A new comprehensive 12-segment approach to right ventricular systolic and diastolic functions by 2D speckle tracking echocardiography in healthy individuals.

BACKGROUND: 2D speckle tracking echocardiography (2DSTE) was proved to be accurate for the assessment of the RV function. However, normal values for RV strain refer mostly to 3- or 6-segment models, excluding the contribution of other RV walls to RV function. We analyze RV function by 2DSTE in a normal population, using parasternal two-(2C) and apical four-chamber (4C) RV views, and creating a new 12-segment model for a potential better definition of RV function. METHODS: We prospectively evaluated 100 normals using 2DE and STE. We assessed the RV systolic function from regional strain (basal, mid, and apical), and at the level of each wall: lateral (LS), septal (SS), inferior (IS), and anterior (AS), and also global strain for 4C (4CGS), and 2C (2CGS). Global systolic strain rate (SRs) was measured from 2C and 4C views. Diastolic function was assessed from early (SRe) and late global strain rate (SRl), for both views. RESULTS: A total of 70 healthy individuals (48±15 years, 34 men) were suitable for concomitant 4C and 2CRV analysis. Feasibility of the STE analysis was 87.8%. We found significantly lower SS by comparison with LS, AS, and IS (P<.001). All S/SR parameters (GS, SRs, and SRe) were higher in 2C view than in 4C view (P<.001). All systolic S/SR parameters did not change with age. The early diastolic SR decreased, while the late diastolic SR increased with age. CONCLUSION: Our 12-segment RV strain model is feasible. Moreover, 2DSTE analysis using 2C and 4C views of the RV does not provide similar information. Rather, they offer complementary data. This might be of particularly clinical interest in diseases with regional RV dysfunction.

Growth hormone deficiency in adults impacts left ventricular mechanics: a two-dimensional speckle-tracking study.

BACKGROUND: Growth hormone deficiency (GHD) in adults is associated with increased cardiovascular events, but detailed assessment of cardiac and vascular function is lacking. Thus we assessed cardiac, arterial, and endothelial functions, using conventional and speckle-tracking echocardiography, in adults with GHD compared with controls with similar cardiovascular risk. METHODS: Fifty-two patients with GHD (47 ± 16 years; 34 men) and no cardiovascular disease or diabetes were enrolled prospectively and compared with 50 age- and sex-matched controls. Comprehensive echocardiography was performed in all participants. Regional left ventricular (LV) function was assessed from global longitudinal strain (GLS), global radial strain (GRS), and global circumferential strain (GCS), whereas LV torsion (LVtor) was calculated from basal (RotB) and apical (RotA) rotations. Arterial function was assessed from intima-media thickening, local wave speed, and beta index of stiffness, whereas endothelial function was assessed from flow-mediated dilation. Levels of pro-brain natriuretic peptide (proBNP) were measured. RESULTS: GLS and GCS were decreased more in patients with GHD than in controls (-17.2% ± 2.7% vs. -19.3% ± 3.3% and -15.9% ± 5.4% vs. -18.8% ± 3.5%; both P < 0.01), whereas GRS was similar. RotB and LVtor were also decreased in patients with GHD (-4.8° ± 2.6° vs. -6.2° ± 2.1°/cm and 1.8° ± 0.6° vs. 2.3° ± 1.1°/cm; both P < 0.05). ProBNP was increased in patients with GHD (61.0 ± 74 pg/dL vs. 24.7 ± 21 pg/dL; P = 0.002). Arterial and endothelial functions were similar between groups. CONCLUSIONS: In conclusion, adults with GHD had LV longitudinal dysfunction and increased proBNP levels compared with controls, suggesting intrinsic myocardial disease. Further studies are needed to assess if this cardiac impairment in adults with GHD is reversible after GH replacement.

Acute heart failure and a pseudo cystic image in the left ventricle.

The association between acute heart failure (AHF) and cardiac tumor may change the short and long term management of both conditions. A 51-year-old man presented with signs of AHF. ECG showed sinus tachycardia and left ventricular (LV) hypertrophy. Chest x-Ray found dilated heart and pulmonary congestion. There were no significant changes in blood tests. Transthoracic echocardiography revealed chambers dilation, and LV ejection fraction (LVEF) of 17%. Unexpectedly, we found an apical 2/2 cm cystic image in the LV. This had a myocardium-like membrane, seen better in 3D echocardiography, suggestive for hydatic cyst. Cerebral, thoracic, and abdomino-pelvic CT scan showed no hydatic lesions. Anti-Echinococcus antibodies were negative. Initially the clinical challenge was the management of the tumor in a patient with AHF and dilated cardiomyopathy. He was treated for AHF and followed up for the cystic image. He exhibited significant improvement of the clinical status and LVEF (increased to 42 %), with important cardiac reverse remodeling. Surprisingly, the apical cystic image disappeared. However, we found a hypertrophic aberrant cordae from apex to mid-septum, in the same position as the previous image. Thus, we believe that this cordae, by important remodeling and torsion generated the cystic image. This case highlights the importance of serial 2D and 3D echo examinations in patients with severely remodeled LV, and also with tumoral images.

