Systolic Dyssynchrony Research Articles

LEFT VENTRICULAR DYSSYNCHRONY CAN BE SEEN IN ASYMPTOMATIC HEART TRANSPLANTATION PATIENTS WITH NORMAL LVEF: A TRI-PLANE SPECKLE TRACKING STUDY

ObjectivesThe current study aims to explore whether asymptomatic heart transplantation patients with normal LVEF have left ventricular systolic dysfunction or dyssynchrony by using Tri-plane Speckle Tracking Imaging (T-STI).MethodsFifteen asymptomatic heart...

Diastolic Heart Failure and LV Dyssynchrony

Our knowledge of diastolic heart failure (DHF) is still limited with regard to pathophysiology, diagnosis and clinical treatment. Amongst others, LV dyssynchrony was suggested to be an additional factor involved in the pathogenesis of subgroup of patients with DHF. In 20-30% of patients with DHF a systolic LV dyssynchrony could be detected and about 20% DHF patients evidenced a diastolic dyssyncrony. Both systolic and diastolic dyssynchrony may contribute to the impairment of cardiac function and clinical manifestation in DHF. Opposite to the systolic heart failure, wide QRS complex is uncommon which incriminates that dyssynchrony in DHF is rather related to regional disperse in contractility than to electromechanical coupling delay. Asynchronous LV relaxation and impairment of ventricular restoring forces may also impair the LV filing and lead to a diastolic dyssynchrony. Particularly in patients with preserved LV contractility mechanical LV dyssynchrony induces energy wastage and consequently reduces cardiac reserves. However, up to date it is not clear to what degree LV dyssynchrony is involved in the pathomechanisms of this subpopulation of DHF.

Dynamic Dyssynchrony and Impaired Contractile Reserve of the Left Ventricle in Beta-Thalassaemia Major: An Exercise Echocardiographic Study

BackgroundPerformance of the left ventricle during exercise stress in thalassaemia patients is uncertain. We aimed to explore the phenomenon of dynamic dyssynchrony and assess contractile reserve in patients with beta-thalassaemia major and determine their relationships with myocardial iron load.Methods and ResultsThirty-two thalassaemia patients (16 males), aged 26.8±6.9 years, without heart failure and 17 healthy controls were studied. Their left ventricular (LV) volumes, ejection fraction, systolic dyssynchrony index (SDI), and myocardial acceleration during isovolumic LV contraction (IVA) were determined at rest and during submaximal bicycle exercise testing using 3-dimensional and tissue Doppler echocardiography. Myocardial iron load as assessed by T2* cardiac magnetic resonance in patients were further related to indices of LV dyssynchrony and contractile reserve. At rest, patients had significantly greater LV SDI (p<0.001) but similar IVA (p = 0.22) compared with controls. With exercise stress, the prevalence of mechanical dyssynchrony (SDI>4.6%, control+2SD) increased from baseline 25% to 84% in patients. Δ SDIexercise-baseline correlated with exercise-baseline differences in LV ejection fraction (p<0.001) and stroke volume (p = 0.006). Compared with controls, patients had significantly less exercise-induced increase in LV ejection fraction, cardiac index, and IVA (interaction, all p<0.05) and had impaired contractile reserve as reflected by the gentler IVA-heart rate slope (p = 0.018). Cardiac T2* in patients correlated with baseline LV SDI (r = −0.44, p = 0.011) and IVA-heart rate slope (r = 0.36, p = 0.044).ConclusionsResting LV dyssynchrony is associated with myocardial iron load. Exercise stress further unveils LV dynamic dyssynchrony and impaired contractile reserve in patients with beta-thalassaemia major.

