Tissue Doppler velocity is superior to strain imaging in predicting long-term cardiovascular events after cardiac resynchronisation therapy.

OBJECTIVE: To examine the predictive value of systolic dyssynchrony measured by tissue Doppler velocity versus tissue Doppler strain imaging on long-term outcome after cardiac resynchronisation therapy (CRT). DESIGN: Cohort study. SETTING: Two university hospitals. PATIENTS: Two hundred and thirty-nine patients (65 (SD 12) years, 76% males) who underwent CRT. INTERVENTIONS: Baseline echocardiography with tissue Doppler imaging (TDI) and clinical follow-up for 37 (20) months. MAIN OUTCOME MEASURES: The time to peak systolic velocity during ejection phase (Ts) and the time to peak systolic strain (T(epsilon)) were assessed for dyssynchrony, that is the maximal delay in Ts and the maximal delay in T(epsilon) among the four left ventricular basal segments. Occurrence of cardiovascular endpoints between patients with and without dyssynchrony was compared by Kaplan-Meier curves, followed by Cox regression analysis for potential predictor(s). RESULTS: There were 78 (33%) deaths, with cardiovascular causes in 64 (27%) patients, while 136 (57%) patients were hospitalised for cardiovascular events, including decompensated heart failure in 87 (36%) patients. Patients with the maximal delay in Ts of > or =65 ms showed a lower event rate for cardiovascular mortality (19% vs 38%, logrank chi2 = 7.803, p = 0.005) and other prognostic endpoints. In Cox regression analysis, the maximal delay in Ts (hazard ratio (HR) 0.463, 95% CI 0.270 to 0.792, p = 0.005) and ischaemic aetiology (HR 2.716, 95% CI 1.505 to 4.901, p = 0.001) were independent predictors of cardiovascular mortality. In contrast, the maximal delay in T(epsilon) of > or =80 ms failed to predict any cardiovascular event. CONCLUSIONS: Echocardiographic evidence of prepacing systolic dyssynchrony measured by TDI velocity, but not TDI strain, predicted lower long-term cardiovascular events after CRT.

Disease chronicity and activity predict subclinical left ventricular systolic dysfunction in patients with systemic lupus erythematosus.

OBJECTIVE: This study investigates parameters that could predict subclinical cardiac dysfunction in systemic lupus erythematosus (SLE) in the absence of valvular, clinical coronary artery and pericardial disease. DESIGN: A case-control trial. SETTING: Rheumatology clinic, a university teaching hospital. PATIENTS: Eighty-two female SLE patients (49 (SD 9) years) and 82 female normal subjects (49 (13) years) matched for age, body mass index, blood pressure and heart rate. INTERVENTIONS: All underwent standard echocardiography and tissue Doppler imaging. MAIN OUTCOME MEASURES: Twenty-two (27%) patients had evidence of impaired left ventricular (LV) long-axis function with mean myocardial peak systolic velocity (Sm) of basal six segments <4.4 cm/s and also subnormal stress-corrected midwall fractional shortening. Thirty-four (42%) patients demonstrated impaired right ventricular (RV) long-axis function. These occurred in the presence of comparable normal LV ejection fraction, cardiac index, and RV fractional area change to the control group. Patients with subnormal mean Sm were older (49 (8) vs 44 (9); p = 0.043) and had a higher prevalence of hypertension (46% vs 22%; p = 0.034), longer disease duration >10 years (82% vs 50%, p = 0.01), higher disease activity score (73% vs 48% for Systemic Lupus Erythematosus Disease Activity Index (SLEDAI)> or =1, p = 0.049) and end-organ damage index (64% vs 47% with Systemic Lupus International Collaborating Clinics Damage Index (SLICC)> or =1, p = 0.049) than those with normal values. Disease duration >10 years, disease activity index and increased arterial stiffness provided additional incremental predictive value of LV long-axis function. CONCLUSION: SLE patients have subclinical long and short-axis dysfunctions. Regular monitoring of cardiac function by tissue Doppler echocardiography may be indicated for patients who had SLE for >10 years, frequent flare or when arterial stiffening is demonstrated.

Difference in long-term clinical outcome after cardiac resynchronisation therapy between ischaemic and non-ischaemic aetiologies of heart failure.