Accuracy of fluoroscopic and electrocardiographic criteria for pacemaker lead implantation by comparison with three-dimensional echocardiography.

BACKGROUND: Fluoroscopic and electrocardiographic (ECG) criteria for the documentation of pacing lead positioning (apical and alternative sites) have been described, but data regarding their accuracy are lacking. METHODS: Fifty patients (27 men; mean age, 76 ± 9 years) with permanent right ventricular (RV) pacing leads were included. RV lead position was classified as apical, mid septal, mid RV free wall, RV outflow tract (RVOT) septal, or RVOT free wall. Exact anatomic lead position was documented using three-dimensional (3D) transthoracic echocardiography (TTE). Cohen's κ coefficient was used to assess agreement between fluoroscopic or ECG criteria and 3D TTE. RESULTS: True lead positions were as follows: 15 apical, 24 mid septal, three mid RV free wall, and eight RVOT septal wall; no leads were implanted into the RVOT free wall. Fluoroscopy (κ = 0.56; 95% confidence interval [CI], 0.37-0.76) and electrocardiography (κ = 0.43; 95% CI, 0.25-0.60) had moderate overall agreement with 3D TTE. Fluoroscopy had moderate agreement with 3D TTE for apical (κ = 0.57; 95% CI, 0.32-0.83), mid septal (κ = 0.48; 95% CI, 0.25-0.72), and mid free wall sites (κ = 0.54; 95% CI, 0.08-1.00) and moderate to good agreement for the RVOT septal wall (κ = 0.61; 95% CI, 0.30-0.90). Fluoroscopy misclassified as mid septal six of the 15 RV apical leads. ECG criteria had moderate agreement with 3D TTE for apical positions (κ = 0.55; 95% CI, 0.34-0.77) and RVOT sites (κ = 0.47; 95% CI, 0.21-0.73). Electrocardiography misclassified as apical 10 and as RVOT six of the 24 mid septal leads. CONCLUSIONS: Fluoroscopic and ECG criteria are only moderately accurate in discriminating between RV apical, mid septal, mid free wall, and RVOT pacing sites. These data suggest that both fluoroscopy and electrocardiography may not be adequate techniques for the correct documentation of RV pacing lead position for routine clinical practice or research purposes.

Cardiac adaptation in acute hypertensive pulmonary edema.

The aim of this study was to evaluate the role of left ventricular (LV) dysfunction (global and regional, systolic and diastolic) acute dyssynchrony, ischemic mitral regurgitation (MR), and afterload changes in acute hypertensive pulmonary edema (AHPE). Forty-four consecutive patients were evaluated by comprehensive echocardiography during clinical and radiologic pulmonary edema (63 ± 29 minutes after first dose of treatment) and after 48 to 92 hours. Twenty age- and gender-matched asymptomatic hypertensive and diabetic subjects served as controls. AHPE was associated with increased afterload (estimated arterial elastance 3.0 vs 2.3 mm Hg/ml, p = 0.024) and subsequent decreased longitudinal LV systolic function (mean strain of 6 basal segments -11.0% vs -15.4%; p = 0.015) compared to the stable follow-up state. However, global LV systolic function was maintained (estimated ventricular elastance 1.7 vs 1.6 mm Hg/ml, stroke work 76.7 vs 84.5 cJ, ejection fraction 0.33 vs 0.37, all nonsignificant). Except for diastolic filling time (ratio to cardiac cycle 0.41 vs 0.49, p <0.001), other indexes of diastolic function, dyssynchrony, and MR severity were similar between evaluations. Patients with AHPE had worse ventricular-arterial coupling, systolic function, estimated diastolic stiffness, and filling pressures compared to asymptomatic controls, suggesting a decreased capacity to adapt to changes in loading. In conclusion, acute alterations of systolic and diastolic LV function, myocardial synchrony, and ischemic MR are unlikely mechanisms of AHPE. Rather, AHPE is likely to develop in patients with decreased systolic and diastolic capacity to adapt to acute changes in loading.