881 INDEPENDENT DETERMINANTS FOR PRESENCE AND DEGREE OF LEFT VENTRICULAR SYSOLIC DYSSYNCHRONY IN TREATMENT-NAIVE PATIENTS OF HYPERTENSION

Backgrounds: Prevalence of left ventricular (LV) systolic dyssynchrony is over 40% in treatment-naïve patient of hypertension.(1) We investigated the factors associated with LV systolic dyssynchrony. Methods: The study groups consisted of 266 treatment-naïve patients of hypertension undergoing laboratory, echocardiographic (Echo), arterial stiffness (pulse wave velocity and ankle-brachial index), central blood pressure, and 24-hour (h) ambulatory BP monitoring evaluations. Standard deviation (SD) of time from ECG Q to systolic peak velocity of 12 LV segments (Ts-SD12) and maximal difference between peak systolic velocities of any 2 of the 12 segments (Ts-Max) were measured by Echo. A Ts-SD12 ≥33 or Ts-Max ≥100 ms was a presence of LV systolic dyssynchrony. Peak systolic velocity (Sa), as a subclinical systolic function, peak early diastolic velocity (Ea) and mitral E velocity/Ea (E/Ea), as a subclinical diastolic function, were measured. Results: Treatment-naïve hypertensives were divided into patients without LV systolic dyssynchrony (n = 151, 56.8%) or with LV systolic dyssynchroy (n = 115, 43.2%). In multivariate analysis for presence of LV systolic dyssynchrony, Sa was independently and inversely associated (OR 0.67, 95% CI 0.51-0.89, P = 0.005). In multivariate analysis for degree of it, serum potassium levels, E/Ea, and Sa were independently associated (potassium, β=0.193, P = 0.006; E/Ea, β=0.211, P = 0.017; and Sa, β=-0.301, P < 0.001). Conclusion: Subclinical LV systolic function is independently associated with presence and degree of LV systolic dyssynchrony in treatment-naïve patients of hypertension. Subclinical LV diastolic function and serum potassium levels are independently associated with degree of it. Arterial stiffness and BPs are not a determinant. References Kwon BJ, Choi KY, Kim DB, Jang SW, Cho EJ, Youn HJ, et al. Systolic synchrony is impaired in nonleft ventricular hypertrophy of never-treated hypertensive patients. J Hypertens. Nov 2011; 29(11):2246-54.

Early pacing-induced systolic dyssynchrony is a strong predictor of left ventricular adverse remodeling: Analysis from the Pacing to Avoid Cardiac Enlargement (PACE) trial

BackgroundRight ventricular apical (RVA) pacing is associated with adverse left ventricular (LV) remodeling and biventricular (BiV) pacing may prevent it although the mechanisms remain unclear. The current study aimed to assess the role of early pacing-induced systolic dyssynchrony (DYS) to predict adverse LV remodeling. MethodsPatients with standard pacing indications and normal LV ejection fraction were randomized either to BiV (n=89) or RVA pacing (n=88). Pacing-induced DYS, defined as the standard deviation of the time to peak systolic velocity (Dyssynchrony Index) >33ms in a 12-segmental model of LV, was measured by tissue Doppler echocardiography at 1month. ResultsAt 1month, 59 patients (33%) had DYS which was more prevalent in RVA than BiV pacing group (52% vs. 15%, χ2=28.3, p<0.001), though Dyssynchrony Index was similar at baseline (30±14 vs. 26±11ms, p=0.06). At 12months, those developing DYS had significantly lower LV ejection fraction (55.1±9.7 vs. 62.2±7.9%, p<0.001) and larger LV end-systolic volume (35.3±14.3 vs. 27.0±10.4ml, p<0.001) when compared to those without DYS. Reduction of ejection fraction ≥5% occurred in 67% (39 out of 58) of patients with DYS, but only in 18% (21 out of 115) in those without DYS (χ2=40.8, p<0.001). Both DYS at 1month (odds ratio [OR]: 4.725, p=0.001) and RVA pacing (OR: 3.427, p=0.009) were independent predictors for reduction of ejection fraction at 12months. ConclusionEarly pacing-induced DYS is a significant predictor of LV adverse remodeling and the observed benefit of BiV pacing may be related to the prevention of DYS. Clinical trial registrationCentre for Clinical Trials number, CUHK_CCT00037 (URL: http://www.cct.cuhk.edu.hk/Registry/publictrialrecord.aspx?trialid=CUHK_CCT00037).

