In Protocol 1, 2DSTE data in the apical four-chamber view (iE33, Philips) and CMR images (Philips 1.5T scanner) were obtained in 20 patients. The 2DSTE data were analysed using custom software, which automatically performed speckle tracking analysis throughout the cardiac cycle. LV volume curves were generated using the single-plane Simpson's formula, from which end-diastolic volume (LVEDV), end-systolic volume (LVESV), and LVEF were calculated. In Protocol 2, the 2DSTE and RT3DE data were acquired in 181 subjects. RT3DE data sets were acquired, and LV volumes and LVEF were measured using QLab software (Philips). In Protocol 1, excellent correlations were noted between the methods for LVEDV (r = 0.95), ESV (r = 0.95), and LVEF (r = 0.88). In Protocol 2, LV volume waveforms suitable for analysis were obtained from 2DSTE images in all subjects. The time required for analysis was <2 min per patient. Excellent correlations were noted between the methods for LVEDV (r = 0.95), ESV (r = 0.97), and LVEF (r = 0.92). However, 2DSTE significantly underestimated LVEDV, resulting in a mean of 8% underestimation in LVEF. Intra- and inter-observer variabilities of 2DSTE were 7 and 9% in LV volume and 6 and 8% in LVEF, respectively.

Two-dimensional speckle tracking echocardiography measurements resulted in a small but significant underestimation of LVEDV and EF compared with RT3DE. However, the accuracy, low intra- and inter-observer variabilities and speed of analysis make 2DSTE a potentially useful modality for LV functional assessment in the routine clinical setting.

Seven patients (mean age of 65 years) with ischaemic mitral regurgitation underwent mitral valve annuloplasty with the Geoform ring and coronary artery bypass surgery. Pre- and post-operative 3D echocardiograms were performed. Following mitral annuloplasty, mitral regurgitation decreased from 3.4 ± 0.2 to 0.9 ± 0.3 (P-value < 0.0001), mitral valve tenting volume from 13 ± 1.7 to 3.2 ± 0.3 mL (P-value < 0.001), annulus area from 12.6 ± 1.0 to 3.3 ± 0.2 cm² (P-value < 0.0001), valve circumference from 13 ± 0.5 to 7.3 ± 0.3 cm (P-value < 0.0001), septolateral distance from 2.1 ± 0.1 to 1.4 ± 0.06 cm (P-value < 0.01) and intercommissural distance from 3.4 ± 0.1 to 2.7 ± 0.03 cm (P-value < 0.03). There was significant decrease in the septolateral distance at the level of A2–P2 with respect to other regions. These geometric changes were associated with the improvement in the NYHA class from 3.1 ± 0.3 to 1.3 ± 0.3 (P-value < 0.002).

The mitral valve annuloplasty with the Geoform^® ring restores leaflet coaptation and eliminates mitral regurgitation by effectively modifying the mitral annular geometry.

Coronary blood flow direction was assessed in the epicardial collaterals [distal LAD (dLAD), obtuse marginal branches and right posterior descending artery (PDA)] and intramyocardial collaterals [LAD septal branch (SB LAD) and RCA septal branch (SB RCA)]. The sensitivity and specificity of retrograde flow for identification of the occluded LAD by TTE in the dLAD only were 78 and 96%, respectively, and those in both dLAD and SB LAD were 89 and 96%, respectively. The retrograde SB LAD flow detects proximal LAD occlusion with 88% sensitivity and 75% specificity. The sensitivity and specificity of retrograde flow for identification of the occluded RCA by TTE in the PDA only were 79 and 97%, respectively, and those in both PDA and SB RCA were 89 and 97%, respectively. The retrograde SB RCA flow does not allow us to differentiate between proximal and non-proximal RCA occlusion. Transthoracic echocardiography is not a method for diagnosing Cx occlusions as the success in visualizing the Cx epicardial collaterals was achieved in 31% of cases only.

TTE is a sensitive and highly specific non-invasive method for diagnosis of LAD and RCA occlusions, based on the detection of the coronary blood flow direction in the epicardial and intramyocardial collaterals.

LV geometry was determined from LV mass/body surface area and relative wall thickness in combination. At end of the study, 52% of patients with initial LV hypertrophy had normal geometry (P < 0.001). In particular, concentric remodelling was reduced by 82% and concentric LV hypertrophy by 84%. Development of LV hypertrophy was seen in <5%. In Cox regression analyses including LV geometric patterns as time-varying variables and adjusting for treatment, Framingham risk score, race, and time-varying systolic blood pressure, the patterns independently predicted higher risk of primary composite endpoints [HR 2.99 (1.16–7.71) for concentric remodelling, HR 1.79 (1.17–2.73) for eccentric hypertrophy, and HR 2.71 (1.13–6.45) for concentric hypertrophy; all P < 0.05].

In hypertensive patients with ECG LV hypertrophy, in-treatment LV geometry by echocardiography adds information on risk of cardiovascular events.

