Systolic and diastolic regional myocardial motion of pacing-induced versus idiopathic left bundle branch block with and without left ventricular dysfunction

To demonstrate systolic and diastolic asynchrony in patients with left bundle branch block (LBBB), tissue Doppler imaging (TDI) of 4 different walls was performed in 27 normal controls, 29 patients with right ventricular pacing and normal left ventricular (LV) ejection fraction (EF; pacing LBBB), and 35 patients with idiopathic LBBB. Patients with idiopathic LBBB were further classified into those with LVEF >50% and those with LVEF <35%. Asynchrony was calculated as the coefficient of variation of the time intervals from the QRS complex to the peak systolic velocity and to the peak of early diastolic relaxation. Patients with pacing and idiopathic LBBB had significantly longer QRS durations (162 +/- 20 vs 92 +/- 7 ms, p <0.001) and larger systolic (15.9 +/- 5.0% vs 4.1 +/- 2.1%, p <0.001) and diastolic (3.7 +/- 2.0% vs 1.4 +/- 0.6%, p <0.001) asynchrony than controls. Those with idiopathic LBBB and low EF had significantly larger diastolic asynchrony (5.7 +/- 2.1%) than those with pacing LBBB (2.9 +/- 1.1%) and those with idiopathic LBBB and normal EF (2.0 +/- 0.6%). Diastolic asynchrony was the only independent factor that correlated with LVEF (r = -0.64, p <0.001). Thus, idiopathic LBBB with LV dysfunction is characterized not only by systolic but also by diastolic asynchrony.     

Intra- and interatrial asynchrony in patients with heart failure

Heart failure (HF) is associated with atrial conduction delay. Color tissue Doppler imaging was used to evaluate intra- and interatrial asynchrony in patients with HF, patients with structural heart disease without HF, and controls. Twenty-three controls (mean age 65 +/- 13 years), 29 patients with structural heart disease without HF (mean age 68 +/- 9 years), and 29 patients with HF (mean age 67 +/- 9 years) were studied. Patients had no histories of atrial fibrillation. Echocardiographic color tissue Doppler imaging of the atria was performed. Measurements below the atrioventricular plane were selected on the right atrial (RA) free wall, interatrial septum (IAS), and left atrial (LA) free wall. The time difference from the onset of the P wave to the onset of the A wave at the right atrium (P-RA), the IAS (P-IAS), and the left atrium (P-LA) was measured. Asynchrony was defined as the differences between P-IAS and P-RA (RA asynchrony), P-LA and P-IAS (LA asynchrony), and P-LA and P-RA (interatrial asynchrony). In patients with HF, a significant increase in RA asynchrony was observed compared with controls and patients without HF (30 +/- 21 vs 12 +/- 13 and 14 +/- 15 ms, p <0.001). LA asynchrony was not different (19 +/- 26 vs 25 +/- 13 vs 25 +/- 14 ms, p = NS). Interatrial asynchrony was significantly increased in patients with HF (49 +/- 24 vs 37 +/- 9 and 39 +/- 17 ms, p = 0.04). There were moderate but significant correlations of RA asynchrony with log N-terminal-pro-B-type natriuretic peptide (r = 0.3, p = 0.01) and the ejection fraction (r = -0.4, p <0.001). In conclusion, in patients with HF, significant RA and interatrial asynchrony was documented, evaluated by noninvasive color tissue Doppler imaging. Asynchrony was related to N-terminal-pro-B-type natriuretic peptide and to the ejection fraction.     

Cardiac resynchronization therapy tailored by echocardiographic evaluation of ventricular asynchrony

OBJECTIVES: The value of interventricular and intraventricular echocardiographic asynchrony parameters in predicting reverse remodeling after cardiac resynchronization therapy (CRT) was investigated. BACKGROUND: Cardiac resynchronization therapy has been suggested as a promising strategy in patients with severe heart failure and left bundle branch block (LBBB), but the entity of benefit is variable and no criteria are yet available to predict which patients will gain. METHODS: Interventricular and intraventricular mechanical asynchrony was evaluated in 20 patients (8 men and 12 women, 63 +/- 10 years) with advanced heart failure caused by ischemic (n = 4) or nonischemic dilated cardiomyopathy (n = 16) and LBBB (QRS duration of at least 140 ms) using echocardiographic Doppler measurements. Left ventricular end-diastolic volume index (LVEDVI) and left ventricular end-systolic volume index (LVESVI) were calculated before and one month after CRT. Patients with a LVESVI reduction of at least 15% were considered as responders. RESULTS: Cardiac resynchronization therapy significantly improved ventricular volumes (LVEDVI from 150 +/- 53 ml/m(2) to 119 +/- 37 ml/m(2), p < 0.001; LVESVI from 116 +/- 43 ml/m(2) to 85 +/- 29 ml/m(2), p < 0.0001). At baseline, the responders had a significantly longer septal-to-posterior wall motion delay (SPWMD), a left intraventricular asynchrony parameter; only QRS duration and SPWMD significantly correlated with a reduction in LVESVI (r = -0.54, p < 0.05 and r = -0.70, p < 0.001, respectively), but the accuracy of SPWMD in predicting reverse remodeling was greater than that of the QRS duration (85% vs. 65%). CONCLUSIONS: In patients with advanced heart failure and LBBB, baseline SPWMD is a strong predictor of the occurrence of reverse remodeling after CRT, thus suggesting its usefulness in identifying patients likely to benefit from biventricular pacing.     

