Thirty-three patients with stable coronary artery disease, scheduled for PCI, underwent CSE and quantitative coronary angiography (QCA) before and 9 months after PCI. Regional myocardial perfusion was analysed blinded to QCA results. QCA identified 38 significant stenoses (≥50% diameter reduction). Before PCI, perfusion during stress was significantly reduced in regions supplied by stenotic arteries; blood flow velocity (β) –3.9 (–9.0 to 0.5) s^–1, perfusion rate (Axβ) –175.0 (–518.0 to 58.5) s^–1, and refilling time (rt) 210 (–22 to 452)ms, compared with the perfusion increase seen in regions supplied by non-stenotic arteries; β 1.6 (–0.7 to 4.4) s^–1, Axβ 151.7 (–67.0 to 300.5) s^–1, and rt –47 (–195 to 89) ms, all P < 0.05. At follow-up, regional stress-induced perfusion improved in 29 regions with successful PCI; β 0.1 (–2.7 to 3.6), Axβ 30.5 (–133.3 to 232.1), and rt –99 (–247 to 125), all P ≤ 0.01, although there was no improvement in nine regions with restenosis; β 0.9 (–1.5 to 5.3), Axβ 65.7 (–40.8 to 412.6), and rt –79 (–268 to 163), P = NS.

Quantitative CSE has the potential to detect angiographically significant coronary artery stenoses as well as angiographic success after PCI.

Trial registration: ClinicalTrials.gov Identifier: NCT00354081.

Database search was performed through January 2008. We included studies evaluating accuracy of quantitative stress MCE for detection of CAD compared with coronary angiography or single-photon emission computed tomography (SPECT) and measuring reserve parameters of A, β, and Aβ. Data from studies were verified and supplemented by the authors of each study. Using random effects meta-analysis, we estimated weighted mean difference (WMD), likelihood ratios (LRs), diagnostic odds ratios (DORs), and summary area under curve (AUC), all with 95% confidence interval (CI). Of 1443 studies, 13 including 627 patients (age range, 38–75 years) and comparing MCE with angiography (n = 10), SPECT (n = 1), or both (n = 2) were eligible. WMD (95% CI) were significantly less in CAD group than no-CAD group: 0.12 (0.06–0.18) (P < 0.001), 1.38 (1.28–1.52) (P < 0.001), and 1.47 (1.18–1.76) (P < 0.001) for A, β, and Aβ reserves, respectively. Pooled LRs for positive test were 1.33 (1.13–1.57), 3.76 (2.43–5.80), and 3.64 (2.87–4.78) and LRs for negative test were 0.68 (0.55–0.83), 0.30 (0.24–0.38), and 0.27 (0.22–0.34) for A, β, and Aβ reserves, respectively. Pooled DORs were 2.09 (1.42–3.07), 15.11 (7.90–28.91), and 14.73 (9.61–22.57) and AUCs were 0.637 (0.594–0.677), 0.851 (0.828–0.872), and 0.859 (0.842–0.750) for A, β, and Aβ reserves, respectively.

Evidence supports the use of quantitative MCE as a non-invasive test for detection of CAD. Standardizing MCE quantification analysis and adherence to reporting standards for diagnostic tests could enhance the quality of evidence in this field.

One hundred and thirty-two patients were evaluated (81 type 1 diabetic patients and 51 healthy volunteers). The detailed M-mode, two-dimensional, colour Doppler; PW Doppler; and TDI analyses were performed on resting subjects in a regular setting. Posterior wall thickness, left atrial indexed diameter, and A velocity were significantly higher in the diabetics when compared with control group (P = 0.019, <0.001, 0.033, respectively). Rest of the M-mode and PW Doppler parameters of diabetics were comparable with those of control subjects (P > 0.05 for all). However, both septal E' and lateral E' velocities were significantly lower in diabetics than in the control subjects on TDI echocardiographic examination (P < 0.001 and 0.011, respectively). In addition, E'/septal E' and E/lateral E' ratios were significantly higher in the diabetic group (P < 0.001 and 0.008, respectively).