Myocardial function was evaluated in 110 Parkinson patients [mean age (63.4 ± 9.0 years)] treated for at least 6 months with either EDDA (n = 71) or non-EDDA (n = 39). LV ejection fraction did not differ between EDDA and non-EDDA patients [63 ± 4% vs. 65 ± 4% (ns)]. There was no difference in prevalence of diastolic dysfunction between EDDA and non-EDDA patients [7% vs. 8% (ns)]. Finally, averaged LV systolic myocardial strain and longitudinal displacement analysed by means of two-dimensional speckle tracking showed no difference between EDDA and non-EDDA patients [strain: 19 ± 3% vs. 19 ± 2% (ns) and longitudinal displacement: 12 ± 2 mm vs. 12 ± 2 mm (ns)]. Elevated p-NT-proBNP was found in 38% of EDDA patients and in 59% of non-EDDA patients (ns).

In contrast to the well-established association between EDDA treatment and valvular fibrosis, EDDA did not have a detectable adverse impact on myocardial systolic and diastolic function.

We studied the accuracy of Doppler pressure gradients derived from regurgitant jet peak velocities using the simplified Bernoulli equation (SBE) using an in vitro flow model of atrio-ventricular valve regurgitation. We observed overall a good correlation (r = 0.89, P < 0.0001) with actual pressure gradient, when there is normal fluid viscosity and the jet is free of wall interaction. However, we observed various degrees of underestimation of pressure gradient by Doppler when regurgitant chamber size was reduced (P = 0.0003), when fluid viscosity was increased (P < 0.0001), or in the presence of wall interaction (P < 0.0001). Chamber compliance had no effect on the accuracy of pressure gradient prediction (P = 0.36). Significant underestimation error in pressure gradient prediction by Doppler of up to 43.2% was observed.

When jet impingement or wall interaction are present, or when viscosity is increased, caution should be used in applying the SBE to a regurgitant jet, as significant underestimation in pressure gradient prediction may occur.

Thirty patients (26 males, age 58 ± 9.6 years) underwent dobutamine stress echocardiography (DSE) and myocardial perfusion imaging (MPI) as well as coronary angiography (CA) with intravascular ultrasound (IVUS). Ultrasound images were analysed off-line, evaluating (1) wall motion and thickening at high mechanical index (‘conventional evaluation’), (2) the MCE loops stored during continuous infusion of contrast agent with regard to visual changes (stress vs. rest, ‘visual grading’), and (3) the replenishment curves of the contrast agent at low mechanical index after bubble destruction (‘quantitative grading’). CA/IVUS plus MPI showed ischaemia in seven and myocardial scars in nine patients. Sensitivity, specificity, NPV, PPV and accuracy for the detection of ischaemia representing functionally relevant CAV were, respectively, 0.71, 0.83, 0.90, 0.55 and 0.80 for the conventional evaluation alone, 0.71, 0.91, 0.91, 0.71 and 0.87 for additional visual grading and 0.86, 0.91, 0.95, 0.75 and 0.90 for additional quantitative grading.

Real-time MCE including visual and quantitative analysis is feasible for screening patients after HTX and is highly accurate in the diagnosis of haemodynamically relevant CAV.

A diluted ultrasound contrast bolus (SonoVue^®) was injected intravenously in 31 patients (19 male, age 65 ± 11) with known or suspected heart disease. A total of 68 recordings were made. The developed algorithm used the left atrium and LV IDC for LV ejection fraction measurement. Biplane enhanced LV ejection fraction measurements with pure ultrasound contrast (SonoVue^®) were determined in multiple four- and two-chamber recordings as reference.

The mean LV ejection fraction measured by biplane and IDC method was 33 ± 17% and 35 ± 18%, respectively. A correlation coefficient r = 0.93 was observed between the two methods. Bland–Altman analysis demonstrated a slight LV ejection fraction overestimation with IDC (mean 1.9 ± 6.3%).

A new fast method for LV ejection fraction assessment based on IDC principles is described and comparison with contrast enhanced biplane LV ejection fraction quantification shows accurate results.

Fifty-seven patients eligible for CRT were assessed for transmural scar with gadolinium-enhanced MRI and for left ventricular (LV) dyssynchrony with tissue Doppler. After implant, both atrioventricular and interventricular pacing intervals were optimized. LV reverse remodeling was defined as ≥10% decrease in LV end-systolic volume after 3 months. Sixteen patients had transmural scar in the posterolateral (PL) area (LV lead location), 14 at a remote site (non-PL) and 27 patients had no scar. LV reverse remodeling was observed in respectively 25%, 64% and 89% (P = 0.0001). Univariate analyses showed a relation with LV dyssynchrony (P = 0.004) and with absence of PL scar (P = 0.04) but not with QRS duration and the extent of LV scar tissue. In multivariate analysis, only LV dyssynchrony (OR: 19.62; 95% CI: 2.5–151.9; P = 0.004) independently predicted LV reverse remodeling.

In this study LV dyssynchrony remains the most important determinant of response to CRT, even in the presence of posterolateral scar provided atrioventricular and interventricular pacing intervals are optimized.