Hypertensive heart disease: MR tissue phase mapping reveals altered left ventricular rotation and regional myocardial long-axis velocities

The aim of this study was the evaluation of left ventricular (LV) segmental 3D velocities in patients with hypertensive heart disease using magnetic resonance (MR) tissue phase mapping (TPM). LV radial, long-axis and rotational myocardial velocities were assessed by TPM in patients with LV hypertrophy and preserved EF (n = 18, age = 53 ± 12 years) and volunteers (n = 20, age = 51 ± 4 years). Systolic and diastolic peak and time-to-peak velocities were mapped onto a 16-segment LV model. 3D myocardial motion was displayed on an extended visualisation model. Correlation coefficients were calculated to investigate differences in regional dynamics. Patients revealed diastolic dysfunction as expressed by decreased peak long-axis velocities in all (except apical) segments (basal, P ≤ 0.01; two midventricular segments, P = 0.02, P = 0.03). During systole, hypertrophy was associated with heterogeneous behaviour for long-axis velocities including an increase in anteroseptal apical and midventricular regions (P = 0.001), a reduction in mid-inferior segments (P = 0.03) and enhanced septal velocities (P < 0.05). Segmental correlation analysis revealed altered dynamics of LV base rotation and increased dyssynchrony of lateral long-axis motion. Patients with hypertensive heart disease demonstrated alterations in systolic long-axis motion, basal rotation and dyssynchrony. Longitudinal studies are needed to investigate the value of regional wall motion abnormalities regarding disease progression and outcome.

Effect of Ranolazine on Left Ventricular Dyssynchrony in Patients With Coronary Artery Disease

We previously reported that ranolazine improves exercise myocardial perfusion. Ranolazine ameliorates myocardial ischemia by augmenting myocardial blood flow; likely by a reduction in the extravascular compression of small vessels. We hypothesized that ranolazine could improve left ventricular (LV) dyssynchrony as assessed by phase analysis of gated single photon emission computed tomographic myocardial perfusion imaging. Patients (n = 32) with known or suspected coronary artery disease and reversible perfusion defects on a clinically indicated stress myocardial perfusion imaging were restudied 4 weeks after ranolazine (500 to 1,000 mg orally twice daily) was added to their conventional treatment in an open-label trial (data previously reported). The LV systolic and diastolic dyssynchrony indexes were obtained using automated phase analysis before and after ranolazine. No significant changes were found in the heart rate or blood pressure (at rest or during stress) after treatment. The perfusion pattern improved in 13 of 18 patients who had undergone exercise testing, but in only 3 of 14 patients who had undergone vasodilator stress testing. No significant changes were seen in the LV ejection fraction or volume after treatment. The systolic and diastolic LV dyssynchrony improved after ranolazine therapy; there was a significant decrease in the systolic phase SD (21 ± 17 vs 18 ± 13, p = 0.04), systolic bandwidth (69 ± 60 vs 53 ± 38, p = 0.03), diastolic SD (29 ± 18 vs 24 ± 15, p = 0.047) and diastolic bandwidth (91 ± 61 vs 72 ± 45, p = 0.02). In conclusion, the present study is the first to show improvements in diastolic and systolic LV synchrony with ranolazine as measured by automated phase analysis of gated single photon emission computed tomographic myocardial perfusion imaging.

Tethering Symmetry Reflects Advanced Left Ventricular Mechanical Dyssynchrony in Patients With Ischemic Mitral Regurgitation Undergoing Restrictive Mitral Valve Repair

We evaluated the papillary muscle systolic dyssynchrony (DYS-PAP) using two-dimensional speckle tracking echocardiography (2D-STE) in patients with chronic ischemic mitral regurgitation (CIMR) showing different preoperative leaflet pattern and investigated the impact of baseline tethering pattern in the prediction of significant post-repair desynchronized papillary muscle contraction. We recruited 152 CIMR consecutive patients (64.4% male, mean age 65.9 ± 7.1 years) who survived coronary artery bypass grafting (CABG) and (undersized mitral ring annuloplasty, performed between 2001and 2010. The assessment of DYS-PAP was performed preoperatively and at follow-up (median 41.5 months [IQR 23-61]) by 2D-STE in the apical 4-chamber view for anterolateral papillary muscle and apical long-axis view for posteromedial papillary muscle). Based on the cutoff value (anterior-posterior tethering angle ratio α/β ≥ 0.76) patients were classified in 2 groups; symmetrical (group 1, n = 73, mean α/β = 0.81 ± 0.6) and asymmetrical preoperative tethering pattern (group 2, n = 79, mean α/β = 0.66 ± 0.4). Recurrent MR occurred in 67.1% (n = 49) in group 1 versus 3.8% (n = 3) in group 2 (p < 0.001). Comparing both groups at baseline, patients in group 1 had higher DYS-PAP (57.7 ± 5.3 vs 29.8 ± 2.4 ms in group 2, p < 0.001) that significantly worsened at follow-up (78.1 ± 8.8 ms, p < 0.001 versus baseline), whereas in group 2 it improved (26.6 ± 6.0 ms, p < 0.001 versus baseline). Tethering symmetry significantly correlated with DYS-PAP (r = 0.90, p < 0.001) and it was a strong multivariable predictor of significant postoperative DYS-PAP (odds ratio 4.2; 95% confidence level 3.4 to 5.2, p < 0.001). Tethering symmetry is an easy and immediate tool to identify CIMR patients with advanced DYS-PAP who are unlikely to benefit from mitral repair with undersized mitral ring annuloplasty.