OBJECTIVE: To examine the impact of heart failure (HF) aetiology on long-term outcome after cardiac resynchronisation therapy (CRT). DESIGN: Prospective cohort study. SETTING: University hospital. PATIENTS: 119 patients (44% with ischaemic and 56% non-ischaemic aetiology) who underwent CRT. INTERVENTIONS: Clinical follow-up for 39 (24) months. MAIN OUTCOME MEASURES: Cardiovascular mortality, HF and cardiovascular hospitalisation were compared by Kaplan-Meier curves between the two groups, followed by Cox regression analysis for prognostic predictor(s). RESULTS: 41 (34%) patients died, in whom cardiovascular causes were identified in 32 (27%) patients. The ischaemic group had a higher cardiovascular mortality (log-rank chi(2) = 4.293, p = 0.038) and cardiovascular hospitalisation (log-rank chi(2) = 5.123, p = 0.024) when compared with the non-ischaemic group, though no difference was found in HF hospitalisation (log-rank chi(2) = 0.019, p = 0.892). At three months, left ventricular reverse remodelling occurred in 52% of the ischaemic group and 55% of the non-ischaemic group (chi(2) = 0.128, p = 0.720). By Cox regression analysis, ischaemic aetiology and absence of reverse remodelling at three months were independent predictors of cardiovascular mortality (HR = 2.698, p = 0.032; HR = 3.541, p = 0.030) and cardiovascular hospitalisation (HR = 1.905, p = 0.015; HR = 2.361, p = 0.004). Furthermore, these two factors had an incremental value in predicting cardiovascular mortality when compared with either alone (left ventricular reverse remodelling, log-rank chi(2) = 10.275 vs 6.311, p = 0.05; Ischaemic aetiology, log-rank chi(2) = 10.275 vs 4.293, p<0.05). CONCLUSION: Ischaemic aetiology of HF is an independent predictor of higher cardiovascular mortality and hospitalisation after CRT. This may implicate the progressive nature of coronary heart disease leading to a worse outcome despite similar short-term benefits of CRT.

Hypertension and heart failure: a dysfunction of systole, diastole or both?

The pathological myocardial hypertrophy associated with hypertension contains the seed for further maladaptive development. Increased myocardial oxygen consumption, impaired epicardial coronary perfusion, ventricular fibrosis and remodelling, abnormalities in long-axis function and torsion, cause, to a varying degree, a mixture of systolic and diastolic abnormalities. In addition, chronotropic incompetence and peripheral factors such as lack of vasodilator reserve and reduced arterial compliance further affect cardiac output particularly on exercise. Many of these factors are common to hypertensive heart failure with a normal ejection fraction as well as systolic heart failure. There is increasing evidence that these apparently separate phenotypes are part of a spectrum of heart failure differing only in the degree of ventricular remodelling and volume changes. Furthermore, dichotomizing heart failure into systolic and diastolic clinical entities has led to a paucity of clinical trials of therapies for heart failure with a normal ejection fraction. Therapies aimed at reversing myocardial fibrosis, and targets outside the heart such as enhancing vasodilator reserve and improving chronotropic incompetence deserve further study and may improve the exercise capacity of hypertensive heart failure patients. Hypertension heart disease with heart failure is simply not a dysfunction of systole and diastole. Other peripheral factors including heart rate and vasodilator response with exercise may deserve equal attention in an attempt to develop more effective treatments for this disorder.

Improvement of left ventricular myocardial short-axis, but not long-axis function or torsion after cardiac resynchronisation therapy: an assessment by two-dimensional speckle tracking.