The study included 74 patients undergoing routine CABG. A pre-CABG Doppler echocardiographic assessment of LV dimensions, filling and ejection was performed and t-IVT was determined as [60 – (total ejection time + total filling time)]. Follow-up period was 18 ± 12 months. Of the 74 patients (age 65 ± 16 years, 59 males), 29 underwent hospital admission for a cardiac event or died. There were no differences in age, gender, incidence of previous infarct or mitral regurgitation, LV-EDD (left ventricular end-diastolic dimension), left atrial or right ventricular size in patients with cardiac events compared with those without events. Left ventricular end-systolic dimension (LV-ESD) was greater (4.5 ± 0.9 vs. 3.9 ± 0.9 cm, P = 0.003), fractional shortening (FS) was lower (21 ± 4 vs. 32 ± 8%), E:A ratio and Tei index were higher (2.1 ± 0.8 vs. 1.0 ± 0.6 and 0.9 ± 0.3 vs. 0.6 ± 0.3, all P < 0.001), and t-IVT was longer (16 ± 5 vs.10 ± 4 s/min, P < 0.001) in patients with events. Multivariate predictors of post-CABG events (odds ratio 95% confidence interval) were low FS [0.66 (0.50–0.87), P < 0.001], high E:A ratio [l4.13 (1.17–14.60), P = 0.028], large LV-ESD [0.19 (0.05–0.84), P = 0.029], and long t-IVT [1.37 (1.02–1.84), P = 0.035].

Despite satisfactory surgical revascularization, long t-IVT and systolic dysfunction suggest persistent ventricular dyssynchrony that contributes to post-CABG cardiac events. Early assessment of such patients for potential benefit from electrical resynchronization may optimize their cardiac performance and hence clinical outcome.

Forty-six patients undergoing contrast enhanced dobutamine stress echo were imaged with novel 3D LMI power modulation software. All patients underwent contrast enhanced 2D and RT3DE acquisitions, in left ventricular opacification (LVO), and LMI perfusion modes. The data sets were evaluated segmentally for wall motion (WM) and myocardial contrast enhancement. Of the 736 evaluated segments, WM could be assessed in 726 (98.6%) of the 2D and 708 (96.2%) 3D segments (P = 0.007). Perfusion could be assessed in 721 (98%) of 2D and 701 (95.2%) of 3D segments (P = 0.006). Six hundred and sixty-one segments had normal WM and thickening in 2D and of these RT3DE demonstrated normal myocardial opacification in 77.2% of basal, 85% of mid, and 91.8% of apical segments. Thirty-four segments were akinetic, with no evidence of perfusion in 2D, and of these RT3DE revealed a perfusion defect in 31 (91%, P = NS).

LMI RT3DE evaluation of myocardial perfusion is feasible in most segments. It has the potential to accurately locate and possibly quantify perfusion defects.

Ultrasonic and angiographic findings were compared visually and using quantitative measurements in 50 patients. One hundred and seventy-one vessels were examined by FRC-TEE. The total lengths visualized were 9.6 ± 1.7 cm for the right coronary artery, 7.0 ± 1.1 cm for left circumflex, 3.9 ± 1.2 cm for left anterior descending (LAD), and 1.5 ± 0.8 cm for the left main coronary artery. There was high concordance between results of both procedures. Sixty-three stenoses were detected using FRC-TEE. The mean difference in degree of stenosis between techniques was 0.2 ± 5.1%. Stents could be visualized in 19 segments. FRC-TEE detected distal stenoses of the coronary arteries to only a limited extent: 14 stenoses and 2 stents, predominantly in the LAD artery (n = 13), were not identified.

FRC-TEE is a potential method for diagnosing coronary artery disease. FRC-TEE and angiography yield comparable findings during the evaluation of coronary lesions. Further investigations are needed to verify the encouraging findings and define FRC-TEE's applications.

Regional rotation in six subdivisions of the circumference at three levels was studied by using speckle-tracking echocardiography in 40 healthy subjects. At the basal level the inferoseptal segments rotated significantly more clockwise during systole than the opposing anterolateral segments. At the papillary level the inferoseptal segments differed significantly from the anterolateral segments, where the inferoseptal segments rotated clockwise and the anterolateral segments rotated counter-clockwise. The apical level showed significant difference in regional rotation only at aortic valve opening. In early systole, untwist before the main systolic twist was seen at the basal and apical levels; however, the duration of the basal untwist was much longer than that of the apical. The diastolic phases of rotation at the basal and apical levels matched the different filling phases.

Large regional differences in rotation are present at the basal and papillary levels in healthy subjects. The diastolic untwist matches the phases of both the E-wave and A-wave and seems to be related with intraventricular pressure differences, indicating that untwist plays an important role in the filling of the ventricle.