6 VENTRICULAR INTER‐ AND LEFT VENTRICULAR INTRA VENTRICULAR SYSTOLIC ASYNCHRONY IN PATIENTS WITH DILATED CARDIOMYOPATHY AND THE EFFECT OF CARDIAC RESYNCHRONIZATION THERAPY

Aim: Data dealing with the effect of cardiac resynchronization therapy (CRT) on myocardial or interventricular systolic asynchrony derived by pulsed Doppler tissue imaging (PDTI) and pulsed flow Doppler imaging are scare. The purpose of this study was to evaluate ventricular inter‐ and left ventricular intraventricular systolic asynchrony and to describe the effects of CRT on Doppler imaging in patients with dilated cardiomyopathy (DCM) and reduced left ventricular ejection fraction (LVEF). Methods: 217 consecutive patients (96 patients with left bundle branch bloc[LBBB]) with DCM underwent a standard and PDTI echocardiography examination. We measured the interval between Q wave in the electrocardiogram and the beginning of the systolic velocity profile (Q ‐ Sb) recorded from the right and left ventricular outflow tract by pulsed Doppler imaging (PWD) and from 5 basal segments (right ventricle, septal‐, lateral‐, anterior‐, inferior left ventricle) by PDTI from an apical approach. In 18 patients a biventricular pacing system was implanted and the effect of the cardiac resynchronization therapy was evaluated 1 month after implantation by echo examination. Results: A high‐grade interventricular systolic asynchrony (> 60 ms) was measured in 3 patients (2.5%) without LBBB versus 33 patients (16%) with LBBB. A severe left ventricular intraventricular systolic asynchrony (> 60 ms) was documented in 33 patients (27%) without LBBB versus 27 patients (28%) with LBBB. CRT in 18 patients reduced the interventricular systolic asynchrony from 52 ± 29 (20–116) ms to 14 ± 10 (0–32) ms (p < 0.01). Left ventricular intraventricular systolic asynchrony was reduced from 87 ± 35 (42–168) ms to 29 ± 14 (4–52) ms (p < 0.001). All patients with CRT showed an improvement in NYHA functional status. Conclusions: Patients with LBBB and DCM showed a significant intense degree of interventricular systolic asynchrony compared with patients without LBBB. The incidence of high‐grade left ventricular intraventricular systolic asynchrony was not influenced by LBBB. CRT is able to reduce inter‐ and left ventricular intraventricular systolic asynchrony. We recommend the use of PWD and PDTI in all patients with DCM as an additional important selection criteria for CRT.     

Benefits of cardiac resynchronization therapy for heart failure patients with narrow QRS complexes and coexisting systolic asynchrony by echocardiography.

OBJECTIVES: This study was designed to evaluate the role of cardiac resynchronization therapy (CRT) in heart failure (HF) patients with narrow QRS complexes (<120 ms) and echocardiographic evidence of mechanical asynchrony. BACKGROUND: Cardiac resynchronization therapy is currently recommended to advanced HF patients with prolonged QRS duration. Echocardiographic assessment of systolic mechanical asynchrony has been proven useful to predict a favorable response after CRT. METHODS: A total of 102 HF patients with New York Heart Association (NYHA) functional class III or IV were enrolled. Among them, 51 had wide QRS (>120 ms) and 51 had narrow QRS (<120 ms). Tissue Doppler imaging (TDI) was employed to select patients with systolic asynchrony (increased asynchrony index) in the narrow-QRS group. Clinical and echocardiographic assessments were performed at baseline and 3 months after CRT. RESULTS: There was a significant reduction of left ventricular (LV) end-systolic volume in both narrow (122 +/- 42 cc vs. 103 +/- 47 cc, p < 0.001) and wide (148 +/- 74 cc vs. 112 +/- 64 cc, p < 0.001) QRS groups. Improvement of NYHA functional class (both p < 0.001), maximal exercise capacity (both p < 0.05), 6-min hall-walk distance (both p < 0.01), ejection fraction (both p < 0.001), and mitral regurgitation (both p < 0.005) was also observed. In both groups, the degree of baseline mechanical asynchrony determined LV reverse remodeling to a similar extent, as shown by the superimposed regression lines. Withholding CRT for 4 weeks resulted in loss of echocardiographic benefits. CONCLUSIONS: Cardiac resynchronization therapy for HF patients with narrow QRS complexes and coexisting mechanical asynchrony by TDI results in LV reverse remodeling and improvement of clinical status. The amplitude of benefit is similar to the wide-QRS group provided that similar extent of systolic asynchrony is selected.     

