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.

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.

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.