We evaluated 90 hypertensive patients and 30 healthy volunteers. The hypertensive patients were divided into three groups: (i) HTN-N: normal remodelling (n= 30), (ii) HTN-CR: concentric remodelling (n= 30), and (iii) HTN-CH: concentric hypertrophy (n= 30). Mitral annular early diastolic (Ea) velocities were recorded. Filling pressures (E/Ea), relative wall thickness, LV mass index, DT, isovolumic relaxation time (IVRT), E/A ratio, and longitudinal wall stress (LWS) were also measured. Diastolic dysfunction (DD) was diagnosed based on published criteria. Progressive and increased incidence of DD with advancement of LV remodelling and an increase in LV mass was noted. Wall stress-loading was higher in the HTN-N group and lower in the HTN-CR and HTN-CH groups, despite the more deteriorated diastolic function in the latter groups. DD appeared early, even in the HTN-N group, which had a 36.6% incidence of DD compared to a 13% age-related incidence in the control group (P < 0.05). When the control group was used to define the reference values for septal Ea with the cut-off set as 2SD below the mean, the HTN-N, HTN-CR, and HTN-CH groups had abnormal diastolic function at 16.6, 26.6, and 56.6% incidence rates, respectively. Septal (Ea) was correlated with LVMI (r= –0.55), RWT (r= –0.56), Age (r= –0.52), BMI (r= –0.31), SBP (r= –0.54), PP (r= –0.55), and MAP (r= –0.39), all at P < 0.05. The correlations of blood-pool indices (DT, IVRT, and E/A) with the above parameters were less than that of tissue Doppler imaging (Septal and mean Ea). In a multivariate model, LVMI (β= –0.25), SBP (β = –0.26), and age (β= –0.24) R²= 0.49 were found to be independent predictors of DD.

DD appears early in hypertensive disease, before the onset of abnormal remodelling or LV hypertrophy. With progression of the remodelling process and the advance of LVH, diastolic function progressively deteriorates. Tissue Doppler indices are better correlated with clinical and echocardiographic parameters of LV remodelling compared to blood-pool indices.

We studied 100 consecutive normal foetuses (gestation range: 20–32 weeks; no evidence of structural cardiovascular disease by 2D echo and Doppler study) using 2D-S imaging. Left ventricle (LV) and right ventricle (RV) peak myocardial negative strain values were obtained.

Strain data were obtained from all the studied subjects, the duration of post processing was 3 ± 2 min for each patient dataset. Peak longitudinal deformation parameters were homogeneous in all the three studied walls (strain: septum = –25 ± 5%; lateral wall = –25 ± 4%; RV free wall = –24 ± 4%; P = NS). There were significant correlations between gestational age and peak longitudinal strain (P < 0.001; R: –0.73). Inter and intra-observer variability for strain was good, <3 and <6%, respectively.

This study demonstrated that 2D-S is a feasible and reproducible approach to assess regional ventricular function in the foetal heart, ready for the clinical application.

We performed echocardiograms on children with (i) isolated asymmetric septal HCM, (ii) isolated concentric HCM, (iii) Friedreich's ataxia associated with concentric HCM, and (iv) healthy controls. Wall thickness, left ventricular dimensions, ejection fraction, and mitral inflow were measured. Peak early diastolic myocardial velocities, peak systolic myocardial velocities, peak systolic strain rate (SR), peak systolic strain (), post-systolic shortening and time to maximal were measured in the basal and mid-septum and basal lateral wall to evaluate longitudinal myocardial function. Similar data were acquired and analysed in the anterior septum and infero-lateral wall to evaluate the radial myocardial function. All three groups with HCM had had increased wall thickness, reduced left ventricular dimensions, and evidence of impaired diastolic filling compared to controls. All forms of HCM had reduced early diastolic and systolic myocardial velocities and peak systolic SR and peak systolic compared with controls in all myocardial segments investigated. Children with asymmetric septal HCM had reduced systolic deformation, increased post-systolic shortening, and prolonged time to maximal in the basal septum compared with the other two groups with HCM. There were no differences in any echocardiographic variable between patients with isolated concentric HCM and Friedreich's ataxia and resulting HCM.

Myocardial deformation is abnormal in all forms of paediatric HCM. Myocardial deformation is more reduced and associated with post-systolic shortening in the more hypertrophied basal septum in patients with asymmetric septal HCM. In contrast, this reduction is uniformly distributed in all myocardial segments in patients with concentric HCM irrespective of whether HCM results from isolated or secondary HCM. Our findings suggest the pattern of hypertrophy influences myocardial deformation more than the underlying cause of HCM.

We retrospectively analysed 1229 consecutive echocardiograms (57% males) for the utility of echocardiographic measures including left atrial volume index (LAVI), left ventricular mass index (LVMI), and pulmonary venous and mitral inflow Doppler. LAVI of 40 ml/m² provided the greatest sensitivity and specificity of 76 and 77%, respectively, with reference to E/e' for the detection of diastolic dysfunction. The ESC definition of raised LVMI yielded a sensitivity and specificity of 32 and 99%, respectively. We found that the mitral and pulmonary inflow provided little incremental information. These results remained consistent between those with normal and abnormal ejection fraction.

There appears to be little incremental value of pulmonary and mitral Doppler measures beyond the measure of mitral E wave. An LAVI cut-off of 40 ml/m² maximizes both sensitivity and specificity. However, ESC guidelines of raised LVMI in patients with HFPEF would appear to heavily trade sensitivity for specificity.