Effects of regional systolic asynchrony on left ventricular global diastolic function in patients with coronary artery disease.

Patients with coronary artery disease often have impaired left ventricular diastolic filling despite normal global systolic function. The influence of regional systolic asynchrony on diastolic function was assessed by radionuclide angiography in 60 patients with coronary artery disease and normal ejection fraction at rest: group 1 (n = 30) with normal wall motion at rest and group 2 (n = 30) with abnormal wall motion. Data were compared with those obtained from 19 normal volunteers. Age, heart rate, ejection fraction and echocardiographic end-diastolic dimension did not differ among the three groups. Peak filling rate in group 1 and group 2 was similar (2.5 +/- 0.5 and 2.3 +/- 0.6 end-diastolic counts/s, respectively) and significantly lower than that in the normal subjects (2.8 +/- 0.7 end-diastolic counts/s; p less than 0.01 vs. group 2, p less than 0.05 vs group 1). Time to peak filling rate was prolonged in group 2 (184 +/- 27 ms) compared with that in normal subjects (162 +/- 19 ms; p less than 0.01) and group 1 (172 +/- 15 ms; p less than 0.05). Left ventricular end-diastolic pressure was significantly higher in group 2 than in group 1 (14 +/- 7 vs. 10 +/- 5 mm Hg, respectively; p less than 0.05). Asynchrony was assessed by sector analysis of the radionuclide left ventricular region of interest. Diastolic asynchrony was similar in the two patient groups (30 +/- 23 ms in group 2, 26 +/- 16 ms in group 1) and was higher in both groups than in the normal subjects (16 +/- 8 ms; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventricular asynchrony predicts a better outcome in patients with chronic heart failure receiving cardiac resynchronization therapy

OBJECTIVES: The aim of this study was to evaluate whether the clinical benefit of cardiac resynchronization therapy (CRT) can be prospectively predicted by means of the baseline evaluation of left ventricular asynchrony. BACKGROUND: The reverse remodeling associated with CRT is more evident in patients with severe heart failure (HF) and left bundle branch block (LBBB) who have left ventricular asynchrony. METHODS: Baseline left ventricular asynchrony was assessed in 60 patients with severe HF and LBBB by calculating the electrocardiographic duration of QRS and the echocardiographic septal-to-posterior wall motion delay (SPWMD). Left ventricular size and left ventricular ejection fraction (LVEF), mitral valve regurgitation, and functional capacity were also evaluated. The progression toward HF (defined as a worsening clinical condition leading to a sustained increase in conventional therapies, hospitalization, cardiac transplantation, and death) was assessed during follow-up, as were the changes in LVEF after six months. RESULTS: During the median follow-up of 14 months, 16 patients experienced HF progression. Univariate analysis showed that ischemic cardiomyopathy, changes in the QRS duration after implantation, and SPWMD significantly correlated with events. At multivariate analysis, a long SPWMD remained significantly associated with a reduced risk of HF progression (hazard ratio: 0.91; 95% confidence interval: 0.83 to 0.99; p <0.05). An improvement in LVEF was observed in 79% of the patients with a baseline SPWMD of > or =130 ms and in 9% of those with an SPWMD of <130 ms (p <0.0001). CONCLUSIONS: Baseline SPWMD is a strong predictor of long-term clinical improvement after CRT in patients with severe HF and LBBB.     

Quantification of radial mechanical dyssynchrony in patients with left bundle branch block and idiopathic dilated cardiomyopathy without conduction delay by tissue displacement imaging

Cardiac resynchronization therapy has made assessment of cardiac dyssynchrony clinically important. To test the hypothesis that echocardiographic displacement imaging can quantify dyssynchrony, 22 patients with left bundle branch block (LBBB), 14 with idiopathic dilated cardiomyopathy (IDC) without electrical conduction delay, and 22 normal controls were studied using radial angle-corrected displacement imaging. Control subjects had coordinated wall movement, whereas patients with LBBB had dyssynchrony characterized by early inward anteroseptal movement and markedly delayed posterior, lateral, or inferior regions (157 +/- 99 ms; p <0.001 vs normal). An interesting subset of patients with IDC without conduction delay (36%) had dyssynchrony with anteroseptal to posterior wall delays of 169 +/- 56 ms (p <0.001 vs normal), similar to patients with LBBB.     