TDI is a more accurate and powerful method than PW or M-mode in determination of early cardiac involvement related to type 1 DM even in the subclinical phase as well as hereditary cardiomyopathies.

Seventy-nine patients undergoing routine full dose dobutamine stress-echo (DSE) were divided into two groups based on resting wall motion and DSE response: DSE negative (DSE_neg) (35 of 79 patients) and positive (DSE_pos) (44 of 79 patients) which were compared with 32 healthy volunteers. Aortic CW-Doppler traces at rest were analysed semi-automatically; time-to-peak (T_mod), ejection-time (ET_mod), rise-time (t_rise), and fall-time (t_fall) were quantified. Asymmetry (asymm) was calculated as the normalized difference of left and right half of the spectrum. Normal curves were triangular, early-peaking, whereas patients showed more rounded shapes and later peaks. T_rise was longest in DSE_pos. T_fall was shortest in DSE_pos, followed by controls and DSE_neg. Asymm was lowest in DSE_pos, followed by controls and DSE_neg. Abnormally symmetric profiles (asymm <0.25) were found in none of the controls, 2.9% DSE_neg, and 27.3% DSE_pos. A good correlation was found between assym and ejection fraction (EF) and T_mod/ET_mod and EF. Notably, an LV dynamic gradient was induced in 71.4% DSE_neg and in 18.2% DSE_pos, associated with LV hypertrophy and supernormal (very asymmetric) traces.

Decreased myocardial function results in a more symmetrical outflow, while very asymmetrical traces suggest increased contractility, potentially inducing intra-cavity gradients during DSE. Therefore, including outflow symmetry as a clinical measurement provides additional information on patients with CAD.

LA volumes during reservoir, conduit, and contractile phases were measured in 27 MR patients and 25 controls. LA ejection fraction (EF) and ejection force were calculated. Reservoir (SR-R), conduit (SR-C), and contractile phase (SR-A) strain rates, and reservoir phase strain were obtained. LA volumes were higher in MR in all phases. In MR, ejection force was increased (21.5 vs. 12.3 kdynes, P = 0.001); reservoir phase strain (32.91 ± 14.26%), SR-R (2.65 ± 0.87), SR-C (–2.02 ± 0.58), and SR-A (–2.55 ± 1.31 s^–1) were increased (23.14 ± 7.96%, 1.62 ± 0.53, –1.29 ± 0.59, –1.98 ± 0.65 s^–1, in controls, respectively, P ≤ 0.004). Regional deformation correlated with corresponding volumetric parameters. Despite enhanced SR-A in MR, LA EF was unchanged (31.34 vs. 29.23%, P = ns), and LA contractile tissue velocity (A') was reduced (–5.39 ± 1.95 vs. –6.91 ± 1.80 cm/s, P = 0.006). The LA contractile contribution to left ventricular filling was significantly reduced in MR.

LA deformation is increased in all phases in MR. Unchanged LA EF and reduced A' may reflect the reduced contractile contribution to left ventricular filling.

Fourteen healthy volunteers and 20 patients with repaired ToF (mean age 31 ± 14) underwent 3DE and MRI within the same day. Right ventricular end-systolic volume (ESV) and end-diastolic volume (EDV) and EF were measured by two observers using 3DE and compared with MRI measurements. Intra- and interobserver variability of 3DE and agreement between both methods were evaluated using Bland–Altman analysis. Over or underestimation of 3DE in comparison to MRI was assessed using paired t-test. Intra- and interobserver variability of 3DE was excellent with intraclass coefficient of correlation (ICC) ranging from 0.85 to 0.99 and from 0.85 to 0.98, respectively. Three-dimensional echocardiography underestimated ESV and EDV (P < 0.001) but agreement between 3DE and MRI was excellent (ICC = 0.88 and 0.87, respectively). Ejection fraction was 47.7 ± 7.8 with 3DE and 47.9 ± 6.7 with MRI, agreement between both methods was good (ICC = 0.72).