Evaluation of left ventricular systolic dyssynchrony in chronic heart failure patients by two-dimensional speckle tracking imaging

Objective To evaluate the left ventricular mechanical dyssynchrony in patients with chronic heart failure(CHF)by two dimensional speckle tracking imaging(2D-STI).Methods 37 CHF patients were enrolled in this study.According to left ventricular ejection fraction(LVEF),the patienst were classified into two subgroups:group A,LVEF≤ 35 ％;group B,35 ％＜LVEF＜50 ％.35 healthy volunteers constituted the control group(group C).Standard 2D images were acquired in the 2-,3-and 4-apical views as well as the parasternal short-axis views at the level of the mitral valve and papillary muscles.The time to peak-systolic strain and strain rate were measured for each segment in the level of the mitral valve and papillary muscles in Qlab software.Dyssychrony parameters were defined as the standard deviation and the maximal time delay of the time to peak-systolic strain and strain rate for 12 segments.Parameters were compared among the three groups respectively.The correlation between dyssynchrony parameters and LVEF were analysed in CHF patients.The cut-off value of each parameter were derived from group C based on statistical principles.Dyssychrony rate of each parameter were calculated in group A and B,and compared within each group respectively.Results Compared with group C,all the dyssychrony parameters in group A were significant higher(P＜0.05),and part of the parameters(Tsl-12SD,Tsl-12Dif,Tslr-12SD,Tslr-12Dif and Tsr-12SD)in group B were remarkable higher(P＜0.05).Dyssychrony parameters in CHF patients correlated closely with LVEF(P＜0.05).Significant differences among dyssychrony rates were noted in both group A and B(P＜0.05),and Ts1-12SD showed the highest value in both subgroups.Conclusions 2D-STI is useful in quantifying left ventricular systolic dyssychrony in CHF patients,and the longitudinal parameters are more efficient to detect mechanical dyssychrony than the radial parameters and circumferential parameters. Key words: Echocardiography; Heart failure,congestive; Ventricular function,left; Speckle tracking imaging

Improved coronary artery blood flow following the correction of systolic dyssynchrony with cardiac resynchronization therapy

BackgroundCoronary blood flow (CBF) is improved by cardiac resynchronization therapy (CRT) and impaired by right ventricular apical (RVA) pacing in patients with heart failure. However, the underlying mechanism remains unclear. MethodsTwenty-nine non-ischemic heart failure patients who responded to CRT underwent transthoracic echocardiography examination including both left anterior descending (LAD) CBF and tissue Doppler imaging in 3 pacing modes: intrinsic conduction, RVA pacing and biventricular (BiV) pacing. LAD velocity-temporal integral (LAD-VTI) and duration were measured. Systolic dyssynchrony was assessed with the standard deviation of a 12-left ventricular segmental model (Ts-SD). ResultsBiV pacing improved while RVA pacing reduced CBF compared to intrinsic conduction (all p<0.05). Both Ts-SD and ventricular septal velocity deteriorated during RVA pacing but improved during BiV pacing (all p<0.05). When systolic dyssynchrony was induced, lower LAD-VTI (9.5±3.4 versus 12.7±5.1cm, p=0.001) and shorter LAD diastolic duration (483±92 versus 542±106ms, p=0.010) were detected than synchronous status. Systolic dyssynchrony was inversely related to septal velocity (r=−0.41), p<0.001 and LAD-VTI (r=−0.30, p=0.007), with the latter found to be moderately correlated to septal velocity (r=0.30, p=0.007). ConclusionRegional LAD flow was improved in patients subjected to BiV but worsened in those treated with RVA pacing in non-ischemic heart failure CRT responders. Systolic dyssynchrony was more commonly observed in patients subjected to RVA pacing. Reduction of septal velocity with dyssynchrony may directly lead to reduced LAD flow. Improvement of septal velocity by CRT and hence LAD flow may be an important mechanism in determining the response to CRT.