In 300 patients referred for exercise echocardiography, assessment of DLVOTO at rest and with Valsalva and of the presence of systolic anterior motion of the mitral valve leaflets (SAM) was performed. Within 90 s post-exercise, wall motion, SAM, and DLVOTO were assessed again. A significant DLVOTO was defined as late-peaking Doppler velocity of ≥2.5 m/s (25 mmHg). Excluded were 7 patients with HOCM and 13 with inadequate image quality. There were 280 patients, aged 64(11) years. Coronary artery disease was found in 38% of patients; 44% were receiving beta-blocker therapy and 35% had hypertension. At rest, ejection fraction was 59 ± 9%; left ventricular hypertrophy (LVH) was present in 21%, SAM in 16%, DLVOTO ≥25 mmHg at rest in 0.7%, and with Valsalva in 3%. At peak, echocardiographic signs of ischaemia occurred in 44%, and significant DLVOTO in 5% (13 patients). By multivariate analysis, it was found that independent predictors of significant DLVOTO at peak were chordal SAM at peak, smaller left ventricle at end-systole, higher systolic blood pressure at peak, younger age and increased septal wall thickness. Significant DLVOTO was a possible cause of symptoms and/or ischaemia in at least 6 of the 13 patients.

Haemodynamically significant exercise-induced DLVOTO can occur without HOCM. Chordal SAM at peak, small, hyperdynamic left ventricles, increased septal wall thickness, and younger age are the best predictors.

Data from 71 hospital inpatients with preserved left ventricular systolic function who underwent standard two-dimensional echocardiography was analysed using an off-line speckle tracking software package. Early diastolic mitral inflow velocity (e), mitral septal annular tissue Doppler velocity (e'), and the rate of early diastolic apical untwist in degrees per second (rotR) from a parasternal short-axis view of the apex were all measured. Of the 71 patients, 14 had normal diastolic function, 25 had an abnormal relaxation pattern, 27 had a pseudonormalized pattern, and 5 had a restrictive pattern as defined by standard echocardiography criteria. Both e' and the ratio of e:e' correlated with the rate (speed) of early diastolic apical untwist (rotR) (P < 0.001 for both).

This non-invasive assessment of apical diastolic untwist is related to established echocardiographic measures of diastolic function and may illustrate the importance of a ventricular suction effect in varying left ventricular filling states.

In 25 heart failure patients [15 with left ventricular ejection fraction (LVEF) < 40%; 10 with LVEF ≥ 50%], Doppler echocardiography and invasive bi-ventricular pressure–volume haemodynamics were obtained at baseline and 30 min after infusion of the recombinant B-type natriuretic peptide vasodilator nesiritide. RV and LV intra-ventricular dyssynchrony was measured invasively using a pressure–conductance catheter. Patients with reduced LVEF had greater LV dyssynchrony (31 ± 3 vs. 24 ± 7%; P = 0.003) compared to those with preserved LVEF. Tricuspid annular plane systolic excursion (TAPSE) had the highest correlation with LV dyssynchrony (r = –0.52; P = 0.0002) compared to other RV echocardiographic parameters. The association between TAPSE and LV dyssynchrony was independent of RVEF and LVEF (P = 0.008). There were no acute changes in the correlations between LV dyssynchrony and TAPSE after nesiritide.

TAPSE and LV dyssynchrony are strongly associated, independent of RV and LV ejection fraction. Of the RV echocardiographic parameters, TAPSE has the highest predictive value of LV dyssynchrony, and remained significant after vasodilator unloading.

Forty-five consecutive patients (age 59 ± 10, 31 males) referred for coronary angiography were examined by contrast-enhanced RT3DE. Wall motion analysis was performed off-line by dedicated software. New or worsening wall motion abnormalities were detected in 17 of 28 patients with significant CAD (sensitivity 61%), and in two of 17 patients without significant CAD (specificity 88%). The sensitivity for detection of single-vessel CAD was 8/15 patients (53%), for two-vessel CAD 4/6 (67%), and for three-vessel CAD 5/7 (71%). In 35 patients, comparison with conventional RT3DE was available. The image quality index at rest improved from 2.5 ± 1.2 to 3.2 ± 1.0 (P < 0.001) with contrast and at peak stress from 2.3 ± 1.2 to 3.1 ± 1.0 (P < 0.001). Interobserver agreement on the diagnosis of myocardial ischaemia improved from 26 of 35 studies (74%, = 0.44) with conventional stress RT3DE to 30 of 35 studies (86%, = 0.69) with contrast-enhanced stress RT3DE. Sensitivity increased from 50 to 55% and specificity from 69 to 85% with contrast-enhanced stress RT3DE in this subset of patients.

Despite some important practical and theoretical benefits, contrast-enhanced stress RT3DE currently has only moderate diagnostic sensitivity due to several technical limitations as temporal and spatial resolution.

