induced cardiovascular disease (CVD) when combined with additional space travel stressors, e.g., microgravity.

Association Between Endothelial Dysfunction and Left Ventricular Diastolic Stiffness - Subanalysis of the Flow-Mediated Dilation Japan (FMD-J) Study.

Endothelial dysfunction and increased left ventricular (LV) stiffness are associated with the incidence of heart failure with preserved ejection fraction (HFpEF). This study evaluated the association between endothelial dysfunction and LV diastolic stiffness. Endothelial dysfunction evaluated by flow-medicated vasodilation (FMD) and the reactive hyperemia index (RHI), which reflects endothelial dysfunction in the microvasculature, was measured in 112 subjects with hypertension in the Flow-Mediated Dilation Japan (FMD-J) study. Using transthoracic echocardiography, LV diastolic stiffness was evaluated by measuring diastolic wall strain (DWS) in the LV posterior wall. In this cross-sectional study, associations among FMD, RHI, and DWS were investigated using multiple regression analyses. The mean (±SD) age of the subjects 65±9 years, and 63% were men. DWS was significantly associated with RHI, but not FMD, on multivariate linear regression analysis (β=0.39; P<0.0001). This association was preserved in subjects without LV hypertrophy (β=0.46; P<0.0001). A DWS ≤median, suggesting increased LV diastolic stiffness, was significantly associated with RHI on multivariate logistic regression analysis (odds ratio 20.58; 95% confidence interval 4.83-87.63; P<0.0001). The receiver operating characteristic curve presented a cut-off value of 2.21 for RHI, with a sensitivity of 77% and a specificity of 71%, for DWS ≤median. RHI, rather than FMD, was associated with DWS. Endothelial dysfunction in the microvasculature may be associated with increased LV diastolic stiffness.

Thymidine Phosphorylase Deficiency or Inhibition Preserves Cardiac Function in Mice With Acute Myocardial Infarction.

Background Ischemic cardiovascular disease is the leading cause of death worldwide. Current pharmacologic therapy has multiple limitations, and patients remain symptomatic despite maximal medical therapies. Deficiency or inhibition of thymidine phosphorylase (TYMP) in mice reduces thrombosis, suggesting that TYMP could be a novel therapeutic target for patients with acute myocardial infarction (AMI). Methods and Results A mouse AMI model was established by ligation of the left anterior descending coronary artery in C57BL/6J wild-type and TYMP-deficient (Tymp-/-) mice. Cardiac function was monitored by echocardiography or Langendorff assay. TYMP-deficient hearts had lower baseline contractility. However, cardiac function, systolic left ventricle anterior wall thickness, and diastolic wall strain were significantly greater 4 weeks after AMI compared with wild-type hearts. TYMP deficiency reduced microthrombus formation after AMI. TYMP deficiency did not affect angiogenesis in either normal or infarcted myocardium but increased arteriogenesis post-AMI. TYMP deficiency enhanced the mobilization of bone marrow stem cells and promoted mesenchymal stem cell (MSC) proliferation, migration, and resistance to inflammation and hypoxia. TYMP deficiency increased the number of larger MSCs and decreased matrix metalloproteinase-2 expression, resulting in a high homing capability. TYMP deficiency induced constitutive AKT phosphorylation in MSCs but reduced expression of genes associated with retinoid-interferon-induced mortality-19, a molecule that enhances cell death. Inhibition of TYMP with its selective inhibitor, tipiracil, phenocopied TYMP deficiency, improved post-AMI cardiac function and systolic left ventricle anterior wall thickness, attenuated diastolic stiffness, and reduced infarct size. Conclusions This study demonstrated that TYMP plays an adverse role after AMI. Targeting TYMP may be a novel therapy for patients with AMI.