Left ventricular electromechanical delay in patients with heart failure and normal QRS duration and in patients with right and left bundle branch block.

AIMS: We sought to define the reference values of intra-left ventricular (LV) electromechanical delay (EMD), and to assess the prevalence (and pattern) of intra-LV dyssynchrony in patients with heart failure (HF) and normal QRS and in patients with right and left bundle branch block. METHODS AND RESULTS: We used tissue Doppler imaging echocardiography and a six-LV wall model to study LV EMD in 103 patients [41 with HF and normal QRS, 22 with right bundle branch block (RBBB), and 40 with left bundle branch block (LBBB)], and in 59 controls. In controls, the median intra-LV EMD was 17 ms, (inter-quartile range 13-30); 95% of controls had a value < or =41 ms. Patients showed a longer intra-LV EMD than controls: 33 ms (20-57) in patients with normal QRS, 32 ms (23-50) in RBBB patients, and 50 ms (30-94) in LBBB patients. Intra-LV dyssynchrony (defined as intra-LV EMD >41 ms) was present in 39, 36, and 60% of the patients, respectively. On average, HF patients showed the same pattern of activation as controls, from the septum to the posterior wall, but activation times were significantly prolonged. In RBBB patients the activation sequence was directed from inferior to anterior and in LBBB from anterior to inferior wall. CONCLUSIONS: Left ventricular dyssynchrony was present in several patients with HF and normal QRS, and in patients with RBBB; conversely, 40% of LBBB patients showed values of LV EMD within the normal range. Left ventricular activation sequence was different between groups. Assessment of LV synchronicity by means of imaging techniques may be more important than QRS duration or morphology in selecting patients for cardiac resynchronization treatment.     

Phasic coronary flow pattern and flow reserve in patients with left bundle branch block and normal coronary arteries

OBJECTIVES: The purpose of this study was to determine whether scintigraphic myocardial perfusion defects in patients with left bundle branch block (LBBB) and normal coronary arteries are related to abnormalities in coronary flow velocity pattern and/or coronary flow reserve. BACKGROUND: Septal or anteroseptal defects on exercise myocardial perfusion scintigraphy are common in patients with LBBB and normal coronary arteries. METHODS: Thirteen patients (7 men, age 61+/-8 years) with LBBB and normal coronary arteries underwent stress thallium-201 scintigraphy and cardiac catheterization. In all patients and in 11 control subjects coronary blood flow parameters were calculated from Doppler measurements of flow velocity in the left anterior descending coronary artery (LAD) before and after adenosine administration. RESULTS: The time to maximum peak diastolic flow velocity was significantly longer both for the seven patients with (134+/-19 ms) and for the six without (136+/-7 ms) exercise perfusion defects than for controls (105+/-12 ms, p < 0.05), whereas the acceleration was slower (170+/-54, 186+/-42 and 279+/-96 cm/s2, respectively, p < 0.05). Coronary flow reserve in the patients with exercise perfusion defects (2.7+/-0.3) was significantly lower than in those without (3.7+/-0.5, p < 0.05) or in the control group (3.4+/-0.5, p < 0.05). CONCLUSIONS: Patients with LBBB have an impairment of early diastolic blood flow in the LAD due to an increase in early diastolic compressive resistance resulting from delayed ventricular relaxation. Furthermore, exercise scintigraphic perfusion defects in these patients are associated with a reduced coronary flow reserve, indicating abnormalities of microvascular function in the same vascular territory.     

Impaired left ventricular synchronicity in hypertensive patients with ventricular hypertrophy

OBJECTIVES: The influence of left ventricular hypertrophy (LVH) on left ventricular synchronicity, and the prevalence of left ventricular dyssynchrony in hypertensive patients with LVH are unknown. The purpose of this study was to determine the influence of LVH on left ventricular synchronicity in hypertensive subjects. METHOD: Tissue Doppler imaging (TDI) was performed in 115 hypertensive and 30 control individuals. Hypertensive patients were divided into a LVH group and a non-LVH group according to the left ventricular mass index (LVMI). Diastolic and systolic asynchrony was determined by measuring the maximal differences in time to peak myocardial systolic contraction (Ts-max) and early diastolic relaxation (Te-max) between any two of the left ventricular segments and the standard deviation of time to peak myocardial systolic contraction and early diastolic relaxation of all 12 segments. RESULTS: Ts-max was greater in both the non-LVH and LVH groups than in controls, (96.68 +/- 26.21 versus 79.30 +/- 25.19 versus 53.20 +/- 15.24 ms, both P < 0.001) and in the LVH group than in the non-LVH group (96.68 +/- 26.21 versus 79.30 +/- 25.19 ms, P < 0.01). Te-max was prolonged in both patient groups, being most advance in the LVH group (67.39 +/- 11.01 versus 57.18 +/- 11.42 versus 46.72 +/- 13.24 ms, both P < 0.001 versus control group and P < 0.001 versus non-LVH group). LVH patients had shown a greater prevalence of both systolic and diastolic asynchrony than non-LVH patients. A Ts-max value greater than 88 ms had 68% sensitivity and 71% specificity for detecting hypertensive patients with LVH. CONCLUSION: Left ventricular systolic synchronicity was impaired in hypertensive patients with LVH. TDI was shown to be useful for the detection of myocardial abnormalities in such patients.     

