Left Ventricular Diastolic Dyssynchrony Research Articles

P1488Single wave mitral inflow pattern caused by left ventricular diastolic dyssynchrony in patients with heart failure

Abstract Background Mitral E and A waves could fuse to form a single wave in tachycardia. Patients with heart failure (HF) occasionally show single wave mitral inflow despite of non-tachycardiac condition. Purpose To investigate mechanisms of single wave mitral inflow in HF patients with sinus rhythm and normal heart rate. Methods A total of 60 HF patients, including 20 single wave (SW), 20 impaired relaxation (IR) and 20 pseudonormalized (PN) mitral inflow patterns were retrospectively enrolled. All the patients were in sinus rhythm under 85 bpm. Patients with bundle branch blocks and first-degree heart block were excluded. We compared basic echo measurements, magnitude of left ventricular (LV) diastolic dyssynchrony, isovolumic relaxation time (IRT) and BNP levels among 3 groups. Diastolic dyssynchrony was determined as standard deviation of interval between aortic valve closure and peak early diastolic wave of longitudinal strain across 16 LV myocardial segments using 2D speckle tracking echocardiography. Results There was no significant difference in heart rate among 3 groups. Patients with SW showed significantly large magnitude of diastolic dyssynchrony (4.1±1.1) compared to those with IR (2.7±0.7) and PN (2.9±0.9ms), respectively. Likewise, IRT of SW (7.1±2.7) was longer than IR (3.2±0.8) and PN (2.4±0.9ms). BNP level in patients with IR (153±111) was significantly lower than those with SW (558±432) and PN (523±263pg/ml). Representative cases Conclusion HF patients with SW could be caused by LV diastolic dyssynchrony and their BNP levels are comparable to those with PN.

Impact of Left Bundle Branch Block on Left Atrial Dyssynchrony and Its Relationship to Left Ventricular Diastolic Function in Patients with Heart Failure and Dilated Cardiomyopathy.

Background and ObjectivesThe impact of left bundle branch block (LBBB) on left atrial (LA) dyssynchrony in heart failure (HF) patients with non-ischemic dilated cardiomyopathy (DCM) has not been clearly elucidated.MethodsEighty consecutive symptomatic HF patients with non-ischemic DCM (left ventricular ejection fraction, LVEF<35%) were included. LBBB was defined on electrocardiography. Left ventricular (LV) systolic and diastolic dyssynchrony index and LA dyssynchrony index were obtained by color-coded tissue Doppler imaging.ResultsThere was no significant difference in LV size, LVEF, LV global longitudinal strain, peak atrial longitudinal strain and LA volume between patients with LBBB (n=38) and no LBBB (n=42). There was a significant difference in LV systolic dyssynchrony index (p=0.014) and there was a mild difference in LV diastolic synchronicity index (p=0.045) between patients with LBBB and no LBBB. However, there was no difference in LA dyssynchrony index between the 2 groups (p=0.60). LA dyssynchrony index was not related to LV systolic and diastolic dyssynchrony indexes, but it was related to the deceleration time of mitral early diastolic velocity (E), the ratio of E to mitral annular early diastolic velocity (E/e′) and LA volume. E/e′ was most related to LA dyssynchrony index (r2=0.325, p=0.002).ConclusionsLBBB influences both LV systolic and diastolic dyssynchrony, but not LA dyssynchrony. LA dyssynchrony was related to LV diastolic function regardless of the presence of LBBB in in patients with non-ischemic DCM.

Relationship between left ventricular diastolic dyssynchrony and systolic dyssynchrony in hypertrophic cardiomyopathy by single-cardiac real-time three-dimensional ultrasonography.

