Search

: ObjectivesThe aim of this study was to ascertain if left ventricular mitral annulus velocities measured by tissue Doppler imaging (TDI) are more powerful predictors of outcome compared with clinical data and standard Doppler-echocardiographic parameters.: BackgroundTissue Doppler imaging of basal or mitral annulus velocities provides rapid assessment of ventricular long axis function. But it is not known if TDI-derived velocities in systole and diastole add incremental value and are superior to the standard Doppler-echocardiographic measurements as a predictor of outcome.: MethodsThe study population consisted of 518 subjects, 353 with cardiac disease and 165 normal subjects who had full Doppler two-dimensional–echocardiographic studies with measurement of mitral inflow velocities in early and late diastole, E-wave deceleration time (DT), peak systolic mitral annular velocity (Sm) early and late diastolic mitral annular velocity (Em and Am) by TDI, early diastolic flow propagation velocity, and standard chamber dimensions. All subjects were followed up for two years. The end point was cardiac death.: ResultsTissue Doppler imaging mitral annulus systolic and diastolic velocities were all significantly lower in the non-survivors (all p < 0.05) as was DT (p = 0.024). In the Cox model the best predictors of mortality were Em, Sm, Am, left ventricular ejection fraction, left ventricular mass, and left atrial diameter in systole (LADs). By backward stepwise analysis Em and LADs were the strongest predictors. After forcing the TDI measurements into the covariate model with clinical and mitral DT <0.16 s, Em provided significant incremental value for predicting cardiac mortality (p = 0.004).: ConclusionsMitral annulus velocity measured by TDI in early diastole gives incremental predictive power for cardiac mortality compared to clinical data and standard echocardiographic measurements. This easily available measurement adds significant value in the clinical management of cardiac patients. [Copyright &y& Elsevier]

Objectives: The present study aimed to examine whether diastolic and systolic asynchrony exist in diastolic heart failure (DHF) and their prevalence and relationship to systolic heart failure (SHF) patients. Background: Few data exist on mechanical asynchrony in DHF. Methods: Tissue Doppler echocardiography was performed in 373 heart failure patients (281 with SHF and 92 with DHF) and 100 normal subjects. Diastolic and systolic asynchrony was determined by measuring the standard deviation of time to peak myocardial systolic (Ts-SD) and peak early diastolic (Te-SD) velocity using a 6-basal, 6-mid-segmental model, respectively. Results: Both heart failure groups had prolonged Te-SD (DHF vs. SHF vs. controls subjects: 32.2 ± 18.0 ms vs. 38.0 ± 25.2 ms vs. 19.5 ± 7.1 ms) and Ts-SD (31.8 ± 17.0 ms vs. 36.7 ± 15.2 ms vs. 17.6 ± 7.9 ms) compared with the control group (all p < 0.001 vs. control subjects). Based on normal values, the DHF group had comparable diastolic (35.9% vs. 43.1%; chi-square = 1.48, p = NS), but less systolic asynchrony than the SHF group (39.1% vs. 56.9%; chi-square = 8.82, p = 0.003). Normal synchrony, isolated systolic, isolated diastolic, and combined asynchrony were observed in 39.1%, 25.0%, 21.7%, and 14.1% of DHF patients, respectively, and these were 25.6%, 31.3%, 17.4%, and 25.6%, correspondingly, in SHF (chi-square = 10.01, p = 0.019). The correlation between systolic and diastolic asynchrony, and between the myocardial velocities and corresponding mechanical asynchrony appeared weak. A wide QRS duration (>120 ms) was rare in DHF (10.9% vs. 37.7% in SHF) (chi-square = 16.69, p < 0.001). Conclusions: Diastolic and/or systolic asynchrony was common in 61% of DHF patients despite narrow QRS complex. The presence of asynchrony was not related to myocardial systolic or diastolic function. Systolic and diastolic asynchrony were not tightly coupled, implying distinct mechanisms. [Copyright &y& Elsevier]

Objectives: We sought to examine whether cardiac resynchronization therapy (CRT) improves atrial function and induces atrial reverse remodeling. Background: Cardiac resynchronization therapy is an established therapy for advanced heart failure with prolonged QRS duration, which improves left ventricle (LV) function and is associated with LV reverse remodeling. Methods: A total of 107 heart failure patients (66 ± 11 years) who received CRT and were followed up for 3 months were studied. Atrial function was assessed by M-mode, 2-dimensional echocardiography, transmitral Doppler, tissue Doppler velocity, and strain (ε) imaging. Left atrial (LA) emptying fraction based on the change in areas (LAA-EF) and volumes (LAV-EF) were calculated. The LV reverse remodeling was defined by a reduction of LV end-systolic volume >10%. Results: In the responders of LV reverse remodeling (n = 62), LAA-EF and LAV-EF were significantly increased (p < 0.001). Responders also had significant decrease in LA size area and volumetric measurements, both before (p < 0.05) and after atrial systole (p < 0.001). However, these parameters were unchanged in the nonresponders (n = 45, p = NS). In the responders, tissue Doppler velocity analysis showed improvement of contraction velocity in both left (p = 0.005) and right atria (p = 0.018), whereas ε in both atria were increased in all the phases of cardiac cycle, namely ventricular end-systole (p < 0.001), early diastole (p < 0.001), and late diastole (p = 0.007). Conclusions: Cardiac resynchronization therapy improves both left and right atrial pump function. The increase in atrial ε throughout the cardiac cycle is likely reflecting the improvement of atrial compliance. These changes lead to LA reverse remodeling with reduction of LA size before and after atrial systole. [Copyright &y& Elsevier]

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. [Copyright &y& Elsevier]

Objectives: The aim of this study was to determine if strain rate imaging (SRI) correlates with the transmural extent of myocardial infarction (MI) measured by contrast-enhanced magnetic resonance imaging (Ce-MRI). Background: Identification of the transmural extent of myocardial necrosis and degree of non-viability after acute MI is clinically important. Methods: Tissue Doppler echocardiography with SRI and Ce-MRI were performed in 47 consecutive patients with a first acute MI between days 2 and 6 and compared to 60 age-matched healthy volunteers. Peak myocardial velocities and peak myocardial deformation strain rates were measured. Location and size of the infarct zone was confirmed by Ce-MRI using the delayed enhancement technique with a 16-segment model. Results: Contrast-enhanced MRI identified transmural infarction in 21 patients, non-transmural infarction in 15 (mean transmurality of infarct 72.3 ± 10.6%), and another 11 patients with subendocardial infarction (&#60;50% transmural extent of the left ventricular wall). Peak systolic strain rate (SRs) of the transmural infarction segments was significantly lower compared to normal myocardium or with non-transmural infarction segments (both p &#60; 0.0005). A cutoff value of SRs >−0.59 s−1 detected a transmural infarction with high sensitivity (90.9%) and high specificity (96.4%), and −0.98 s−1 >SRs >−1.26 s−1 distinguished subendocardial infarction from normal myocardium with a sensitivity of 81.3% and a specificity of 83.3%. Conclusions: Peak myocardial deformation by SRI can differentiate transmural from non-transmural MI, and it allows noninvasive determination of transmurality of the scar after MI and thereby the extent of non-viable myocardium. [Copyright &y& Elsevier]