Functional abnormalities in isolated left bundle branch block. The effect of interventricular asynchrony

Eighteen patients with isolated left bundle branch block (LBBB) were compared with 10 normal control subjects. Apexcardiograms, phonocardiograms, electrocardiograms, two-dimensional and dual M-mode echocardiograms, and radionuclide ventriculograms (RNV) were performed. There were no differences in the timing of right ventricular events between LBBB and normal subjects; however, striking delays in left ventricular systolic and diastolic events were apparent in the LBBB group. The delay was associated with shortening of left ventricular diastole and resultant increase in the ratio of right to left ventricular diastolic time in LBBB (1.2 +/- 0.08) compared with normal (1.0 +/- 0.06), p less than 0.0001. First heart sound (S1) amplitude, expressed as the ratio S1/S2, was decreased in LBBB compared with normal (0.67 +/- 0.2 compared with 1.34 +/- 0.25, p less than 0.01), in part due to wide separation of the valvular contributors to S1. The abnormal interventricular septal motion in LBBB corresponded to periods of asynchrony in contraction, ejection, end systole, and end diastole between right and left ventricles. Radionuclide ventriculograms revealed decreased regional ejection fraction of the septum in LBBB (40 +/- 16%) compared with 67 +/- 7% in normal subjects (p less than 0.001), while the apical and lateral regional ejection fractions were similar in the two groups. This loss of septal contribution resulted in a reduction in global ejection fraction in LBBB compared to normals (54 +/- 7% compared with 62 +/- 5%, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

Intra-ventricular resynchronization for optimal left ventricular function during pacing in experimental left bundle branch block

oBJECTIVES: We sought to investigate to what extent intra-ventricular asynchrony (intraVA) and inter-ventricular asynchrony (interVA) determine left ventricular (LV) function in canine hearts with left bundle branch block (LBBB) during ventricular pacing. BACKGROUND: Pacing therapy improves LV pump function in patients with heart failure and abnormal ventricular conduction supposedly due to resynchronization. However, the relationship between LV pump function and measures of asynchrony is not well established. METHODS: In 15 experiments, LV (various sites) and biventricular (BiV) pacing was performed at atrioventricular (AV) delays of 20 to 140 ms. Measured were the maximum rate of increase (dP/dt(max)) of LV pressure and LV stroke work (SW) (conductance catheter), interVA (time delay between the upslope of LV and RV pressures), and intraVA (from endocardial electrical activation maps). RESULTS: Induction of LBBB increased interVA (-6.4 +/- 8.6 to -28.4 +/- 8.5 ms [RV earlier]) and intraVA (4.9 +/- 2.4 to 18.0 +/- 3.3 ms), whereas LV dP/dt(max) and SW decreased (-13 +/- 18% and -39 +/- 24%, respectively). During LBBB, LV and BiV pacing increased LV dP/dt(max) and SW (mean increases 14% to 21% and 11% to 15%, respectively) without changing diastolic function or preload. Optimal improvement in LV function was obtained consistently when intraVA returned to pre-LBBB values, while interVA remained elevated. Normalization of intraVA required AV delays shorter than the baseline PQ time during LV apex and BiV pacing, thus excluding endogenous LV activation, but AV delays virtually equal to the baseline PQ time (difference 4 +/- 9 ms, p = NS) during pacing at (mid)lateral LV sites to obtain fusion between pacing-induced and endogenous activation. CONCLUSIONS: In LBBB hearts, optimal restoration of LV systolic function by pacing requires intra-ventricular resynchronization. The optimal AV delay to achieve this depends on both the site of pacing and baseline PQ time.     

Evidence of left ventricular dyssynchrony resulting from right ventricular pacing in patients with severely depressed left ventricular ejection fraction.