The relationship between left ventricular diastolic and systolic dyssynchrony in hypertrophic cardiomyopathy (HCM) was investigated by single-cardiac real-time three-dimensional ultrasonography. A total of 52 patients with HCM were selected in Jining No. 1 People's Hospital from July 2016 to June 2017. Additionally, a total of 52 healthy people were selected to serve as the control group. All participants received real-time two- and three-dimensional ultrasonography to evaluate left ventricular morphology, function and systolic and diastolic function. The relevant parameters included left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular ejection fraction (LVEF), end-systolic/diastolic sphericity index (ESSI/EDSI), systolic dyssynchrony index (SDI), diastolic dyssynchrony index (DDI), dispersion end systole (DISPES), diastolic dyssynchrony index-late (DDI-late) and dispersion end diastole (DISPED-late). The LVEF of observation group was significantly lower than that of the control group, while LVEDV, LVESV, E/A and E/Ea were significantly higher than those in control group (P<0.05); EDSI, DDI-late and DISPED-late were significantly higher in observation than in control group (P<0.05); ESSI, SDI and DISPES in observation were significantly higher than those in control group (P<0.05); The 16-segment time-volume curve of observation group was disordered without synchronization, while the curve of control group was regular and smooth with synchronization; Pearson's correlation analysis showed that SDI and DDI were positively correlated (P<0.05). In conclusion, three-dimensional ultrasonography can be used to effectively evaluate left ventricular diastolic and systolic dyssynchrony in HCM. The severity of diastolic is positively correlated with systolic dyssynchrony.

Ventricular dyssynchrony in pregnant women: A tissue Doppler study.

The aim of the study was to assess the left ventricular (LV) synchronicity in pregnant women and to identify the main determinants of LV dyssynchrony in asymptomatic pregnant women. One hundred sixty-seven pregnant women consecutively and 48 age-matched nonpregnant controls were enrolled. For the assessment of LV systolic dyssynchrony, the standard deviation of the time from QRS onset to peak systolic (Tps-LV- standard deviation [SD]) velocity and the maximal difference of the time from QRS onset to peak systolic velocity (Tps-LV) from 12 segments at the apical views. For the LV diastolic dyssynchrony, the standard deviation of the time from QRS onset to peak diastolic (Tpe-LV-SD) velocity and the maximal difference of the time from QRS onset to peak diastolic velocity (Tpe-LV) were calculated. Both systolic and diastolic dyssynchrony indexes were significantly higher in pregnant women than in the normal controls (Tps-LV; P<.01, Tps-LV-SD; P<.03, Tpe-LV, P<.05 and Tpe-LV-SD; P<.02). A total of 28 (16.8%) of the pregnant women had a dyssynchrony index above the accepted value for LV dyssynchrony (>34.4msec). There was a significant correlation between LV dyssynchrony indexes with, multiparty, multifetal pregnancies, systolic blood pressure in pregnant women with LV dyssynchrony. Additionally LV dyssynchrony was significantly associated with elevated E/e" and brain natriuretic peptide (BNP). Both systolic synchronicity and diastolic synchronicity were affected in pregnant women compared to nonpregnant women. LV dyssynchrony was significantly correlated with age, multiparity, and BNP level. Early detectable changes in systolic and diastolic synchrony may be present in pregnant women at higher risk of peripartum cardiomyopathy.

Afterload-induced left ventricular diastolic dysfunction during myocardial ischaemia and reperfusion.

What is the central question of this study? While the load dependence of the diastolic function is established for the normal heart, little is known about the response of the acutely ischaemic and reperfused myocardium to alterations in afterload. What is the main finding and its importance? Using a model that simulates the clinical scenario of acute ischaemia-reperfusion, we show that increased afterload aggravates diastolic dysfunction during both acute ischaemia and reperfusion. In addition, increased afterload induces diastolic dyssynchrony, which might be the underlying mechanism of the diastolic dysfunction of the ischaemic myocardium. These findings provide us with new information regarding how better to manage patients who undergo revascularization therapy after acute myocardial infarction. The effects of changes in left ventricular (LV) afterload on diastolic function of acutely ischaemic and reperfused myocardium have not been studied in depth. We examined the following factors: (i)the consequences of increasing the LV afterload on LV diastolic function during acute ischaemia and reperfusion; (ii)whether the myocardial response to afterload elevation is stable throughout a 2h reperfusion period; and (iii)the role of LV wall synchrony in the development of afterload-induced diastolic dysfunction. We instrumented 12 anaesthetized, open-chest pigs with Millar pressure catheters and piezoelectric crystals before ligating mid-left anterior descending coronary artery for 1h, followed by reperfusion for 2h. Six of the animals survived throughout the 2h of reperfusion, and their data were used for comparisons across the different experimental phases. Left ventricular afterload was increased by inflating an intra-aortic balloon. Data were recorded at baseline, after 20min of coronary occlusion and at 30 and 90min of myocardial reperfusion. The increased afterload for 2min lengthened the isovolumic relaxation during ischaemia and during early and late reperfusion but had no significant effect on isovolumic relaxation before coronary artery occlusion. Increasing the afterload aggravated LV diastolic dyssynchrony during coronary artery occlusion, but not during reperfusion. The afterload-induced prolongation of isovolumic relaxation was positively correlated with afterload-induced diastolic dyssynchrony. These observations indicate that, during myocardial ischaemia and throughout reperfusion, LV diastolic function is afterload dependent. Afterload-induced diastolic dyssynchrony might be an underlying mechanism of diastolic dysfunction during acute ischaemia.