Can we explore AF–pacemakers’ relationship using clinical and echocardiographic parameters in patients with permanent pacemaker? (Echocardiography and subclinical AF in permanent pacemaker)

Patients on implanted permanent pacemakers frequently develop atrial fibrillation (AF). We aimed to determine the Echocardiographic and clinical parameters predicting AF in patients with a dual-chamber (DDD) pacemaker. This retrospective study included 208 patients with permanent pacemaker, classified according to development of AF during follow up into 2 groups: AF (77, 37%) and non AF (131, 63%), baseline: clinical, ECG(P-wave dispersion) and echo {diastolic wall strain (DWS),left arial volume index (LAVI), left ventricular stiffness index(LVSI)} data were assessed. AF group were older with more P wave dispersion, lesser DWS, greater LVSI& LAVI, LVSI at a cut off > 0.13 and DWS at a cut off < 0.34 were predictors of AF in patients with DDD pacemakers. LVSI and DWS could be used as simple good predictors for AF in patients with DDD pacemakers, for timely initiation of anticoagulants according to CHA2DS2VASc score to decrease ischemic stroke burden.

Amplifying effect of chronic lisinopril therapy on diastolic function and the angiotensin-(1-7) Axis by the G1 agonist in ovariectomized spontaneously hypertensive rats

G protein-coupled estrogen receptor (GPER) activation by G1 attenuates diastolic dysfunction from estrogen loss, which may be partly due to suppression of angiotensin II pathological actions. We aimed to determine the independent effects of 8 weeks of G1 (100 µg/kg/d, subcutaneous pellet), ACE-inhibition (ACEi; lisinopril 10 mg/kg, drinking water), or combination therapy versus vehicle in the ovariectomized (OVX) spontaneously hypertensive rat (SHR) on cardiac function and morphometrics (echocardiography), serum equilibrium of angiotensins (mass spectroscopy) and cardiac components of the RAS (Western blotting). G1 alone and when combined with ACEi enhanced myocardial relaxation (é: 30 and 17%) and diastolic wall strain (DWS: 76 and 68%) while reducing relative wall thickness (RWT: 20 and 33%) and filling pressures (E/é: 30 and 37%). Cardiac expression levels of Mas receptor (Mas-R) and ACE2 also increased in the presence of G1. Strong antihypertensive effects of lisinopril monotherapy were associated with reductions in RWT, collagen deposition and E/é without overtly altering é or DWS. Chronic ACEi also increased cardiac levels of Mas-R and AT1-R and tilted the circulating RAS toward the formation of Ang-(1-7), which was amplified in the presence of G1. In vitro studies further revealed that an inhibitor to prolyl endopeptidase (PEP), but not to neprilysin, significantly reduced serum Ang-(1-7) levels in G1-treated rats, suggesting that G1 might be increasing Ang-(1-7) formation via PEP. We conclude that activating GPER with G1 augments components of the cardiac RAS and improves diastolic function without lowering blood pressure, and that lisinopril-induced blood pressure control and cardiac alterations in OVX SHR are permissive in facilitating G1 to augment Ang-(1-7) in serum, thereby strengthening its cardioprotective benefits.

Left ventricular stiffness assessed by diastolic wall strain predicts asymptomatic atrial high rate episodes in patients with pacemaker implantation

Abstract Background Asymptomatic atrial fibrillation has been reported to be associated with an increased risk of embolism. Purpose We investigated whether the left ventricular (LV) stiffness assessed by diastolic wall strain (DWS) predicts atrial high rate episodes (AHREs) in patients with pacemaker implantation (PMI). Methods One hundred forty seven patients (76 males, 75.2±8.9 years, 62 with sick sinus syndrome; SSS and 85 with atrioventricular block) who did not show atrial tachyarrhythmia before PMI were studied. DWS and other measurements were assessed using transthoracic echocardiography before DDD-pacemaker implantation. DWS was calculated from the M-mode echocardiographic measurement of the LV posterior wall thickness at end-systole (PWs) and end-diastole (PWd), and DWS was defined as (PWs-PWd)/PWs. Results AHREs (&amp;gt;5 min and &amp;gt;180 beats/min) were detected in 50/147 patients during follow-up periods (38.3±13.8 months). Patients with AHREs showed reduced DWS (0.29±0.07 vs. 0.39±0.06, p&amp;lt;0.0001), larger left atrial volume index, elevated E/e' ratio, thicker LV PWd, higher prevalence of SSS, and left bundle branch block pattern during ventricular pacing. On multivariate analysis, DWS was only independently associated with AHREs (p&amp;lt;0.0001, HR 1.987 for each 0.1 decrease in DWS, 95% CI 1.553–2.650). Patients with reduced DWS (&amp;lt;0.33) had a higher risk of incidences of AHREs (Figure 1). Conclusions LV stiffness assessed by DWS predicts AHREs in patients with PMI. Figure 1 Funding Acknowledgement Type of funding source: None