Left Ventricular Dyssynchrony and Its Effects on Cardiac Function in Patients with Newly Diagnosed Hypertension

Left ventricular (LV) systolic synchrony, defined as simultaneous peak contractions of corresponding cardiac segments, is well documented to be impaired in hypertension but its effect on LV function is not clear. The aim of this study was to assess the impacts of LV systolic dyssynchrony on LV function in newly diagnosed hypertensives. Forty-eight newly diagnosed hypertensive patients and 33 controls were enrolled. All study population underwent a comprehensive echocardiographic evaluation including tissue synchrony imaging. The time to regional peak systolic tissue velocity (Ts) in LV by 12 segmental models was measured and two parameters of systolic dyssynchrony were computed. Baseline demographic characteristics were similar in both study groups. Dyssynchrony parameters prolonged in newly diagnosed hypertensive patients compared to controls: the standard deviation (SD) of 12 LV segments Ts (40.2 ± 21 vs. 26.2 ± 13.4, P = 0.003); the maximal difference in Ts between any 2 of 12 LV segments (123.3 ± 61.5 vs. 79.8 ± 37.9, P = 0.001). In multivariable analysis, Ts-SD-12 was found to be an independent predictor for systolic function (β=-0.29, P = 0.008). But, both diastolic and global functions were not independently related to Ts-SD-12. LV synchronization is impaired in newly diagnosed hypertensive patients. LV dyssynchrony is one of the independent predictors of systolic function in hypertensive patients.

Incremental value of global systolic dyssynchrony in determining the occurrence of functional mitral regurgitation in patients with left ventricular systolic dysfunction

The aim of this study was to assess the contribution of left ventricular (LV) systolic dyssynchrony to functional mitral regurgitation (MR). Patients (n = 136) with LV systolic dysfunction (ejection fraction <50%) and at least mild MR were prospectively recruited. The effective regurgitant orifice area (EROA) was assessed by the proximal isovelocity surface area method. Left ventricular global systolic dyssynchrony [the maximal difference in time to peak systolic velocity among the 12 LV segments (Ts-Dif)] and regional systolic dyssynchrony (the delay between the anterolateral and posteromedial papillary muscle attaching sites) were assessed by tissue Doppler imaging. Left ventricular global and regional remodelling, systolic function, indices of mitral valvular and annular deformation were also measured. The size of the EROA correlated with the degrees of mitral deformation, LV remodelling, systolic function, and systolic dyssynchrony. By multivariate logistic regression analysis, the mitral valve tenting area (OR = 1.020, P < 0.001) and the Ts-Dif (OR = 1.011, P = 0.034) were independent determinants of significant functional MR (defined by EROA ≥20 mm(2)). From the receiver-operating characteristic curve, the tenting area of 2.7 cm(2) (sensitivity 83%, specificity 82%, AUC 0.86, P < 0.001) and the Ts-Dif of 85 ms (sensitivity 66%, specificity 72%, AUC 0.74, P < 0.001) were associated with significant functional MR. The assessment of Ts-Dif showed an incremental value over the mitral valve tenting area for determining functional MR (χ(2) = 53.92 vs.49.11, P = 0.028). This cross-sectional study showed that LV global, but not regional systolic dyssynchrony, is a determinant of significant functional MR in patients with LV systolic dysfunction, and is incremental to the tenting area that is otherwise the strongest factor for mitral valve deformation.