Left ventricular diastolic dyssynchrony in patients with treatment-naive hypertension and the effects of antihypertensive therapy.

The presence of left ventricular diastolic dyssynchrony is well known to be a frequent and important manifestation in heart failure. We investigated diastolic dyssynchrony in patients with treatment-naive hypertension, compared with normal controls; the determinants of the presence of diastolic dyssynchrony by performing comprehensive studies including laboratory, arterial stiffness, central blood pressure (BP), ambulatory BP monitoring (ABPM), and transthoracic echocardiography (TTE) evaluations; the effects of 6-month antihypertensive therapy on diastolic dyssynchrony; and the predictors associated with the change of diastolic dyssynchrony after medical therapy. A total of 325 treatment-naive hypertensive patients and 172 normal controls were prospectively enrolled. Hypertensive patients were followed up at 6 months after medical therapy, and were assessed by serial TTE (at baseline and 6-month follow-up visit) and clinical evaluations. The time-to-peak myocardial early diastolic velocity (Te) of the 12 left ventricular segments was measured with reference to the QRS complex. The standard deviation (SD) of Te of all 12 left ventricular segments (Te-SD12) and the maximal difference in Te between any two of the 12 left ventricular segments (Te-Max) were calculated. A Te-SD12 at least 34 or Te-Max at least 113 ms was regarded as indicating the presence of diastolic dyssynchrony. Diastolic dyssynchrony was more prevalent in treatment-naive hypertensive patients, compared with normal controls (15.4 versus 7.0%, P = 0.007). Male sex [odds ratio (OR), 9.36 (1.93-45.41)], magnesium [OR per 1 SD, 2.54 (1.32-4.90)], night-time heart rate [HR; OR per 1 SD, 2.44 (1.18-5.05)], and mitral E/A [OR per 1 SD, 0.13 (0.04-0.45)] were independent determinants for the diastolic dyssynchrony in hypertensive patients. A 6-month follow-up, echocardiography was performed in 74 of 275 patients without diastolic dyssynchrony (group 1) and 26 of 50 patients with diastolic dyssynchrony (group 2). Diastolic dyssynchrony (Te-SD12, Δ = -8.3 ms; Te-Max, Δ = -27.6 ms; prevalence, Δ = -42.3%; all P < 0.05) improved in group 2, whereas it did not in group 1. Baseline daytime HR (P = 0.008) and magnesium levels (P = 0.029) and changes of the midwall fractional shortening (P = 0.026), mitral E/A (P = 0.003), mean annulus Ea (P = 0.003), mean annulus Ea/Aa (P = 0.020), and mitral peak E (P = 0.042) were independent predictors for changes of Te-SD12. Diastolic dyssynchrony is not rare in treatment-naive hypertensive patients. Male sex, magnesium levels, night-time HR, and mitral E/A are independent determinants for the impaired diastolic dyssynchrony. Antihypertensive therapy reduces both the severity and prevalence of diastolic dyssynchrony in patients with impaired diastolic dyssynchrony. Daytime HR, magnesium levels, and indications of systolic or diastolic dysfunction are independent predictors for improvements in diastolic dyssynchrony. Thus, magnesium levels, HR, and diastolic dysfunction seem to have important implications for diastolic dyssynchrony in hypertensive patients, whereas left ventricular hypertrophy, office BPs, arterial stiffness, central BPs, and ABPM parameters do not.