Increased left ventricular stiffness assessed by diastolic wall strain causes symptoms in patients with premature ventricular contraction

Abstract Background Premature ventricular contraction (PVC) is one of common arrhythmias and only some patients complain of PVC-related symptoms, however the mechanisms which cause the symptoms remain unclear in patients with PVCs. Purpose We investigated whether the left ventricular (LV) stiffness assessed by diastolic wall strain (DWS) relate symptoms or not in patients with PVC. Methods We studied 109 patients (48 males, age 60±19) with frequent monomorphic PVCs who underwent 12-leads electrocardiogram (ECG), signal-averaged electrocardiogram (SAECG), 24h-Holter ECG recording, and transthoracic echocardiography (TTE). Patients with structural heart disease or other arrhythmias such as atrial fibrillation were excluded. Clinical factors, blood samples for atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), and filtered QRS duration (f-QRS) and root mean square voltage of the terminal 40ms of the QRS complex (RMS40) obtained by SAECG were evaluated. We assessed PVC-SV (stroke volume during PVC), PVC-CI (CI between the previous sinus beat and VPC), and left ventricular (LV) stiffness assessed by diastolic wall strain (DWS). DWS was calculated from the M-mode echocardiographic measurement of the LV posterior wall thickness at end-systole (PWs) and end-diastole (PWd) during sinus rhythm, and DWS was defined as (PWs − PWd)/PWs. Results 31patients (28%) had PVC-related symptoms (18 palpitation and 13 pulse deficit). Patients with PVC-related symptoms showed shorter PVC coupling interval index (52±10 vs. 58±11%, p=0.0140), reduced PVC-SV (21±12 vs. 29±17ml, p=0.0103) and decreased DWS (0.38±0.06 vs. 0.42±0.06, p=0.0011). Meanwhile, the level of BNP and ANP, f-QRS, RMS40, QRS morphology of PVC and the total number of PVC per day were not associated with PVC-related symptoms. On multivariate analysis, decreased DWS was only independently associated with PVC-related symptoms (p=0.0357, OR 2.3629 for each 0.1 decrease in DWS 95% CI 1.0583–5.5815). Conclusion The reduced diastolic wall strain relates with PVC-related symptoms. The increased left ventricular stiffness might cause symptoms in patients with PVC. Funding Acknowledgement Type of funding source: None

Left ventricular stiffness assessed by diastolic Wall strain predicts asymptomatic atrial high-rate episodes in patients with pacemaker implantation

BackgroundCardiac implantable electronic device-detected atrial high-rate episodes (AHREs) have been reported to be associated with thromboembolic risks. The present study aimed to investigate the association of echocardiographic and clinical parameters with the occurrence of AHREs in patients with a dual-chamber pacemaker (PMI). MethodsOne hundred forty-seven patients (76 males, 75.2 ± 8.9 years) who did not show atrial tachyarrhythmia before the implantation of the PMI were studied. Diastolic wall strain (DWS) and other measurements were assessed during sinus rhythm using transthoracic echocardiography before the PMI. DWS was calculated from the M-mode echocardiographic measurement of the left ventricular (LV) posterior wall thickness at end-systole (PWs) and end-diastole (PWd), and DWS was defined as (PWs-PWd) / PWs. ResultsAHREs (defined as AHREs duration >6 min and atrial rate >180 bpm) were detected in 50 / 147 patients during follow up (38.3 ± 13.8 months). Patients in the AHREs group had reduced DWS (0.29 ± 0.07 vs. 0.39 ± 0.06, p < 0.0001), larger left atrial volume index, thicker LV posterior diameter, higher rate of patients taking β-blocker / diuretics, and higher prevalence of sinus node dysfunction. On multivariable analysis, only DWS was independently associated with AHREs. Patients with reduced DWS (<0.33) had a higher risk of incidences of AHREs. ConclusionLV stiffness assessed by DWS was associated with AHREs in patients with a PMI.