A randomized study of haemodynamic effects and left ventricular dyssynchrony in right ventricular apical vs. high posterior septal pacing in cardiac resynchronization therapy

The effect on left ventricular (LV) systolic function and LV dyssynchrony by alternative right ventricular (RV) lead position in cardiac resynchronization therapy (CRT) is unclear. In the present study, RV apical (RV-A) was compared with RV high posterior septal (RV-HS) lead position in CRT. In 85 consecutive CRT patients (mean age 66 ±11 years) the RV lead placement was randomized to RV-A (n = 43) or RV-HS (n = 42). The LV lead was targeted to the latest activated LV segment (concordant LV lead), identified by two-dimensional speckle tracking radial strain (ST-RS) echocardiography. Concordant LV leads were obtained in 72%, similar in RV-A and RV-HS (79% vs. 64%; P = 0.13). Six months after CRT, no difference was found in LV reverse remodelling (reduction of LV end-systolic volume ≥15%) according to RV-A and RV-HS leads [26 (65%) vs. 25 (64%); P = 0.93]. Superior LV reverse remodelling was observed in concordant LV leads compared with discordant LV leads [41 (73%) vs. 10 (43%); P = 0.01]. At 6-month follow-up, LV reverse dyssynchrony (reduction of anteroseptal to posterior delay ≥50%) using ST-RS imaging was similar in RV-A and RV-HS [25 (63%) vs. 24 (62%); P = 0.93]. More LV reverse dyssynchrony was found in concordant LV leads vs. discordant LV leads [39 (70%) vs. 10 (43%); P = 0.03]. A concordant LV lead was an independent predictor of LV reverse remodelling (odds ratio, 3.65; P = 0.01) and LV reverse dyssynchrony (odds ratio, 4.22; P = 0.02) 6 months after CRT. RV-A and RV-HS in CRT demonstrated similar LV reverse remodelling and LV reverse dyssynchrony at 6-month follow-up. Concordant LV leads provided superior LV reverse remodelling and LV reverse dyssynchrony.

003 Validating markers of mechanical dyssynchrony by experimental manipulation of interventricular timings: what is needed to make them a reasonable prospect for cardiac resynchronisation therapy selection?

<h3>Background</h3> Any dyssynchrony marker proposed for selection of patients for cardiac resynchronisation therapy (CRT) should be stable between heartbeats but change markedly when interventricular delay is experimentally manipulated; the marker should also minimise at some “optimal” interventricular delay. <h3>Methods and Results</h3> We performed 3264 echocardiographic measurements in 13 patients with CRT: separate, replicate measurements at interventricular delays from RV-first 40 ms to LV-first 60 ms, in 20-ms intervals of (1) 3D systolic dyssynchrony index (SDI), (2) Tissue Doppler imaging (TDI), (3) aortic pre-ejection time, (4) interventricular mechanical delay (IVMD), (5) LVOT VTI and (6) QRS duration. In each patient, we identified with blinding on several successive repetitions, an apparently-optimal (minimally-dyssynchronous) interventricular delay for each variable. Agreement between successive optimisations was low: κ values of 0.24 for SDI, 0.02 for TDI, 0.36 for aortic pre-ejection time, 0.14 for IVMD, 0.40 for LVOT VTI and 0.47 for QRS duration. Intraclass correlation coefficient, indicating measurement reproducibility, was low when single measurements were taken (ranging across methods from 0.32 to 0.63), but improved when pairs of measurements were averaged (0.51 to 0.74, p=0.0008). Using averages of pairs of measurements reduced the disagreement between replicate optimisations p=0.007. <h3>Conclusions</h3> Under blinded conditions these mechanical dyssynchrony markers cannot reliably discriminate even large changes in interventricular delay, and can be quickly rejected as candidates for predicting clinical benefit from CRT. It would save time and expense if markers considered for clinical trialling under formal scientific conditions first underwent screening for plausibility by such a stage of inexpensive, active experimentation.

005 Cardiac MRI: understanding myocardial motion to predict remodelling pre cardiac resynchronisation therapy

IntroductionA significant number of patients undergoing Cardiac Resynchronisation Therapy (CRT) do not remodel. Assessing global dyssynchrony has the potential to improve patient selection. We developed a framework for comparing measures...