Early diastolic dyssynchrony in relation to left ventricular remodeling and function in hypertension

BackgroundCardiac synchronization is important in maintaining myocardial performance, but the mechanism of diastolic dyssynchrony leading to failing myocardium is unclear. We aim to study the relation of left ventricular (LV) diastolic dyssynchrony with diastolic dysfunction in patients with hypertension. MethodsTwo-D, three-D and Doppler echocardiography were performed using the GE Vivid E9 system on 230 subjects. Among them, 154 patients with hypertension were divided into group 1 (86 patients with mild to moderate hypertension, BP 152±8/91±11mmHg) and group 2 (68 patients with severe hypertension, BP 188±12/105±24mmHg), age 76, gender matched normotensive subjects (119±6/76±9mmHg) as control. The routine 2D and Doppler parameters were measured and LV systolic and diastolic dyssynchrony indices were determined as the standard deviation of the time interval from the peak R of the QRS complex to peak myocardial systolic strain rate (Ts-SD), and to early diastolic strain rate (Te-SD) of 12 LV segments. ResultsLV relative wall thickness, mass index, and Te-SD were significantly higher in patients with hypertension than in control group (p<0.0001), but Ts-SD showed no significant differences. Te-SD and diastolic dysfunction worsened progressively with increasing severity of hypertension (p<0.05). Te-SD was significantly and independently associated with parameters of LV remodeling and diastolic function. ConclusionOur study demonstrated that LV diastolic dyssynchrony was associated with LV remodeling, which seems to contribute to diastolic dysfunction in hypertension. This diastolic dyssynchrony index derived from speckle tracking echocardiography can be used as a marker for studying the LV function and effects of therapy in hypertensive heart disease.