INCREASED LEFT VENTRICULAR STIFFNESS IN PATIENTS WITH SYMPTOMATIC PREMATURE VENTRICULAR CONTRACTION

Premature ventricular contraction (PVC) is one of commonarrhythmias and only some patients complain of PVC-related symptoms, however the mechanisms which cause the symptoms remain unclear. We assessed the left ventricular (LV) stiffness assessed by diastolic wall strain (DWS)in patients with PVC-

LEFT VENTRICULAR STIFFNESS ASSESSED BY DIASTOLIC WALL STRAIN PREDICTS ASYMPTOMATIC ATRIAL HIGH RATE EPISODES IN PATIENTS WITH PACEMAKER IMPLANTATION

Asymptomatic atrial fibrillation has been reported to be associated with an increased risk of embolism. We investigated whether the left ventricular (LV) stiffness assessed by diastolic wall strain (DWS) predicts atrial high rate episodes (AHREs) in patients with pacemaker implantation (PMI). One

Left ventricular stiffness in paediatric patients with end-stage kidney disease.

We tested the hypothesis that myocardial stiffness is altered in paediatric patients with end-stage kidney disease (ESKD) and explored its association with clinical parameters of chronic kidney disease (CKD). Thirty-five patients with ESKD (16 males) aged 17.5 ± 3years old, 18/35 of whom were receiving dialysis and 17 post kidney transplant, were studied. Left ventricular (LV) myocardial stiffness was determined by measurement of diastolic wall strain (DWS) and stiffness index (SI), while LV diastolic function was interrogated by pulsed-wave and tissue Doppler echocardiography. Compared with available literature data, both dialysis and transplanted patients had significantly lower DWS and greater SI, reduced transmitral early (E) to late diastolic velocity ratio and septal and lateral mitral annular early (e') diastolic velocities, and greater septal and lateral E/e' ratios (all p < 0.05). Multivariate analysis revealed that z score of diastolic blood pressure (β = 0.43, p = 0.004) and the duration of renal replacement therapy (β = 0.55, p < 0.001) were significant determinants of LV SI. Subgroup analysis in post-transplant patients showed z score of diastolic blood pressure (β = 0.54, p = 0.025) remained as a significant determinant of LV SI. Increased LV myocardial stiffness is evident in paediatric dialysis and transplanted patients with ESKD, and is associated with blood pressure and duration of renal replacement therapy.

Left Ventricular Stiffness in Adolescents and Young Adults After Arterial Switch Operation for Complete Transposition of the Great Arteries.

We tested the hypothesis that left ventricular (LV) myocardial stiffness is altered in patients with transposition of great arteries (TGA) after arterial switch operation (ASO) and explored its associations with myocardial calibrated integrated backscatter (cIB) and LV myocardial deformation. Thirty-one patients and twenty-two age-matched controls were studied. LV myocardial stiffness was assessed by diastolic wall strain (DWS) and stiffness indices including (E/e)/LV end-diastolic dimension, (E/LV global longitudinal early diastolic strain rate)/LV end-diastolic volume, and (E/LV global circumferential early diastolic strain rate)/LV end-diastolic volume, where E and e are early diastolic transmitral and mitral annular velocities, respectively. LV myocardial cIB and longitudinal and circumferential myocardial deformation were determined by conventional and speckle tracking echocardiography. Patients had significantly lower DWS, higher stiffness indices, and greater myocardial cIB than controls (all p < 0.05). The LV longitudinal and circumferential systolic strain and systolic and diastolic strain rates were significantly lower in patients than controls (all p < 0.05). Greater average myocardial cIB was associated with lower DWS (r = - 0.44, p = 0.002). Worse DWS and LV stiffness indices were found to correlate with lower mitral annular systolic velocity, mitral annular late diastolic velocity, and LV longitudinal late diastolic strain rate (all p < 0.05). LV longitudinal and circumferential systolic strain and strain rate were also found to correlate with DWS (all p < 0.05). In conclusion, LV myocardial stiffening occurs in adolescents and young adults with TGA after ASO and is associated with impairment of ventricular systolic and diastolic myocardial deformation and myocardial fibrosis.

The role of M-mode echocardiography in patients with heart failure and preserved ejection fraction: A prospective cohort study.