AIMS: Cardiac resynchronization therapy (CRT) has recently emerged as an effective treatment for patients with moderate-to-severe systolic heart failure and left bundle branch block (LBBB). Right ventricular pacing (RVP) leads to an LBBB-like pattern in the electrocardiogram. The aim of this study was to evaluate the frequency of ventricular mechanical dyssynchrony in patients induced by RVP. METHODS AND RESULTS: The study included 33 patients with a conventional single or dual chamber pacemaker, 18 with ejection fraction (EF) > 35% and 15 with EF < or = 35%. In all patients, an intrinsic rhythm without intraventricular conduction delay (QRS < or = 120 ms) was present without RVP. Two-dimensional and Doppler echocardiographic criteria for mechanical dyssynchrony [aortic pre-ejection delay (APE), interventricular mechanical delay (IVMD), delayed activation of the posterior left ventricular wall (PD), septal-to-posterior wall motion delay (SPWMD)] were evaluated in all patients with and without RVP. QRS duration showed no difference between the two EF-groups without RVP (93 +/- 10 vs. 96 +/- 9 ms), but was significantly longer in patients with low EF with RVP (152 +/- 18 vs. 181 +/- 18 ms; P < 0.001). In patients with EF > 35%, only APE was slightly prolonged by RVP (111 +/- 20 vs. 129 +/- 17 ms; P = 0.03), whereas in patients with EF < or = 35% marked pathological differences in APE (118 +/- 29 vs. 169 +/- 24 ms; P < 0.001), IVMD (22 +/- 17 vs. 58 +/- 14 ms; P < 0.001), SPWMD (103 +/- 28 vs. 125 +/- 29 ms; P = 0.004), and PD (-21 +/- 25 vs. - 39 +/- 25 ms; P = 0.005) were found. A significant correlation between QRS duration and mechanical ventricular dyssynchrony was only found for two echocardiographic parameters (IVMD, APE) with RVP. CONCLUSION: In patients with a conventional pacemaker, mechanical dyssynchrony with RVP was shown exceptionally in patients with preserved or moderately depressed systolic left ventricular (LV) function, but in nearly all patients with severely depressed systolic LV function. These patients might benefit from CRT when frequent RVP is required.     

Improved septal contraction and coronary flow velocity after cardiac resynchronization therapy elucidated by strain imaging and pulsed wave Doppler echocardiography

OBJECTIVES: The effects of cardiac resynchronization therapy (CRT) with various atrioventricular conduction delay settings were investigated on cardiac hemodynamic changes involved in coronary flow velocity using color and pulsed wave Doppler modalities and myocardial regional contractility using a novel echocardiographic technique (strain imaging). METHODS: Seven patients with advanced heart failure (left ventricular ejection fraction < 35%) and left bundle branch block(QRS > or = 140 msec) were treated with CRT. Color and pulsed wave Doppler imaging were performed from the apical four-chamber view to examine the cardiac functions such as stroke volume, cardiac output, mitral regurgitant volume and coronary flow velocity. Strain imaging was performed to quantify the asynchrony of both intraventricular and interventricular time delay between the septum and left ventricular free wall (posterior wall) and to assess the regional contractile function. Wall motion was also evaluated. RESULTS: Intraventricular and interventricular asynchrony were improved from 173 +/- 18 to 60 +/- 6 msec, and 69 +/- 25 to 12 +/- 3 msec, respectively. Stroke volume (55.2 +/- 6.2 to 76.8 +/- 10.8 ml; 39% up), cardiac output (3.9 +/- 0.3 to 5.4 +/- 0.5 I/min; 38% up) and coronary flow velocity (24 +/- 3 to 36 +/- 5 cm/sec; 50% up) were greatly increased and mitral regurgitant volume (59.7 +/- 18.0 to 38.9 +/- 11.3 ml; 35% down)was clearly decreased. Septal wall shortening was greatly increased from 10.2 +/- 2.3% to 17.0 +/- 1.8% and septal wall motion (radial thickening)was also improved simultaneously. Atrioventricular interval settings influenced all above parameters. CONCLUSIONS: CRT improved the cardiac hemodynamics involved in coronary flow significantly due to both resynchronization of inter and intra asynchrony, and improvement of the regional myocardial contraction in patients with severe congestive heart failure and complete left bundle branch block.     

Predictors of response to cardiac resynchronization therapy--importance of left ventricular dyssynchrony.