MONITORING OF HYPERTENSION USING SMARTPHONE APPLICATIONS: A SYSTEMATIC REVIEW

s S213 309 MONITORING OF HYPERTENSION USING SMARTPHONE APPLICATIONS: A SYSTEMATIC REVIEW CN Floyd, K Parmesar, A Ferro London, United Kingdom BACKGROUND: Smartphone applications (apps) have become integrated with many aspects of modern life, with >100,000 apps currently available for use in healthcare. Apps are unregulated and potentially place patients at risk if the information they contain is inaccurate. Additionally, any app that transforms clinical data (e.g. calculating a mean blood pressure (BP)) is a Class 1 medical device and should be registered with the Medicines and Healthcare Regulatory Agency in the UK. Here we present a systematic review of blood pressure (BP) monitoring apps available in the UK. METHODS: The Apple App Store (UK) was searched on 15th March 2014 using the terms “hypertension” OR “blood pressure”. Inclusion criteria were iPhone compatibility, free to use, English language, targeted for patient use, ability to record multiple BP readings and app functionality independent of other medical devices. Data were extracted from each app according to a predefined protocol: conformity to guidelines, presence of data transformation, limits to data input and data protection policy. RESULTS: Following the removal of duplicates, 608 apps were identified of which 96 met the inclusion criteria. Five apps provided advice on how to measure BP, of which four claimed conformity to national and/or international guidelines. A further 11 apps providing advice unrelated to BP measurement technique also claimed conformity to guidelines (15 apps in total; 16%). No apps stated approval by recognised societies. Data transformation was performed by 24 apps (25%), none of which displayed regulatory approval. Three apps did recommend using a specific approved sphygmomanometer, with one providing formulae used for subsequent data transformation. Data input was subject to checks in 60% (58 apps) to ensure that diastolic values were lower than systolic. 25% (24 apps) required a passcode to access stored data, but it was unclear where data was stored (e.g. locally on device or on a server) in 89% of apps. CONCLUSION: There are many apps freely available to patients that enable them to record BP measurements. These unregulated apps conform poorly to recognised guidelines and have the potential to harm if their advice or data transformations are inaccurate. 310 LEFT VENTRICULAR DIASTOLIC DYSSYNCHRONY IN PATIENTS WITH TREATMENT-NAIVE HYPERTENSION AND THE EFFECTS OF ANTIHYPERTENSIVE THERAPY B Kwon, J Roh, H Kim, S Ihm Seogwipo, Korea, Republic of BACKGROUND: We investigated (1) DD in patients with treatment-naive hypertension, compared with normal controls; (2) the determinants of the presence of DD by performing comprehensive studies including laboratory, arterial stiffness, central blood pressure (BP), ambulatory BP monitoring (ABPM), and transthoracic echocardiography (TTE) evaluations; (3) the effects of 6-month antihypertensive therapy on DD; and (4) the predictors associated with change of DD after medical therapy. METHODS: 325 treatment-naive hypertensive patients and 172 normal controls were prospectively enrolled. Hypertensive patients were followed up at 6 months after medical therapy, and were assessed by serial TTE (at baseline and 6-month follow-up visit) and clinical evaluations. The time-to-peak myocardial early diastolic velocity (Te) of the 12 LV segments was measured with reference to the QRS complex. The standard deviation (SD) of Te of all 12 LV segments (TeSD12) and the maximal difference in Te between any 2 of the 12 LV segments (Te-Max) were calculated. A Te-SD12 34 or Te-Max 113 ms was regarded as indicating the presence of DD. RESULTS: DD was more prevalent in treatment-naive hypertensive patients, compared with normal controls (15.4% vs. 7.0%, P1⁄40.007). Male (odds ratio [OR], 7.60, 1.6934.30), magnesium (OR per 1 SD, 4.18, 1.54-11.30), nighttime heart rate (HR) (OR per 1 SD, 2.79, 1.19-6.53), and mitral E/A (OR per 1 SD, 0.11, 0.03-0.41) were independent determinants for the DD in hypertensive patients. A 6-month follow-up echocardiography was performed in 74 of 275 patients without DD (group 1) and 26 of 50 patients with DD (group 2). DD (Te-SD12, D1⁄4-8.3 ms and Te-Max, D1⁄4-27.6 ms and prevalence, D1⁄4-42.3%, all P<0.05) improved in group 2, while those did not in group 1. Baseline daytime HR (P1⁄40.008) and magnesium levels (P 1⁄4 0.029) and changes of the mitral E/A (P 1⁄4 0.003), mean annulus Ea (P 1⁄4 0.003), mean annulus Ea/Aa (P 1⁄4 0.020), and mitral peak E (P 1⁄4 0.042) were independent predictors for changes of DD. CONCLUSION: DD is not rare in treatment-naive hypertensive patients. Male gender, magnesium levels, nighttime HR, and mitral E/A are independent determinants for the impaired DD. Antihypertensive therapy reduces both the severity and prevalence of DD in patients with impaired DD. Daytime HR, magnesium levels, and indicative of diastolic dysfunction are independent predictors for improvements in DD. Thus, magnesium levels, HR, and diastolic dysfunction seem to have important implications for DD in hypertensive patients, whereas LV hypertrophy, office BPs, arterial stiffness, central BPs, and ABPM parameters do not.

Left ventricular systolic and diastolic dyssynchrony assessed by phase analysis of gated SPECT myocardial perfusion imaging: a comparison with speckle tracking echocardiography