Epicardial movement during diastole is inversely proportional to myocardial stiffness but systolic regional thickening cannot precisely identify ischemic territories. The aim of the present study was to test the hypothesis that a correlation may be present between M-mode echocardiography parameters and poor outcomes in patients with heart failure and preserved ejection fraction. Patients with known cardiovascular disease were included in the test group (n=1,244) and patients without known cardiovascular disease were included in the control group (n=1,952). Patient records of routine measurements, M-mode echocardiography and mortality were collected. The control population and test population had the same left ventricular end-diastolic dimension (P=0.062) and left ventricular end-diastolic volume (P=0.053). A lower mitral flow velocity (P<0.05), higher Tei index (P<0.0001) and reduced distribution of diastolic wall strain (P<0.0001) were reported in the test populations compared with the control population. Patients of the test population with lower diastolic wall strain (<0.28) demonstrated a higher mortality rate than those with higher diastolic wall strain (≥0.28; P<0.0001) at the 3-year follow-up. M-mode echocardiographic parameters may be of use for predicting poor outcomes in patients with heart failure and preserved ejection fraction.

P3790Left ventricular stiffness assessed by diastolic wall strain predicts infrequent atrial fibrillation

Abstract Background Left ventricular (LV) stiffness as the passive LV filling property in the LV diastolic function has been reported to be related with the prevalence of atrial fibrillation (AF). On the other hand, a novel insertable monitoring (ICM) system is a powerful tool to detect AF with rare appearance in patients with embolic stroke of undetermined source (ESUS). We investigated whether the LV stiffness assessed by diastolic wall strain (DWS) predicts infrequent atrial fibrillation. Methods Fifty-five patients (41 males, 68±14 years) who underwent ICM implantation for ESUS (n=19) or unexplained syncope (n=36) were studied. DWS, left atrial (LA) stiffness and other measurements were assessed using transthoracic echocardiography before the ICM implantation. DWS was calculated from the M-mode echocardiographic measurement of the LV posterior wall thickness at end-systole (PWs) and end-diastole (PWd) during sinus rhythm, and DWS was defined as PWd/PWs. LA stiffness index was defined as the ratio of E/e' to LA peak strain. Results AF was detected in 20 patients (36%) during the follow-up periods (280±243 days). Patients with AF showed reduced DWS (0.30±0.07 vs. 0.41±0.08, p&lt;0.0001), larger LA volume index (39.0±10.9 vs. 32.3±9.0, p=0.0174), and higher age (74.6±10.4 vs. 64.6±14.9, p=0.0105). On the other hand, LA stiffness index, LA function (reservoir, booster, and conduit function estimated by LA volume), and LV relaxation function (E wave, E/A ratio, deceleration time) were not associated with detection of AF. There was no difference on AF detection rate between ESUS and unexplained syncope (26% vs. 42%, p=0.2604). On multivariate analysis, DWS was only independently associated with detection of AF (p&lt;0.0001, OR 5.647 for each 0.1 decrease in DWS, 95% CI 1.084–1.338). Moreover, patients with reduced DWS (&lt;0.38) had a higher risk of incidences of AF than patients with preserved DWS (figure). Figure 1 Conclusions LV stiffness assessed by DWS predicts infrequent AF. Reduced LV stiffness rather than LA dysfunction or LV relaxation dysfunction may be the main cause of AF in the early stages.

P303Prognostic value of diastolic wall strain in patients with asymptomatic severe aortic stenosis