A Pilot Study of Systolic Dyssynchrony Index by Real Time Three‐Dimensional Echocardiography and Doppler Tissue Imaging Parameters Predicting the Hemodynamic Response to Biventricular Pacing in the Early Postoperative Period after Cardiac Surgery

To evaluate systolic dyssynchrony index (SDI) measured by real time three-dimensional echocardiography (RT3DE) and Doppler tissue imaging (DTI) dyssynchrony parameters in predicting the hemodynamic response to biventricular (BIV) pacing in the early postoperative period after cardiac surgery. To compare right ventricular (RV) and BIV pacing using invasively measured hemodynamic values. A prospective randomized clinical study enrolling 11 patients with ischemic heart disease, concomitant valvular heart disease, and left ventricular ejection fraction (LVEF) ≤ 35% comparing preoperative SDI by RT3DE and DTI LV dyssynchrony parameters to hemodynamic values obtained during RV or BIV sequential (DDD) epicardial pacing in the first 72 hours after cardiac surgery. BIV pacing produced a statistically significant higher cardiac output (CO) (6.27 ± 1.55 L/min) and cardiac index (CI) (3.44 ± 0.93 L/min per m(2) ) than RV pacing (CO 5.44 ± 0.97 L/min, CI 3.03 ± 0.83 L/min per m(2) , P < 0.05). We found a statistically moderate correlation between preoperative SDI by RT3DE and CO (r = 0.596, P < 0.05) and a nonsignificant correlation to CI (r = 0.535, P < 0.10) during BIV pacing. No correlation was observed between DTI dyssynchrony parameters and measured hemodynamic values. BIV pacing reduced the ICU stay and inotropic support requirements of patients after heart surgery. SDI measured preoperatively using RT3DE can predict CO during BIV pacing in the early postoperative period after cardiac surgery. BIV pacing is more hemodynamically effective than RV pacing in patients with LV dysfunction after coronary artery bypass grafting with or without a valve procedure.

Comparison of quick optimization of interventricular delay between simple methods: intracardiac electrogram and surface electrocardiogram after cardiac resynchronization therapy

It is time consuming to obtain optimal interventricular (VV) delay by conventional methods. This study is designed to compare quick optimization between intracardiac electrogram (IEGM) with surface electrocardiogram (ECG)-guided VV delay optimization for cardiac resynchronization therapy (CRT). Fifty-one heart failure patients (M/F = 34/17, age = 71 ± 10-year-old) scheduled for CRT implantation were included. After atrioventricular optimization, VV delay optimization was performed by either the IEGM or surface ECG method. Aortic velocity time integral (AVTI) was used as a reference in comparing these two methods. Real-time three-dimensional echocardiography was studied under three varying parameters-CRT switched off or CRT switched on, and VV delay optimized by IEGM guided or surface ECG. The AVTI could be improved equally by either IEGM-guided or surface ECG-guided VV optimization. All the other parameters [QRS width, systolic dyssynchrony index (SDI), left ventricular ejection fraction (LVEF), left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV)] could be improved by either the IEGM or ECG method in these patients. In the multivariate logistic regression analysis, the immediate improvement of acute LVEF was independently related to favourable outcomes (odds ratio 1.23, 95% CI = 1.03-1.47, P = 0.02). The AVTI, QRS width, SDI, LVEF, LVEDV, and LVESV could be improved equally by either IEGM-guided or surface ECG-guided method after CRT.

The Relationship Between Aortic Stiffness and Left Ventricular Dyssynchrony in Hypertensive Patients with Preserved Left Ventricular Systolic Function