The objective of this study was to compare left ventricular (LV) systolic and diastolic dyssynchrony parameters measured by phase analysis on gated single-photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI) with those measured by speckle tracking echocardiography (STE). Two patient groups were enrolled from the Chang Bing Show Chwan Memorial Hospital. The systolic group consisted of patients with reduced LV ejection fraction (LVEF) of <50 % as assessed by routine echocardiography. The diastolic group consisted of patients with normal LVEF (>50 %) and diastolic dysfunction according to routine echocardiography (E/A <1, E/E' >8). LV systolic and diastolic dyssynchrony parameters were calculated using STE as the maximal peak-time delay between peak radial strains of two opposing LV walls and as the standard deviation of the time to peak radial strains in 6 mid-LV segments. All of the patients had gated SPECT MPI within 6 ± 11 days post STE. Phase analysis was performed on the resting gated SPECT MPI images to calculate systolic and diastolic phase standard deviation and phase histogram bandwidth as markers of LV systolic and diastolic dyssynchrony, respectively. Fifty-two consecutive patients (40 men, mean age = 66 ± 13 years, LVEF = 34.4 ± 10.2 %) were enrolled in the systolic group, whereas 30 consecutive patients (15 men, mean age = 69 ± 11 years, LVEF = 72.3 ± 4.7 %, E/A all <1, E/E' = 11.7 ± 2.2) were enrolled in the diastolic group. LV systolic and diastolic dyssynchrony parameters measured by phase analysis of gated SPECT MPI and STE were correlated well in both systolic and diastolic groups, respectively. Phase analysis on gated SPECT MPI showed good correlations with STE and is suitable for the assessment of LV systolic and diastolic dyssynchrony. As assessed with the phase analysis and STE techniques, the patients with severe LV systolic dysfunction had severe LV systolic dyssynchrony, but the patients with LV diastolic dysfunction were not necessarily with LV diastolic dyssynchrony, indicating that the LV diastolic dyssynchrony parameters characterized independent mechanisms of LV regional diastolic function.

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.

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.

Left ventricular diastolic dyssynchrony assessed with phase analysis of gated myocardial perfusion SPECT: a comparison with tissue Doppler imaging

PurposeThe aim of the current study was to evaluate the feasibility of phase analysis on gated myocardial perfusion SPECT (GMPS) for the assessment of left ventricular (LV) diastolic dyssynchrony in a head-to-head comparison with tissue Doppler imaging (TDI).MethodsThe population consisted of patients with end-stage heart failure of New York Heart Association functional class III or IV with a reduced LV ejection fraction of ≤35%. LV diastolic dyssynchrony was calculated using TDI as the maximal time delay between early peak diastolic velocities of two opposing left ventricle walls (diastolic mechanical delay). Significant LV diastolic dyssynchrony was defined as a diastolic mechanical delay of >55 ms on TDI. Furthermore, phase analysis on GMPS was performed to evaluate LV diastolic dyssynchrony; diastolic phase standard deviation (SD) and histogram bandwidth (HBW) were used as markers of LV diastolic dyssynchrony.ResultsA total of 150 patients (114 men, mean age 66.0 ± 10.4 years) with end-stage heart failure were enrolled. Both diastolic phase SD (r = 0.81, p < 0.01) and diastolic HBW (r = 0.75, p < 0.01) showed good correlations with LV diastolic dyssynchrony on TDI. Additionally, patients with LV diastolic dyssynchrony on TDI (>55 ms) showed significantly larger diastolic phase SD (68.1 ± 13.4° vs. 40.7 ± 14.0°, p < 0.01) and diastolic HBW (230.6 ± 54.3° vs. 129.0 ± 55.6°, p < 0.01) as compared to patients without LV diastolic dyssynchrony on TDI (≤55 ms). Finally, phase analysis on GMPS showed a good intra- and interobserver reproducibility for the determination of diastolic phase SD (ICC 0.97 and 0.88) and diastolic HBW (ICC 0.98 and 0.93).ConclusionPhase analysis on GMPS showed good correlations with TDI for the assessment of LV diastolic dyssynchrony.

Myocardial Contractile Inefficiency and Dyssynchrony in Heart Failure With Preserved Ejection Fraction and Narrow QRS Complex

Using speckle-tracking imaging (STI), the aims of this study were to assess dyssynchrony and quantify the myocardial energy wasted by contractility in delayed segments by determining the longitudinal strain delay index (LSDi) in patients with heart failure with preserved ejection fraction (HFpEF). Thirty-eight patients with HFpEF and 33 matched controls were recruited. All subjects underwent clinical examinations, 12-lead electrocardiography, pulmonary function tests, echocardiography, and metabolic exercise tests. LSDi was determined, the magnitude of which is a measure of the amount of wasted energy. Global and segmental systolic and diastolic dyssynchrony was assessed by STI. LSDi was significantly higher in patients with HFpEF than controls (-14.36 +/- 8.24% vs -10.73 +/- 5.62%, P < .05). Patients with HFpEF exhibited left ventricular (LV) systolic and diastolic dyssynchrony, with the LV anterior wall displaying the most delayed motion. Patients with HFpEF exhibited increased myocardial contractile inefficiency. They also exhibited LV systolic and diastolic dyssynchrony, with the LV anterior wall displaying the most delayed motion.