Abstract Background Diastolic wall strain (DWS) has been reported to be associated with left ventricular (LV) stiffness and worse clinical outcomes. We sought to assess the utility of this new index for prediction of prognosis in asymptomatic patients with severe aortic stenosis (AS). Methods Asymptomatic severe AS patients [peak flow velocity (PFV) ≥4.0m/s, mean pressure gradient (mPG) ≥40mmHg, aortic valve area (AVA) ≤1.0cm2, or indexed AVA ≤0.6cm2/m2)] diagnosed between July 2007 and April 2016 were included in this study. Patients with significant mitral valve disease, posterior wall motion abnormality, prior cardiac surgery, hypertrophic cardiomyopathy, and LV ejection fraction &lt;50% were excluded. DWS was calculated with a validated formula [DWS = (posterior wall thickness at end-systole − posterior wall thickness at end-diastole)/posterior wall thickness at end-systole]. All study patients were prospectively followed up to last visit or death until November 2017, and predictive value of all-cause death was assessed using Cox-proportional hazards modeling. Patients who underwent aortic valve replacement (AVR) during the study period were censored on the date of surgery. Results A total of 184 asymptomatic severe AS, 138 (age 76±9year-old, men 41%, PFV 3.9±1.0m/s, mPG 38±19mmHg, AVA 0.83±0.18cm2, indexed AVA 0.56±0.13cm2/m2) met all study criteria. Of whom, 43 (31%) underwent AVR and 28 (20%) died during a mean follow-up of 25±28months. In a multivariable model after adjusting for clinical and echocardiographic variables, advancing age (per10yrs; HR=2.19, 95% CI=1.19–4.03, P&lt;0.05), history of hemodialysis (HR=4.31, 95% CI=1.30–14.35, P&lt;0.05), and low-DWS (DWS &lt;0.30) (HR=2.83, 95% CI=1.25–6.40, P&lt;0.05) were independent predictors of all-cause death. In the Kaplan-Meier estimates of cumulative survival stratified by DWS status were shown (Figure). The Kaplan-Meier estimates of survival Conclusion Low-DWS provides prognostic information in patients with asymptomatic severe AS.

Diastolic wall strain predicts progression from paroxysmal to persistent or permanent atrial fibrillation in structurally normal hearts

BackgroundAtrial fibrillation (AF) is characterized by a progression from paroxysmal to persistent or permanent AF. Recent studies have shown that AF progression is related to a worse morbidity and mortality, and poorer outcomes of radiofrequency catheter ablation (RFCA). We previously showed that left ventricular (LV) compliance assessed by diastolic wall strain (DWS) was a strong determinant of prevalent AF. Methods and resultsWe studied 306 paroxysmal AF patients with structurally normal hearts. The DWS was non-invasively measured with echocardiography. During a follow-up of 35±19 months, AF progression occurred in 60 of 172 (35%) patients treated with medications only (medication group), and 3 of 134 (2%) who underwent RFCA (RFCA group) (p<0.001). In the medication group, patients with a DWS <0.38 had a higher incidence of AF progression than those without (log-rank p<0.001), while the AF progression rate was low irrespective of the DWS in the RFCA group. In a multivariate analysis, the DWS and left atrium volume index (LAVI) were independent predictors of AF progression in the medication group (hazard ratio, 1.13 per 0.01 decrease; 95% CI: 1.08–1.18; p<0.001, and 1.04 per 1mm increase; 95% CI: 1.01–1.08; p=0.012, respectively). In the medication group, AF progression occurred in only 5 of 61 (8%) patients with a DWS ≥0.38, whereas 27 of 40 (68%) with a DWS <0.38 and LAVI >34mL/m2 progressed to persistent or permanent AF. ConclusionsThe LV compliance estimated by the DWS was independently associated with AF progression. The DWS would be useful to stratify patients at risk of AF progression who could benefit from an earlier RFCA intervention.

Diastolic wall strain as a predictor of age-related cardiovascular events in patients with preserved left ventricular ejection fraction.

Diastolic wall strain (DWS) was reported as a simple and feasible echocardiographic index in assessing left ventricular (LV) diastolic stiffness. We sought to evaluate whether DWS predicts age-related cardiovascular events. Patients referred for transthoracic echocardiogram, those with preserved LV ejection fraction and no clinical heart failure were studied. Cardiovascular events were ascertained using Framingham criteria (myocardial infarction, coronary insufficiency, stroke, transient ischemic attack, congestive heart failure, or cardiovascular death). DWS was calculated with a validated formula. Cox proportional hazards modeling was used to assess the risk of cardiovascular events. Of a total number of 962 patients (mean age 60.9 ± 14.9years, 48.0% men), 69 (7.2%) developed at least 1 cardiovascular event during a mean follow-up of 43 ± 32months. After adjusting for cardiovascular comorbidities in a multivariable model, low DWS (≦ 0.33) was a significant independent predictor of cardiovascular events [hazard ratio (HR): 1.87, 95% confidential interval (CI) 1.04-3.36, P = 0.04]. Echocardiographic assessment of DWS may help in identifying the patients at increased risk for future age-related cardiovascular events.