BACKGROUND: Cardiac resynchronization therapy (CRT) is currently used in selected patients with dilated cardiomyopathy and heart failure. However, 30% of patients do not respond to CRT when selection is based on clinical and electrocardiographic criteria. Left ventricular dyssynchrony can be evaluated by tissue Doppler imaging and it has been described as a useful precdictor of response to CRT. OBJECTIVE: To evaluate whether left ventricular dyssynchrony, as measured by tissue Doppler imaging, can be used to predict response to CRT. METHODS: 23 consecutive patients (age 67 +/- 10 years, 13 male) with heart failure refractory to medical therapy and who underwent CRT were studied. Before and six months after the procedure, various characteristics - clinical (including NYHA functional class), electrocardiographic (QRS interval) and echocardiographic (left ventricular ejection fraction [EF] and respective volumes)--were evaluated. In addition, pulsed wave tissue Doppler imaging was used to assess the time interval (QS) between the beginning of the QRS complex and the beginning of the systolic wave on the Doppler signal, in the basal segments of the septal, lateral, anterior and inferior walls. Left ventricular dyssynchrony was quantified as the difference between the maximum and minimum QS interval (QS(max-min)). The patients were divide into two groups: responders, if functional class improved by at least one and EF increased by more than 10%, and non-responders for the remainder. Differences between groups were assessed and predictors of response to CRT were determined. RESULTS: CRT improved functional class by at least one in 87% of patients and EF improved from 21 +/- 6 to 33 +/- 9% (p < 0.001). QS(max-min) was reduced from 80 +/- 38 to 38 +/- 14 ms (p < 0.001). In 15 patients (65%), classified as responders, there was an improvement in functional class and an increase in EF of more than 10%. There were no differences between groups, except for QS(max-min). Patients in the responder group had greater left ventricular dyssynchrony (QS(max-min) 94 +/- 39 vs. 54 +/- 16 ms, p = 0.002). QSmix-min was an independent predictor of response to CRT and a cut-off of 60 ms identified responders with a sensitivity of 87% and specificity of 75%. CONCLUSION: Despite the good results achieved with CRT, about one third of patients do not benefit from it. Left ventricular dyssynchrony can be quantified by tissue Doppler imaging using QS(max-min) and values greater than 60 ms can identify responders to CRT.     

Effects of levosimendan on right ventricular function in patients with advanced heart failure

Right ventricular (RV) dysfunction frequently complicates advanced left ventricular heart failure and contributes to an unfavorable prognosis. Levosimendan is a novel inodilator that beneficially affects hemodynamics and left ventricular systolic and diastolic function in patients with advanced heart failure. However, its effects on RV function have not yet been properly assessed in these patients. In this randomized trial, the impact of levosimendan or placebo on various echocardiographic parameters of RV systolic and diastolic function was investigated in 54 patients with advanced heart failure due to left ventricular systolic dysfunction. Tissue Doppler imaging maximal systolic tricuspid annular velocity (S wave) increased significantly only in the levosimendan group (8.2 +/- 3.2 vs 9.0 +/- 3.0 cm/s, p <0.03). Tissue Doppler imaging RV early diastolic velocity (E wave) and the ratio of early to late diastolic velocities (E/A) also increased significantly after levosimendan administration (p <0.01 and p <0.05, respectively). Systolic pulmonary arterial pressure decreased significantly (54 +/- 11 vs 43 +/- 11 mm Hg, p <0.01) in the levosimendan-treated patients. Levosimendan beneficially modulated neurohormonal and inflammatory status by decreasing B-type natriuretic peptide levels (p <0.05) and by altering the ratio of interleukin-6 to interleukin-10 in favor of the latter (p <0.05). In conclusion, levosimendan could offer further therapeutic advantages in patients with advanced heart failure by improving systolic and diastolic RV function.     

Left ventricular function in normotensive young adults with well-controlled type 1 diabetes mellitus

The aim of this study was to determine whether early myocardial structural and functional systolic and diastolic alterations in asymptomatic and uncomplicated patients with type 1 diabetes mellitus (DM) could be detected using the new highly sensitive echocardiographic techniques of integrated backscatter and color Doppler myocardial imaging. Forty asymptomatic and uncomplicated patients with type 1 DM and 40 gender- and age-matched normal controls were studied. All patients were analyzed by conventional and new echocardiographic techniques (integrated backscatter and color Doppler myocardial imaging). Patients with DM showed reduced systolic function compared with controls, evidenced by significantly lower peak strain, strain rates, and cyclic variation indexes at the septum (p <0.0001, <0.01, and <0.001, respectively) and at the posterior wall level (p <0.0001, <0.0001, and <0.001, respectively). On receiver-operating characteristic curve analysis, systolic strain and the cyclic variation index showed the highest discriminating power for separating patients with DM and control subjects. Neither structural or ultrastructural nor diastolic functional abnormalities were detected. On univariate regression analysis, a significant inverse correlation was found for DM duration with conventional (E/A ratio) and unconventional (tissue Doppler imaging E/A ratio) indexes of diastolic function, in the absence of any correlation for systolic function. In conclusion, highly sensitive ultrasonic techniques demonstrate evidence of left ventricular systolic dysfunction in the early stage of type 1 DM, in the absence of ultrastructural and left ventricular diastolic functional abnormalities.     

