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Abstract: Purpose: The aim of this study was to investigate the use of the electrocardiogram-derived ventricular gradient, projected on the x-axis (VGx), for detection of pulmonary hypertension (PH) and for prediction of all-cause mortality in PH patients. Methods: In patients referred for PH screening (n = 216), the VGx was calculated semiautomatically from the electrocardiogram and was defined as abnormal when less than 24 mV·ms. The VGx of PH patients was compared with the VGx of patients without PH. The association between a reduced VGx and mortality was investigated in PH patients. Results: Patients with PH (n = 117) had a significantly reduced VGx: 14 ± 27 vs 45 ± 23 mV·ms, P < .001. Furthermore, a severely reduced VGx (<0 mV·ms) was associated with increased mortality in PH patients: hazard ratio, 1.025 (95% confidence interval, 1.006-1.045; P = .012) per mV·ms VGx decrease. Conclusion: Reduced VGx is associated with the presence of PH and, more importantly, within PH patients, a severely reduced VGx predicts mortality. [Copyright &y& Elsevier]

Heart rate (HR) at rest is an important marker of prognosis in heart failure, but has not been addressed in pulmonary arterial hypertension (PAH). To determine the prognostic value of HR at rest in patients with PAH, we retrospectively analyzed 140 consecutive patients with idiopathic PAH. Electrocardiogram (ECG)-derived HR at rest was evaluated as a potential predictor of adverse prognosis (death or lung transplantation), in addition to World Health Organization functional class, 6-minute walk distance, and hemodynamics before and approximately 1 year and 2 years after initiation of PAH treatment. During follow-up, 49 patients (35%) died, and 5 patients (4%) underwent lung transplantation. Before treatment initiation and after 1 year and 2 years of treatment, respectively, a higher HR at rest was an independent predictor of adverse prognosis (hazard ratios per 10-beats/min increase 1.76, 95% confidence interval 1.42 to 2.18, 2.31, 95% confidence interval 1.58 to 3.38, 2.1, 95% confidence interval 1.39 to 3.19, respectively, p <0.001 for all). Change in HR between the first and last ECG also independently predicted prognosis (hazard ratio per 1-beat/min increase 1.03, 95% confidence interval 1.01 to 1.06). In conclusion, a higher HR at rest and an important increase in HR at rest during follow-up signify a considerable risk of death in patients with PAH. ECG-derived HR at rest is an important marker of prognosis and should be assessed before and at frequent intervals after initiation of treatment for PAH. [Copyright &y& Elsevier]

Abstract: Background and purpose: Normal limits of the spatial QRS-T angle and spatial ventricular gradient (SVG) are only available from Frank vectorcardiograms (VCGs) of male subjects. We determined normal limits for these variables derived from standard 12-lead electrocardiograms (ECGs) of 660 male and female students aged 18 to 29 years. Methods: A computer algorithm was used that constructed approximated VCG leads by inverse Dower matrix transformation of the 12-lead ECG and subsequently calculated the spatial QRS-T angle, SVG magnitude, and orientation. Results: In female subjects, the QRS-T angle was more acute (females, 66° ± 23°; normal, 20°-116°; males, 80° ± 24°; normal, 30°-130°; P < .001), and the SVG magnitude was smaller (females, 81 ± 23 mV·ms; normal, 39-143 mV·ms; males, 110 ± 29 mV·ms; normal, 59-187 mV·ms; P < .001) than in male subjects. The male SVG magnitude in our study was larger than that computed in Frank VCGs (79 ± 28 mV·ms; P < .001). Conclusions: The spatial QRS-T angle and SVG depend strongly on sex. Furthermore, normal limits of SVG derived from Frank VCGs differ markedly from those derived from VCGs synthesized from the standard ECG. As nowadays, VCGs are usually synthesized from the 12-lead ECG; normal limits derived from the standard ECG should preferably be used. [Copyright &y& Elsevier]

Abstract: Objective: To assess the effect of pulmonary valve replacement (PVR) on the repolarization of patients with tetralogy of Fallot. Background: Pulmonary valve regurgitation may cause right ventricular failure in adult patients with Fallot''s tetralogy. In these patients, prolonged depolarization and disturbed repolarization are associated with ventricular arrhythmias and sudden cardiac death. Methods: Thirty Fallot patients (age 32±9 years, 19 male) eligible for PVR were studied with cardiac magnetic resonance imaging (CMR) before and 6 months after PVR. Electrocardiograms obtained during initial and follow-up CMR were analyzed and occurrence of ventricular arrhythmias was studied. Results: Right ventricular end-diastolic volume (RV EDV) decreased from 322±87 to 215±57 ml after PVR (P <0.0001). The spatial QRS-T angle normalized from 117±34 to 100±35°, P =0.0004 (normal angle <105°). QT dispersion and T-wave complexity did not change significantly. T-wave amplitude decreased from 376±121 to 329±100 μV (P =0.01). T-wave area decreased from 43±15 to 38±13 μV s (P =0.02). Decreases in T-wave amplitude and area were most prominent in the right precordial leads overlying the RV. Three patients had sustained ventricular arrhythmias and one patient died suddenly. These patients had a QRS duration >160 ms. No severe ventricular arrhythmias were found in patients with a RV EDV <220 ml, QRS-T angle <100°, QT dispersion <60 ms or T-wave complexity <0.30. Conclusion: Normal repolarization indices may be associated with the absence of severe ventricular arrhythmias. PVR in Fallot patients with dilated right ventricles has a beneficial effect on electrocardiographic indices of repolarization heterogeneity. [Copyright &y& Elsevier]

Background: Predicting changes in right ventricular (RV) size and function after pulmonary valve replacement (PVR) is important for timely reintervention in adult tetralogy of Fallot patients. Methods: We analyzed the influence of pulmonary regurgitation severity and RV size and function before PVR on the outcome of RV size and function after PVR in 27 adult Fallot patients who had cardiac magnetic resonance imaging before and after PVR. RV dimensions were indexed for body surface area. Results: Pulmonary regurgitation (48% ± 11% of RV stroke volume) was not related to RV dimensions and function before PVR. Moreover, severity of pulmonary regurgitation did not influence changes in RV dimensions after PVR. The indexed RV end-systolic volume before PVR (mean, 98 mL/m2; range, 52 to 235 mL/m2) best predicted the indexed RV end-systolic volume after PVR (mean, 59 mL/m2; range, 24 to 132 mL/m2, r = 0.78, p < 0.001) and the indexed RV end-diastolic volume after PVR (mean, 107 mL/m2; range, 70 to 170 mL/m2, r = 0.73, p < 0.001). Baseline RV ejection fraction corrected for valvular insufficiencies and shunting (21% ± 7%) best predicted the RV ejection fraction after PVR (43% ± 10%, r = 0.77, p < 0.001). Conclusions: Timing of PVR should be based on indexed RV end-systolic volume and corrected RV ejection fraction rather than on severity of pulmonary regurgitation. [Copyright &y& Elsevier]