AIMS: To evaluate whether short-axis function plays a part in determining left ventricular (LV) geometric and functional improvement after cardiac resynchronisation therapy (CRT). METHODS AND RESULTS: 39 patients who received CRT were enrolled. 2D speckle tracking echocardiography was performed at baseline and three months after CRT to assess mean systolic circumferential (epsilon-circum), radial (epsilon-radial) and longitudinal (epsilon-long) strain and torsion. Responders of reverse remodelling (n = 21) had higher baseline mean epsilon-circum than non-responders (p<0.05), who also had improvement in mean epsilon-circum and mean epsilon-radial (both p<0.05) after CRT. Also, the increase in mean epsilon-circum correlated with increase in ejection fraction (r = 0.57, p<0.001) and decrease in mid-cavity width (r = -0.52, p = 0.001). A baseline mean epsilon-circum of >or=6.5% predicted a gain in ejection fraction >or=5%, with a sensitivity of 73% and a specificity of 71%. The baseline epsilon-long was not different between the two groups, and remained unchanged after CRT. The torsion did not improve in responders, but was worsened in non-responders (p<0.05). CONCLUSIONS: The improvement of LV short-axis function but not long-axis function or torsion contributes to the improvement in LV global function and geometry at three-month follow up. A relatively preserved mean epsilon-circum of >or=6.5% might be useful to predict favourable responses after CRT.

The Hong Kong diastolic heart failure study: a randomised controlled trial of diuretics, irbesartan and ramipril on quality of life, exercise capacity, left ventricular global and regional function in heart failure with a normal ejection fraction.

BACKGROUND: Although heart failure with a preserved or normal ejection fraction (HFNEF or diastolic heart failure) is common, treatment outcomes on quality of life and cardiac function are lacking. The effect of renin-angiotensin blockade by irbesartan or ramipril in combination with diuretics on quality of life (QoL), regional and global systolic and diastolic function was assessed in HFNEF patients. METHODS: 150 patients with HFNEF (LVEF >45%) were randomised to (1) diuretics alone, (2) diuretics plus irbesartan, or (3) diuretics plus ramipril. QoL, 6-minute walk test (6MWT) and Doppler echocardiography were performed at baseline, 12, 24 and 52 weeks. RESULTS: The QoL score improved similarly in all three groups by 52 weeks (-46%, 51%, and 50% respectively, all p<0.01), although 6MWT increased only slightly (average +3-6%). Recurrent hospitalisation rates were equal in all groups (10-12% in 1 year). At 1 year, LV dimensions or LVEF had not changed in any group, though both systolic and diastolic blood pressures were lowered in all three groups from 4 weeks onwards. At baseline both mean peak systolic (Sm) and early diastolic (Em) mitral annulus velocities were reduced, and increased slightly in the diuretic plus irbesartan (Sm 4.5 (SEM 0.17) to 4.9 (SEM 0.16) cm/sec; Em 3.8 (SEM 0.25) to 4.2 (SEM 0.25) cm/sec) and ramipril (Sm 4.5 (SEM 0.24) to 4.9 (SEM 0.20) cm/sec; Em 3.3 (SEM 0.25) to 4.04 (SEM 0.32) cm/sec) groups (both p<0.05). NT-pro-BNP levels were raised at baseline (595 (SD 905) pg/ml; range 5-4748) and fell in the irbesartan (-124 (SD 302) pg/ml, p = 0.01) and ramipril (-173 (SD 415) pg/ml, p = 0.03) groups only. CONCLUSIONS: In this typically elderly group of HF patients with normal LVEF, diuretic therapy significantly improved symptoms and neither irbesartan nor ramipril had a significant additional effect. However, diuretics in combination with irbesartan or ramipril marginally improved LV systolic and diastolic longitudinal LV function, and lowered NT-proBNP over 1 year.

Triplane tissue Doppler imaging: a novel three-dimensional imaging modality that predicts reverse left ventricular remodelling after cardiac resynchronisation therapy.

BACKGROUND: Several two-dimensional (2-D) tissue Doppler imaging (TDI) echocardiographic techniques have proved useful to identify responders to cardiac resynchronisation therapy (CRT). Recently a 3-D probe allowing simultaneous acquisition of TDI data in three imaging planes became available. OBJECTIVE: To evaluate the value of triplane TDI to predict reverse left ventricular (LV) remodelling after CRT. METHODS: Sixty patients with heart failure, scheduled for CRT, underwent triplane echocardiography with simultaneous TDI acquisition before and 6 months after implantation. From the triplane dataset a 3-D LV volume was generated and LV volumes and ejection fraction were calculated. Intraventricular dyssynchrony was quantitatively analysed by evaluating time from onset of the QRS complex to peak myocardial systolic velocity in 12 LV segments from the triplane dataset and calculation of the standard deviation (Ts-SD-12). Clinical response was defined as an improvement of at least one New York Heart Association class. Reverse LV remodelling was defined as >/=15% decrease of LV end-systolic volume at 6 months' follow-up. RESULTS: Responders to CRT had significantly more LV dyssynchrony at baseline than non-responders (mean (SD) Ts-SD-12: 42 (14) vs 22 (12), p<0.001). A cut-off value of 33 ms for baseline Ts-SD-12, acquired from the triplane TDI dataset, yielded a sensitivity of 89% with a specificity of 82% to predict clinical response to CRT; sensitivity and specificity to predict reverse LV remodelling were 90% and 83%, respectively. CONCLUSION: Triplane TDI echocardiography predicts clinical response and reverse LV remodelling 6 months after CRT implantation.