Three-dimensional echocardiography combined to semi-automated quantification software shows fair agreement with MRI for RV volumes and EF measurement in patients with repaired ToF and adequate intra- and interobserver variability. These results suggest applicability for serial follow-up of patients with right heart congenital disease. However, the accuracy of 3DE echo diminishes with larger RV volumes, in part due to current difficulty to include the entire RV in the imaged sector. Technical progress in transducers beam geometry is likely to address this issue.

Sixty-five patients with a single- or dual-chamber RV pacemaker were included. Forty-seven patients with ejection fraction (EF) ≤ 35%, 17 with no bundle branch block (BBB), 16 with right bundle branch block (RBBB), and 14 with left bundle branch block (LBBB). Eighteen patients with EF > 35% and no BBB served as a control group. Echocardiographic dyssynchrony parameters [aortic pre-ejection delay (AoPEP), interventricular mechanical delay, delayed posterior left ventricular wall motion, and septal-to-posterior wall motion delay (SPWMD)] were evaluated in all patients with and without RVP. No dyssynchrony was found in patients with no BBB, RBBB, and in the control group, whereas LBBB patients showed significant dyssynchrony in AoPEP and SPWMD. RVP had a significant negative impact on all dyssynchrony parameters in patients with no BBB or LBBB. RVP induced significantly less severe dyssynchrony in RBBB patients. With RVP 100, 94, 56 and 16% of patients with LBBB, without BBB, RBBB, and from the control group, respectively, fulfilled the CARE-HF criteria for ventricular dyssynchrony.

RVP worsens mechanical ventricular dyssynchrony in patients with reduced EF. These effects are most pronounced in patients with either normal QRS width or LBBB during intrinsic rhythm. In contrast, patients with an RBBB during intrinsic rhythm without RVP evidenced a better preserved haemodynamic function and mechanical synchrony with RVP, despite a comparable extent of pacing-induced QRS prolongation.

Five hundred consecutive individuals who presented to the Emergency Department with chest pain, normal electrocardiograms (ECG) and troponin I were selected based on a less than 5 days interval between chest pain episode and performance of contrast flash-replenishment DASE. Analysis of myocardial perfusion with SonoVue© infusion after dipyridamole was routinely added on top of standard wall motion assessment during DASE. Adverse events (AEs) were reported according to standardized terminology and then compared with a historical control group in which contrast was not used. No deaths, myocardial infarctions, sustained arrhythmias, or any other life-threatening events were observed. Adverse events were not significantly different between the study group and the control group. In the selected subgroup of patients (n = 149) who underwent coronary angiography, accuracy of DASE with additional perfusion assessment was higher (88%, 95% C.I. 83–93%) than without (72%, 95% C.I. 65–79%).

DASE with SonoVue© infusion for myocardial perfusion assessment was exceptionally safe even when routinely performed within the first 5 days following a chest pain episode of undetermined origin in subjects without ECG and troponin abnormalities.

Forty patients with HfnEF, 27 young controls and 26 older controls, were prospectively recruited. All subjects underwent clinical examination, 12-lead electrocardiogram, pulmonary function test, echocardiogram, and metabolic exercise test. LV torsion increases with advancing age (older controls vs. young controls, 2.2 ± 0.9 vs. 1.4 ± 0.8°/cm; P = 0.03). Circumferential strain was enhanced in patients with HfnEF (–24.7 ± 4.7 vs. –20.0 ± 4.9%; P = 0.003). Rotational deformation delay (time difference between peak basal rotation and peak apical rotation), global circumferential strain, E-velocity deceleration time, and LV end-diastolic volume index were independent predictors of LV torsion. LV torsion and body mass index were independent predictors of LV untwist rate.