This prospective study included 29 patients (patients; mean age 37 ± 13 years) with genetically, enzymatically and/or biopsy-proven Anderson-Fabry disease and long-time ERT. Data on symptoms, cardiac medications and history of hypertension were collected and all patients had comprehensive echocardiographic examination prior to ERT and at follow-up.

Disease was at an early stage with a total mean Mainz severity score index of only 18.6 ± 13.0. Prior to ERT, 79% of patients reported acroparesthesia. The median creatinine level was 121 ± 108 mcmol/L and LVWT was present in nine patients (31%). Binary appearance of the interventricular septum was found in 20% and posterobasal fibrosis in 83%. At median follow-up of 37 months, acroparesthesia decreased to 55% (P = 0.016). There was no change in creatinine levels. The incidence of LVWT was unchanged, only an increase in interventricular septal wall thickness from 11.7 ± 0.4 to 12.5 ± 0.5 was observed (P = 0.009). Left atrial size and the percentage of patients with binary appearance and posterobasal fibrosis were unchanged. There was a small improvement in diastolic function (29% decrease of E/Ea; P < 0.002).

Our Anderson-Fabry cohort had successful long-time ERT with impressive amelioration of subjective symptoms. Although there was not much improvement in cardiac changes apart from a slight improvement of diastolic function, at least, there was no progression of cardiac disease. For complete reversibility of cardiac changes in Anderson-Fabry disease, ERT might have to be started earlier in life and/or prescribed for a longer time.

We studied 75 hypertensive patients, of whom 45 had diastolic dysfunction and normal EF, and 30 matched controls. All subjects had 2D and colour Doppler myocardial imaging. Mean longitudinal strain (S) and strain rate (SR) were averaged from the basal and mid-LV segments assessed in the longitudinal axis. Early to late diastolic SR ratio <1.1 was defined as altered segmental relaxation [segmental diastolic dysfunction (DD)]. The total number of segmental DD out of the 18 basal-mid-apical segments was calculated for all the participants. Longitudinal systolic function estimated by mean strain and SR was decreased in the hypertensive group, but was further deteriorated in the diastolic dysfunction group compared with controls. Altered Segmental Relaxation was highly correlated with longitudinal systolic dysfunction expressed by strain (r: –0.56)or SR (r: –0.57). A septal mitral annular Ea cut-off of 5.9 cm/s predicted longitudinal systolic dysfunction with a sensitivity of 81% and a specificity of 70%. A multiple linear regression model proved LVMI, systolic blood pressure (SBP) and age as independent predictors of diastolic and longitudinal systolic dysfunction and BMI to independently related to diastolic dysfunction.

Longitudinal systolic dysfunction may be present in hypertensive patients with diastolic dysfunction, especially when septal Ea < 5.9 cm/s. Altered segmental relaxation pattern is highly correlated with longitudinal systolic dysfunction. LV hypertrophy, SBP and aging are important determinants of both diastolic and longitudinal systolic dysfunction, whereas obesity appears to contribute to the appearance of diastolic dysfunction.

We reviewed 57 patients who underwent gastric bypass surgery and had echocardiograms both before and after the operation. A control group was frequency-matched for BMI, sex, age, and for duration of follow-up. After a mean follow-up of 3.6 years, LA volume did not change significantly in patients who underwent bariatric surgery, but increased in the control group by 15 ± 28 ml (P < 0.0001), and 0.1 ± 0.2 ml (P < 0.0001) for height-indexed LA volume, with a difference between cases and controls that remained significant after adjusting for potential confounders (P = 0.01). In the study population as a whole, there was a positive correlation between change in body weight and change in LA volume (r = 0.22, P = 0.006) independent of clinical conditions associated with LA enlargement.

Change in body weight is associated with change in LA size independent of obesity-associated co-morbidities. Successful WL induced by bariatric surgery prevents the progressive increase in LA volume.

Forty-one patients referred for cardiac resynchronization therapy (CRT) were evaluated using tissue Doppler echocardiography. The inter and intra-individual reproducibility of peak systolic myocardial velocities and the intra-ventricular delay in three apical projections was assessed by repeated evaluation of each registered data set. Variability (measured by the coefficient of variation) ranged between 18 and 56% for the peak systolic velocities and between 32 and 117% for the time intervals.

The reproducibility of the tissue Doppler echocardiography parameters (peak systolic myocardial velocity and intra-ventricular delay) was poor in our set of patients with dilated left ventricles and low ejection fraction. The most probable causes of our poor results are discussed including the missing standardization of the TDI measurements.

Eighty-seven consecutive HCM patients (64% men, mean age 45 ± 19 years) underwent physical and Doppler echocardiographic evaluation at our centre from March 1993 to February 2001. Mean length of follow-up was 96 ± 54 months. RFP was found in 14 patients (16%) at index evaluation. Patients with RFP had higher NYHA class, more frequent signs of heart failure and lower left ventricular ejection fraction (P = 0.018, P = 0.002 and P = 0.001, respectively). During follow-up, cardiac death plus heart transplantation was significantly higher in HCM patients with RFP than in those without RFP (P = 0.0001). NYHA class (HR = 5.95, 95% CI: 1.34–26.38, P = 0.019), indexed left atrial diameter (HR = 1.68, 95% CI: 1.01–2.82, P = 0.047) and RFP (HR = 2.94, 95% CI: 1.25–6.88, P = 0.01) were selected as predictors of cardiac death or heart transplantation in a multivariate proportional hazard model. The AUC of ROC curve from multivariate regression models for predicting adverse outcome significantly improved from 0.76 considering only NYHA class to 0.84 after inclusion of RFP and indexed left atrial diameter (P = 0.01).