Left Ventricular Systolic and Diastolic Dyssynchrony in Asymptomatic Hypertensive Patients

Diastolic and systolic dyssynchrony are common in patients with heart failure. However, the presence of dyssynchrony in asymptomatic patients with hypertension who are susceptible to the development of heart failure is not well understood. The aims of this study were (1) to evaluate the prevalence of systolic and diastolic dyssynchrony and (2) to identify the main determinants of left ventricular (LV) dyssynchrony in asymptomatic patients with hypertension. One hundred ten patients with hypertension consecutively enrolled were compared with 55 age-matched and gender-matched normal control subjects. Comprehensive echocardiography was performed, including conventional and Doppler tissue imaging parameters. LV end-systolic wall stress was calculated using a hemodynamic and echocardiographic M-mode data set. For the assessment of LV dyssynchrony, both the standard deviation of the time from QRS onset to peak systolic velocity and the maximal difference of the time from QRS onset to peak systolic velocity from 6 basal segments at the apical views were used and were compared between the two groups. Both systolic and diastolic dyssynchrony indexes were significantly higher in patients with hypertension than in the normal controls (P < .001), with no significant correlation between the systolic and diastolic dyssynchrony indexes. The proportions of patients with hypertension who had LV systolic and diastolic dyssynchrony were 24% and 21%, respectively. Multivariate analysis showed that the E/E' ratio (P < .001) was independently associated with LV systolic dyssynchrony, whereas LV mass index (P = .001) and E/E' (P < .001) were major determinants of LV diastolic dyssynchrony. LV systolic and diastolic dyssynchrony are not uncommon in asymptomatic patients with hypertension and are significantly associated with LV filling pressure. The determinants of LV systolic dyssynchrony are not the same as those of diastolic dyssynchrony, implying that different mechanisms are involved in the development of LV systolic and diastolic dyssynchrony in asymptomatic patients with hypertension.

Left ventricular systolic and diastolic dyssynchrony in coronary artery disease with preserved ejection fraction

The present study aims to evaluate LV (left ventricular) mechanical dyssynchrony in CAD (coronary artery disease) with preserved and depressed EF (ejection fraction). Echocardiography with TDI (tissue Doppler imaging) was performed in 311 consecutive CAD patients (94 had preserved EF > or =50% and 217 had depressed EF <50%) and 117 healthy subjects to determine LV systolic and diastolic dyssynchrony by measuring Ts-SD (S.D. of time to peak myocardial systolic velocity during the ejection period) and Te-SD (S.D. of time to peak myocardial early diastolic velocity during the filling period) respectively, using a six-basal/six-mid-segmental model. In CAD patients with preserved EF, both Ts-SD (32.2+/-17.3 compared with 17.7+/-8.6 ms; P<0.05) and Te-SD (26.2+/-13.6 compared with 20.3+/-8.1 ms; P<0.05) were significantly prolonged when compared with controls, although they were less prolonged than CAD patients with depressed EF (Ts-SD, 37.8+/-16.5 ms; and Te-SD, 36.0+/-23.9 ms; both P<0.005). Patients with preserved EF who had no prior MI (myocardial infarction) had Ts-SD (32.9+/-17.5 ms) and Te-SD (28.6+/-14.8 ms) prolonged to a similar extent (P=not significant) to those with prior MI (Ts-SD, 28.4+/-16.8 ms; and Te-SD, 25.5+/-15.0 ms). Patients with class III/IV angina or multi-vessel disease were associated with more severe mechanical dyssynchrony (P<0.05). Furthermore, the majority of patients with mechanical dyssynchrony had narrow QRS complexes in those with preserved EF. This is in contrast with patients with depressed EF in whom systolic and diastolic dyssynchrony were more commonly associated with wide QRS complexes. In conclusion, LV mechanical dyssynchrony is evident in CAD patients with preserved EF, although it was less prevalent than those with depressed EF. In addition, mechanical dyssynchrony occurred in CAD patients without prior MI and narrow QRS complexes.