Ageing is associated with increased LV torsion secondary to reduced rotational deformation delay and increased peak basal rotation. LV torsion and strain patterns in patients with HfnEF are similar to age-related changes apart from circumferential strain, which is enhanced in patients with HfnEF.

In 29 OSA patients with normal LVEF and 20 control subjects, tissue Doppler imaging (TDI), standard 2D, and Doppler echocardiography were acquired before and immediately after overnight sleep. Peak systolic (S’), early diastolic (E’), and late diastolic (A’) annular velocities at septal and lateral corners were measured and averaged. The prevalence of hypertension was more often, LV mass index (102 ± 16 vs. 89 ± 18 g/m², P < 0.05) and left atrial volume index (25.3 ± 4.0 vs. 22.3 ± 4.4 mL/m², P < 0.05) were larger in OSA patients. Before sleeping, OSA patients had reduced E/A ratio suggesting impaired relaxation. Although no significant differences in S' were noted between the two groups, E' was lower and A' was higher in OSA patients compared with control subjects. Compared with before sleeping, S', E', and A' were significantly reduced after sleeping in both groups, but the per cent reduction of S' and A' was significantly larger in OSA patients. After overnight sleep, A wave velocity was also significantly reduced in OSA patients. A weak but significant correlation between per cent reduction of S'(A’) and apnoea–hypopnoea index was noted.

Overnight sleeping in OSA patients is associated with the development of subclinical systolic dysfunction and exaggerated diastolic dysfunction.

In 44 patients with acute heart failure (HF) with preserved left ventricular (LV) ejection fraction, parameters of LV structure and function were assessed via comprehensive two-dimensional Doppler echocardiography. There was no correlation between cTnT and LV wall thickness, left atrial volume index, or transmitral E wave velocity or deceleration time. There were associations between cTnT and LV end-diastolic dimension (r = –0.34, P = 0.02) and LV mass index (r = 0.32; P = .04). A lower tissue Doppler Ea wave peak velocity was associated with higher cTnT concentrations (r = –0.90, P < 0.001). In multivariate analyses, only LV end-diastolic dimension (t = 2.2; P = 0.04), LV mass index (t = 2.3; P = .03), and tissue Doppler Ea wave peak velocity (t = –4.7; P < .001) emerged as significant predictors of cTnT.

In patients with HF with preserved LV ejection fraction, cTnT is strongly associated with the extent of LV relaxation abnormalities and LV mass.

Twelve consecutive patients (11 women, 1 man) underwent 2D echocardiography on admission and on early follow-up (34 ± 16 days). Two-dimensional images were analysed to measure longitudinal and radial strain and to calculate post-systolic shortening (PSS) and the post-systolic index (PSI). Mean age was 64 ± 14 years. Upon presentation ejection fraction, average longitudinal and radial strains were 42 ± 9%, –10.6 ± 5.5%, and 20.1 ± 17.3%, respectively. Values improved to 59 ± 8%, –17.6 ± 3.0%, and 50.2 ± 17.0%, respectively (all P < 0.001). PSS was present in 69% of segments upon presentation and in 53% of segments upon follow-up. PSI was –0.16 at baseline and improved to –0.06 upon follow-up (P < 0.001).

Patients with TC show abnormal global and regional strain patterns during the acute phase of the disease which improve over time. However, subtle abnormalities of regional LV function seem to persist into the early follow-up period as suggested by the presence of PSS in more than half of LV segments. Long-term follow-up studies are needed to clarify whether these subtle abnormalities will further improve.