RFP is rare, but not exceptional, in HCM. Echo-Doppler evaluation of filling pattern confers additional prognostic power to clinical stratification.

In 92 healthy subjects (age 60.5 ± 18.6, 43.5% women), systolic AVPD was measured after exclusion of isovolumic components using three techniques: (i) M-mode; (ii) temporal integration of pulsed TD systolic wave; and (iii) colour TD-derived tissue tracking. Close correlations of M-mode AVPD with pulsed TD velocity-time integral (VTI) (R = 0.90, P < 0.0001) and colour TD AVPD (R = 0.86, P < 0.0001) were found. However, M-mode AVPD underestimated pulsed TD VTI (mean error –5.1 ± 1.7 mm) and overestimated colour TD AVPD (mean error 3.4 ± 1.3 mm). The concordance between M-mode and pulsed TD increased after adjustment for spectral dispersion of pulsed TD istantaneous velocities (mean error 0.1 ± 1.1 mm).

Despite strict correlations exist between M-mode and TD in the assessment of mitral annulus systolic excursion, the effective concordance between techniques is sub-optimal.

We studied 74 untreated mild to moderate HTNs and 34 matched normotensives (NTN). All had a standard echo including myocardial velocity data for regional radial and longitudinal deformation. Despite the absence of abnormalities in standard functional indices and LVH, non-uniform changes in regional geometry and deformation were observed. Besides a significant increase in wall thickness (WT) in all HTN segments, there was a gradual increase in WT from apex to base resulting in prominent basal septal hypertrophy. In HTN, regional longitudinal peak systolic SR (SSR) and end-systolic S (ESS) were significantly (P < 0.0001) reduced in the basal septum. In the lateral wall there was an increase in peak SSR and ESS (P < 0.05) basally. The basal septal ESS correlated both with mean arterial pressure and basal septal WT, with lower ESS for higher BP and thicker septum.

Regionally differing geometrical remodelling occurs early in HTN. Longitudinal ESS and peak SSR are sensitive markers of early changes occurring in HTN.

Twenty-four patients were enrolled in this prospective, crossover study. Three-dimensional echo and TOE data were collected, analysed and compared, assessing quantitative data including maximum defect diameter, area and circumference. Qualitative morphology such as the presence of fenestrations and the defect margins were noted, and an assessment of the suitability for device closure was made using each modality. Eighteen (75%) of the 3D data sets produced usable data for analysis. In each case the maximum diameter of the defect was larger on 3D echo than on TOE (mean difference = 0.34 cm, P < 0.001). On three occasions suitability for device closure could not be determined using 3D echo. On the other 15 occasions there was agreement between the TOE and 3D echo data.

Three-dimensional echo provides comparable data with TOE when attempting to predict suitability for device closure without the need for general anaesthetic or sedation. It also provides useful additional dynamic and morphological information.

Twelve female patients (mean age 29 ± 7 years) with isolated rheumatic MS, all in sinus rhythm, were studied before and 24–48 h after PTMC. Multiple parameters of global and longitudinal RV function were assessed by conventional and tissue Doppler imaging echocardiography. Immediately following PTMC, mitral valve area increased from 0.91 ± 0.29 cm² to 1.86 ± 0.43 cm² (P < 0.0001) and RV outflow tract fractional shortening (RVOTfs) increased from 57 ± 15% to 72 ± 12% (P = 0.002). There was a significant decrease in systolic pulmonary artery pressure from 46.4 ± 32.1 mmHg to 29.1 ± 13.4 mmHg (P = 0.02), in the RV Tei index from 0.44 ± 0.025 to 0.29 ± 0.17 (P = 0.021), in myocardial acceleration during isovolumic contraction (IVA) at the lateral tricuspid annulus from 0.36 ± 0.11 m/s² to 0.25 ± 0.07 m/s² (P = 0.023), and in isovolumic contraction velocities at the lateral tricuspid annulus from 11.03 ± 3.37 cm/s to 8.50 ± 2.04 cm/s (P = 0.034). In contrast, tissue Doppler velocities at the septal tricuspid annulus remained unchanged. The RV Tei index correlated with systolic pulmonary artery pressure before but not after PTMC (r = 0.70, P = 0.01, and r = 0.270, P = 0.053).

Immediately after successful PTMC, significant decrease in RV contractility as assessed by IVA was observed whereas other parameters of infundibular and global RV function as assessed by RVOTfs and Tei index showed significant improvement. These discordant results may be related to the relative insensitivity of currently available echocardiography parameters of RV function that are not completely immune to loading conditions. Further work using larger numbers of patients is needed to confirm our findings and to assess their utility in patient follow-up and management.