Tissue Doppler velocity is superior to displacement and strain mapping in predicting left ventricular reverse remodelling response after cardiac resynchronisation therapy.

OBJECTIVE: To compare the values of three different forms of tissue Doppler imaging (TDI) processing in predicting left ventricular (LV) reverse remodelling-namely, tissue velocity, displacement and strain mapping. DESIGN: Standard echocardiography with TDI was performed before and 3 months after cardiac resynchronisation therapy (CRT). SETTING: University teaching hospital. PATIENTS: 55 patients with heart failure who received CRT and were followed up for at least 3 months were recruited. INTERVENTIONS: During off-line analysis, the time to peak systolic velocity in the ejection phase, time to peak positive displacement and time to peak negative strain were measured in the six basal, six mid-segmental model. Parameters of systolic asynchrony derived by velocity, displacement and strain mapping were correlated with percentage reduction in LV end systolic volume (LVESV) and absolute gain in ejection fraction (EF). RESULTS: Among the three TDI processing technologies, all parameters of tissue velocity correlated with LV reverse remodelling (r = -0.49 to r = -0.76, all p < 0.001), but the predictive value was strongest in models with 12 LV segments. For displacement mapping, only the two parameters that included 12 LV segments correlated modestly with reduction in LVESV (r = -0.36, p < 0.05) and gain in EF. However, none of the strain mapping parameters predicted a favourable echocardiographic response. The receiver operating characteristic (ROC) curve areas were higher for parameters of tissue velocity based on 12 LV segments (ROC areas 0.88 and 0.94) than the corresponding areas derived from displacement mapping (ROC areas 0.72 and 0.71). CONCLUSION: Tissue velocity parameters of systolic asynchrony are superior to those of displacement and strain mapping in predicting LV reverse remodelling response after CRT.

Variable left ventricular activation pattern in patients with heart failure and left bundle branch block.

OBJECTIVE: To determine the left ventricular (LV) activation pattern in patients with chronic heart failure and left bundle branch block (LBBB) on ECG. DESIGN: Prospective study. SETTING: Tertiary cardiology referral centre in Hong Kong. PATIENTS: Seven patients with LV ejection fraction < 35% and typical LBBB on ECG with QRS duration > or = 130 ms were recruited. Five of them had non-ischaemic dilated cardiomyopathy. METHODS: Non-contact mapping was used to investigate the LV global activation sequences. Tissue Doppler imaging was performed with the LV mapping and correlated with the activation sequences. RESULTS: Three patients had preserved left bundle activation despite LBBB on ECG. Conduction block was detected in four patients during LV activation and the other three had homogeneous depolarisation propagation within the left ventricle. The latest segment of activation was located in either the lateral or the posterior region. Tissue Doppler imaging correlated well with non-contact mapping to locate the conduction block and the latest segment of activation. CONCLUSIONS: LV endocardial activation sequences in patients with chronic heart failure and LBBB are variable. This may have implications for patient selection for treatment with cardiac resynchronisation.

Left ventricular long axis function in diastolic heart failure is reduced in both diastole and systole: time for a redefinition?

OBJECTIVE: To test the hypothesis that, when measured in the long axis, left ventricular systolic function is abnormal in patients with diastolic heart failure. DESIGN: A case-control study. SETTING: University teaching hospital (tertiary referral centre). PATIENTS: 68 patients with heart failure, 29 with a left ventricular ejection fraction (LVEF) of > 0.45 and diastolic dysfunction (diastolic heart failure), 39 with an LVEF of