Hypertensive outpatient without previous cardiovascular events and with normal LV ejection fraction (EF) at rest underwent echocardiographic evaluations of LV size and systolic function by standard, tissue-Doppler, and speckle-tracking methods before and after 2 weeks of treatment with bisoprolol to obtain change in LV systolic mechanics at a stable heart rate reduction (–20 ± 10% from baseline) without significant change in LV mass. In the study sample (n = 26, 62% women, mean age 52 ± 10 years), under bisoprolol, afterload [i.e. circumferential (CESS) and meridional (MESS) end-systolic stress], LV mass, left atrial volume, and EF did not change significantly; LV chamber contractility [i.e. CESS/LV end-systolic volume index (CESS/ESVi) as well as MESS/ESVi] and relative wall thickness (RWT) decreased; stroke volume increased (all P < 0.05). Circumferential LV contractility (i.e. stress-corrected midwall shortening) increased, whereas regional longitudinal strain and strain rate, and global longitudinal strain decreased (all P < 0.05). Peak velocities of the systolic displacement of the lateral and medial mitral anulus did not change under bisoprolol. Parameters of longitudinal LV systolic function did not correlate with preload, afterload, RWT, or with stoke volume.

In hypertensive subjects with preserved LV EF, parameters of longitudinal LV systolic mechanics may not reflect the LV myocardial contractility status in steady-state conditions under short-term treatment with β1-block.

Fifty-three asymptomatic patients with MS and 53 healthy controls were evaluated by the standard echo-Doppler study [mitral valve (MV) area, mean gradient, systolic pulmonary pressure, left atrial (LA) width, LA volumes, LA compliance index] and by Doppler myocardial imaging (velocity, strain, and SR of both atria). The endpoint at 3 year follow-up was symptoms, hospitalization for cardiac cause, atrial fibrillation, thrombo-embolic events, valvular surgery, or percutaneous commissurotomy. LA width, volumes, and systolic pulmonary pressure were significantly increased in MS patients (P < 0.001). Atrial myocardial velocities and deformation indices were significantly compromised in MS patients (P < 0.0001). Significant correlation was found between atrial myocardial velocity and MV area (by pressure half-time method: P = 0.019, R = 0.41; by planimetric method: P = 0.016, R = 0.43). Peak systolic LA myocardial strain and SR were significantly correlated with atrial volumes (strain: P = 0.03, R = –0.28; SR: P = 0.0008, R = –0.42), with atrial compliance index (strain: P = 0.04, R = 0.26; SR: P = 0.04, R = 0.16), with atrial ejection fraction (strain: P < 0.0001, R = 0.56; SR: P = 0.03, R = 0.43). At 3 year follow-up, 22 (41%) patients had events. Comparing the MS patients who had events during the 3 year follow-up with those who did not, the former had bigger LA volumes, although these parameters did not reached a significant value, whereas atrial myocardial systolic SR was significantly impaired in patients with events. In multivariate analysis, the best predictor of adverse events was LA peak systolic SR average (P = 0.04; coefficient: 0.113; SE: 0.055; cut-off value of 1.69 s^–1 for LA peak systolic SR average) with a sensitivity of 88%, specificity of 80.6%, area under the receiver operating characteristic curve of 0.852 (SE: 0.048; 95% CI: 0.74–0.93, P = 0.0001).

Atrial myocardial deformation properties, assessed by SRI, are abnormal in asymptomatic patients with rheumatic MS. The degree of this impairment is predictor of events in a 3 year follow-up. SRI could be helpful in decision-making of asymtomatic patients with MS.

Hundred patients (72 ± 14 years, 59% male) with HF were prospectively enrolled. Fifty-one had preserved EF HF (LVEF > 50%). The prevalence of RV systolic dysfunction in patients with preserved EF HF was 33, 40, and 50%, by using RV fractional area change (FAC), tricuspid annular motion (TAM), and peak systolic tricuspid annular tissue velocity (S') criteria, respectively. Tricuspid S' and TAM correlated the best with LVEF (r = 0. 48, P < 0.01). Patients with preserved EF HF had higher RV FAC (54 ± 18 vs. 36 ± 20%, P < 0.01), TAM (17 ± 1 vs.11 ± 1 mm, P < 0.01), and tricuspid S' (14 ± 6 vs. 9 ± 4 cm/s, P < 0.01) compared with those with reduced EF HF. Of those 51 patients, 34% had tricuspid E/e' > 6 suggestive of elevated RV filling pressures. Early tricuspid inflow (E), early diastolic tricuspid annular tissue (e'), tricuspid E/e', and hepatic vein systolic velocities were also higher in patients with preserved EF HF.