Eighteen closed-chest pigs were randomized into two groups (each with nine animals). In Group I, 4 weeks prior to induction of an acute transmural infarct, a copper coated stent was implanted in the proximal circumflex artery (Cx) to create a coronary artery stenosis of between 30 and 95% lumen diameter. At 4 weeks, the stenotic Cx vessel was occluded for 90 min by inflation of a PTCA balloon placed proximal to the stenosis to produce an acute transmural infarction. In Group II (the control group), 90 min Cx occlusion was performed in a normal vessel. In both groups the resulting acute transmural infarction was reperfused after 90 min by removing the PTCA balloon. For both groups, cardiac ultrasound data, including strain/strain-rate imaging, were collected at all stages of the investigation for subsequent offline analysis.

In both groups, acute reperfusion (TIMI flow 3 or 2), immediately increased infarct zone end-diastolic wall thickness due to the development of oedema. The acute increase in wall thickness was significantly higher in the non-stenotic animals as compared to the ones with a residual stenosis. Neither of the groups showed any tendency to normalize deformation (strain) during the reperfusion period.

In this experimental study, the measurement of end-diastolic wall thickness was a simple and non-invasive tool to monitor acute infarct reperfusion. It also provided information on the presence of a flow limiting stenosis in the infarct related artery after restoration of the flow. The deformation of the myocardium remained impaired during early reperfusion, whether reflow was at full pressure or low pressure due to a residual stenosis in the infarct related artery.

Fourteen patients with a DDD-pacemaker (7 RVA, 7 RVOT) and normal LVF without other cardiac abnormalities were studied. PM dependency, because of sick sinus syndrome with normal atrioventricular and intraventricular conduction, was absent in all, allowing acute programming changes. Wall motion score (WMS), longitudinal LV strain, and tissue Doppler imaging for electromechanical delay were assessed with echocardiography during AAI pacing constituting baseline and DDD pacing. The WMS was normal at baseline (AAI pacing) in all patients and LV dyssynchrony was absent. Acute RVA and RVOT pacing deteriorated WMS, electromechanical delay, and longitudinal LV strain, but no difference of the deterioration between both pacing sites was present and dyssynchrony did not emerge.

Both acute RVA and RVOT pacing negatively affect WMS, longitudinal LV strain, and mechanical activation times, without clear differences between both pacing sites. Thus echocardiographic techniques do not facilitate the selection between RVOT and RVA pacing to exclude adverse effects on LVF during PM implantation in patients with a normal LVF.

Seventeen chronically uremic patients (age 31 ± 10 years), without overt heart disease underwent conventional 2D and Doppler ECHO together with measurement of longitudinal mitral and tricuspid annular motion velocities. Fluid volume removed by HD was 2706 ± 1047 cm³. Haemodialysis led to reduction in LV end-diastolic volume (P < 0.0001), end-systolic volume (P < 0.001), peak early (E wave) transmitral flow velocity (P = 0.0001), and the ratio of early to late Doppler velocities of diastolic mitral inflow (P = 0.021). For the LV, early diastolic (E0) TDI velocities and the ratio of early to late TDI diastolic velocities (E0/A0) only on the septal side of the mitral annulus decreased significantly after HD (P = 0.0001 and P = 0.009, respectively). In a subgroup of seven patients who sustained significantly larger fluid volume loses following HD, E0 and the ratio of E0/A0 at the lateral side of mitral annulus also decreased suggesting a greater resistance of the lateral annulus to preload changes. Systolic velocities decreased after HD on both sides of mitral annulus (septal 6.90 ± 1.10 vs. 5.97 ± 1.48 cm/s, P = 0.006; lateral 8.68 ± 2.67 vs. 6.94 ± 1.52 cm/s, P = 0.011). For the RV, systolic tricuspid annular velocities decreased (13.45 ± 1.47 vs.11.73 ± 1.90 cm/s, P = 0.002) together with early diastolic velocities after HD (13.95 ± 2.90 vs.10.62 ± 2.45 cm/s, P = 0.0001). Both systolic and early diastolic tricuspid annular velocities correlated directly with fluid removal (P < 0.01).

This study shows that both systolic and diastolic TDI velocities of the LV and RV are preload-dependent. However, the lateral mitral annulus is more resistant to preload changes than either the septal mitral annulus or the lateral tricuspid annulus.

We assessed 25 consecutive patients following mitral valve repair with transthoracic real-time 3-dimensional echocardiography (RT3DE) and 2-dimensional echocardiography (2DE). We compared the adequacy of the visualization of the mitral valve Carpentier segments, the site of the repair, and the accuracy of planimetry by RT3DE and 2DE in estimating the postoperative mitral valve area (MVA), compared to the Doppler-derived pressure half-time (PHT) value. Inter-observer variability and feasibility were also assessed for RT3DE. Adequate visualization of the mitral valve segments was more frequently obtained by 3DE imaging (163/170 by 3DE vs. 121/170 by 2DE, P < 0.001). In particular, the mitral valve commissu