Cardiac resynchronization therapy can reverse abnormal myocardial strain distribution in patients with heart failure and left bundle branch block

OBJECTIVES: We studied the effects of cardiac resynchronization therapy (CRT) on regional myocardial strain distribution, as determined by echocardiographic strain rate (SR) imaging. BACKGROUND: Dilated hearts with left bundle branch block (LBBB) have an abnormal redistribution of myocardial fiber strain. The effects of CRT on such abnormal strain patterns are unknown. METHODS: We studied 18 patients (12 males and 6 females; mean age 65 +/- 11 years [range 33 to 76 years]) with symptomatic systolic heart failure and LBBB. Doppler myocardial imaging studies were performed to acquire regional longitudinal systolic velocity (cm/s), systolic SR (s(-1)), and systolic strain (%) data from the basal and mid-segments of the septum and lateral wall before and after CRT. By convention, negative SR and strain values indicate longitudinal shortening. RESULTS: Before CRT, mid-septal peak SR and peak strain were lower than in the mid-lateral wall (peak SR: -0.79 +/- 0.5 [septum] vs. -1.35 +/- 0.8 [lateral wall], p < 0.05; peak strain: -7 +/- 5 [septum] vs. -11 +/- 5 [lateral wall], p < 0.05). This relationship was reversed during CRT (peak SR: -1.35 +/- 0.8 [septum] vs. -0.93 +/- 0.6 [lateral wall], p < 0.05; peak strain: -11 +/- 6 [septum] vs. -7 +/- 6 [lateral wall], p < 0.05). Cardiac resynchronization therapy reversed the septal-lateral difference in mid-segmental peak strain from -46 +/- 94 ms (LBBB) to 17 +/- 92 ms (CRT; p < 0.05). CONCLUSIONS: Left bundle branch block can lead to a significant redistribution of abnormal myocardial fiber strains. These abnormal changes in the extent and timing of septal-lateral strain relationships can be reversed by CRT. The noninvasive identification of specific abnormal but reversible strain patterns should help to improve patient selection for CRT.     

Left ventricular filling characteristics in pulmonary hypertension: a new mode of ventricular interaction.

OBJECTIVE--To examine the effects of pulmonary hypertension on left ventricular diastolic function and to relate the findings to possible mechanisms of interdependence between the right and left sides of the heart in ventricular disease. DESIGN--A retrospective and prospective analysis of echocardiographic and Doppler studies. SETTING--A tertiary referral centre for both cardiac and pulmonary disease. PATIENTS--29 patients with pulmonary hypertension (12 primary pulmonary hypertension, 10 pulmonary fibrosis, five atrial septal defect (ASD), and two scleroderma) were compared with a control group of 10 patients with an enlarged right ventricle but normal pulmonary artery pressure (six ASD, one after ASD closure, one ASD and pulmonary valvotomy, one tricuspid valve endocarditis and repair, and one pulmonary fibrosis). None had clinical or echocardiographic evidence of intrinsic left ventricular disease. MAIN OUTCOME MEASURES--M mode echocardiographic measurements were made of septal thickness, and left and right ventricular internal cavity dimensions. Doppler derived right ventricular to right atrial pressure drop, and time intervals were measured, as were isovolumic relaxation time, and Doppler left ventricular filling characteristics. RESULTS--The peak right ventricular to right atrial pressure gradient was (mean (SD)) 60 (16) mm Hg in pulmonary hypertensive patients, and 18 (5) mm Hg in controls. The time intervals P2 to the end of the tricuspid regurgitation, and P2 to the start of tricuspid flow were both prolonged in patients with pulmonary hypertension compared with controls (115 (60) and 120 (40) v 40 (15) and 45 (10) ms, p values less than 0.001). Pulmonary hypertensive patients commonly had a dominant A wave on the transmitral Doppler (23/29); however, all the controls had a dominant E wave. Isovolumic relaxation time of the left ventricle was prolonged in pulmonary hypertensive patients compared with controls, measured as both A2 to mitral valve opening (80 (25) v 50 (15) ms) and as A2 to the start of mitral flow (105 (30) v 60 (15) ms, p values less than 0.001). The delay from mitral valve opening to the start of transmitral flow was longer in patients with pulmonary hypertension (30 (15) ms) compared with controls (10 (10) ms, p less than 0.001). At the time of mitral opening there was a right ventricular to right atrial gradient of 12 (10) mm Hg in pulmonary hypertensive patients, but this was negligible in controls (0.4 (0.3) mm Hg, p less than 0.001). CONCLUSIONS--Prolonged decline of right ventricular tension, the direct result of severe pulmonary hypertension, may appear as prolonged tricuspid regurgitation. It persists until after mitral valve opening on the left side of the heart, where events during isovolumic relaxation are disorganised, and subsequent filling is impaired. These effects are likely to be mediated through the interventricular septum, and this right-left ventricular asynchrony may represent a hitherto unrecognised mode of ventricular interaction.