Left ventricular (LV) dyssynchrony is often seen in patients with hypertension, even without heart failure. Arterial stiffness is well accepted as an important factor of increasing blood pressure and influencing ventricular function. The purpose of this study was to determine the relationship between aortic stiffness and LV dyssynchrony in hypertensive patients with preserved LV systolic function. Eighty hypertensive patients with preserved LV systolic function (LV ejection fraction > 50%) and 30 controls were studied. The LV systolic and diastolic dyssynchrony indices were determined as the standard deviation of the time interval from onset of the QRS complex to peak myocardial systolic velocity (Ts-SD) and to early diastolic velocity (Te-SD) and the maximal differences in Ts (Ts-Max) and Te (Te-Max) in 12 LV segments. Aortic stiffness index was calculated from aortic diameters in the systolic and diastolic phases, as measured by echocardiography and blood pressure. No relationship was observed between LV systolic and diastolic dyssynchrony indices (r = 0.057, P = .61). In simple regression, aortic stiffness parameter was related to left ventricular mass index (LVMI), E/A ratio, and LV diastolic dyssynchrony index. But using multiple linear regression, Te-Max remained as a single variable related to aortic strain and aortic stiffness index (r = −0.271, P = .008 and r = 0.269, P = .008). LVMI was related to aortic distensibility using multiple linear regression (r = −0.239, P = .02). Aortic stiffness index was related to LV diastolic dyssynchrony index and LVMI. These findings suggest that LV diastolic dyssynchronous changes may be caused by increased LV mass and arterial stiffness.

Relationship between left ventricular dyssynchrony and systolic dysfunction is independent of impaired left ventricular myocardial perfusion in heart failure: Assessment with 99mTc-sestamibi gated myocardial scintigraphy

BackgroundsLeft ventricular (LV) dyssynchrony reduces LV systolic function in patients with heart failure (HF). However, it remains unknown whether this relationship is independent of impaired LV myocardial perfusion. Methods and resultsA total of 105 patients with chronic HF (age 71±13years; 71 men) were enrolled in the present study. 99mTc-sestamibi (MIBI) gated myocardial scintigraphy was performed at rest to assess LV myocardial perfusion as evaluated by the total defect score of perfusion Single Photon Emission Computed Tomography images (TDS-MIBI), LV systolic function as evaluated by LV ejection fraction (LVEF), and LV systolic dyssynchrony as evaluated by the maximal difference of time to end systole (MD-TES), which is the time lag between the earliest and the latest end systole among 17 LV segments analyzed with a novel program, “cardioGRAF”. The mean±SD (minimum and maximum range) of the MD-TES was 147.8±117.5 (14.0–458.3)ms. The MD-TES was significantly higher in patients with LVEF<45% (199.4±117.6ms) than in those with LVEF≥45% (60.5±41.2ms, p<0.001). In a multiple logistic regression analysis, the MD-TES showed an increased odds ratio for LVEF<45% (2.46 [95% CI; 1.51–4.01] per increment in decile of MD-TES rank, p<0.001), after adjusting for the TDS-MIBI, history of myocardial infarction, and other potential confounders. ConclusionsLV dyssynchrony is a significant determinant of LV systolic dysfunction in patients with HF, and this relationship is independent of impaired LV myocardial perfusion and history of myocardial infarction.

Impact of antihypertensive treatment on left ventricular systolic dyssynchrony in treatment-naïve hypertensive patients

Dyssynchrony is common in asymptomatic patients with hypertension. We sought to investigate the impact of antihypertensive treatment on dyssynchrony in patients with hypertension. A total of sixty patients who had uncomplicated hypertension that had never been treated (treatment-naïve hypertensive patients) underwent echocardiographic evaluations of left ventricular (LV) dyssynchrony at baseline and after a 6-month treatment with antihypertensive drugs. The measured parameters were as follows: (1) the s.d. of 12 LV-segment time-to-peak systolic velocities (Ts-SD12), and (2) the maximal difference between peak systolic velocities of any 2 of the 12 segments (Ts-Max). Patients with Ts-SD12 ≥ 33 ms or Ts-Max ≥ 100 ms were regarded as having LV systolic dyssynchrony. Patients with systolic dyssynchrony (group 1, n = 29) and without systolic dyssynchrony (group 2, n = 31) were compared. Among the patients in group 1, antihypertensive treatment significantly improved LV systolic dyssynchrony (ΔTs-SD12, -13.1 ms; P<0.001 and ΔTs-Max, -34.0 ms; P = 0.003), whereas it did not demonstrate additional benefit among group 2 patients. The change in LV systolic dyssynchrony was significantly associated with changes in the mean annulus E' velocity, mean annulus S' velocity and mean annulus E'/A' ratio, but not with changes in blood pressure and LV mass index. It is likely that chronic antihypertensive treatment could reverse the LV systolic dyssynchrony and simultaneously improve subclinical systolic and diastolic function in patients with hypertension and LV systolic dyssynchrony.