The prevalence of RV systolic and diastolic dysfunctions was not uncommon in patients with preserved EF HF. However, patients with preserved EF HF had milder degree of RV systolic and diastolic dysfunctions compared with those with reduced EF HF.

One hundred and sixty-six participants, 79 males and 87 females, aged 29–79 years considered free from clinical and subclinical cardiovascular disease, were included. Normal ranges are defined as 95% reference values for atrial dimensions and reproducibility as coefficients of variations (CVs) for repeated measurements. Upper normal reference values were 41 mL/m² for maximum (max) LAVI and 19 mL/m² for minimum (min) LAVI. The lower normal reference value was 45% for LAEF. The respective values for RA were 47 mL/m², 20 mL/m², and 46%. The only relevant gender difference was a higher upper normal max RAVI among males vs. females. The CVs for repeated measurements were 9% for max LAVI, 8% for max RAVI, 13% for LAEF, and 14% for RAEF.

The present study provides normal ranges for atrial dimensions and contractility with a new, fast, and reproducible technique that can be used bedside without offline analysis.

We retrospectively analysed 166 consecutive patients with CAS and multiple echocardiograms from January 1997 to March 2005. Aortic valve area (AVA) was measured using the continuity equation. CAS severity was categorized using AVA. D and non-D patients were compared for differences in sex, hypertension, smoking, statin use using ² tests. Comparisons between D and non-D for changes in AVA per year were performed using ANOVA. Study cohort included 166 males with age 70 ± 9 years, of which 72 (43%) had D. Baseline CAS was mild in 66 subjects, moderate in 75, and severe in 25. D subjects smoked less (P = 0.02), but all other variables were similar (P > 0.05). The interaction between D and baseline CAS severity was significant (P = 0.0191), indicating comparisons should be viewed by baseline CAS severity. D had significantly larger change in AVA than non-D (P = 0.0016) for those with moderate CAS at baseline only. Adjusting for statin use did not alter the results.

CAS severity progresses faster in D than in non-D in subjects with moderate CAS at baseline. Statins do not affect progression of CAS.

Doppler echocardiography was performed in 40 consecutive patients with CHVP in mitral position. All patients were clinically stable, without evidence of prosthetic valve dysfunction such as significant obstruction or regurgitation, endocarditis, left ventricular dysfunction (ejection fraction <40%), or significant aortic regurgitation. Valve sizes studied included 25, 27, and 29 mm. Mitral valve area was derived both by the PHT method and the continuity equation, using stroke volume measured in the ventricular outflow tract divided by the time-velocity integral of CHVP jet. The peak Doppler gradient ranged from 5 to 21 (mean 11.0) mm Hg, and the mean gradient ranged from 1.7 to 9.2 (mean 4.1) mm Hg. Mean gradient negatively correlated with increase in actual orifice area (AOA) derived from the valve orifice diameter given by the manufacturer (r = –0.45, P = 0.004). Mitral valve area calculated by both PHT and continuity equation increased significantly with increase in AOA (r = 0.42, P = 0.007 and r = 0.32, P = 0.046, respectively). Mitral valve area by the continuity equation averaged 1.55 ± 0.36 cm² (range 0.85 cm² for a 25 mm valve to 2.41 cm² for a 29 mm valve), and was smaller than by the PHT (mean 2.04 ± 0.41 cm², range 1.40–3.14 cm²; P = 0.0001; t-test) irrespective of whether the PHT is less than or more than 110 ms.

The Doppler parameters obtained with CHVP in mitral position are comparable to those obtained with the different prosthetic valves in common use. In selected group of patients with CHVP, assessment of MVA by the PHT method is comparable to that by the continuity equation. Areas by both methods were smaller than the AOA provided by the manufacturer, as seen in other similar design valves.