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The study aimed to assess whether the 12-lead ECG-derived ventricular gradient, a vectorial representation of ventricular action potential duration heterogeneity directed toward the area of shortest action potential duration, can improve ECG diagnosis of chronic right ventricular (RV) pressure load. ECGs from 72 pulmonary arterial hypertension patients recorded 1 with R > 0.5 mV in V1, and QRS axis >90[degrees]) had a sensitivity of 89% and a specificity of 93% for presence of chronic RV pressure load. However, the ventricular gradient not only had a higher diagnostic accuracy for chronic RV pressure load by receiver operating characteristic analysis [areas under the curve (AUC) = 0.993, SE 0.004 vs. AUC = 0.945, SE 0.021, P < 0.05], but also discriminated between mild-to-moderate and severe RV pressure load. CMR identified an inverse relation between the ventricular gradient and RV mass, and a trend toward a similar relation with RV volume. In conclusion, chronically increased RV pressure load is electrocardiographically reflected by an altered ventricular gradient associated with RV remodeling-related changes in ventricular action potential duration heterogeneity. The use of the ventricular gradient allows ECG detection of even mildly increased RV pressure load. hypertension; pulmonary; right ventricular hypertrophy; diagnosis; ventricular gradient; electrocardiogram

The study aim was to assess three-dimensional electrocardiogram (ECG) changes during development of pulmonary arterial hypertension (PAH). PAH was induced in male Wistar rats (n = 23) using monocrotaline (MCT; 40 mg/kg sc). Untreated healthy rats served as controls (n = 5). ECGs were recorded with an orthogonal three-lead system on days O, 14, and 25 and analyzed with dedicated computer software. In addition, left ventricular (LV)-to-right ventricular (RV) fractional shortening ratio was determined using echocardiography. Invasively measured RV systolic pressure was 49 (SD 10) mmHg on day 14 and 64 (SD 10) mmHg on day 25 vs. 25 (SD 2) mmHg in controls (both P < 0.001). Baseline ECGs of controls and MCT rats were similar, and ECGs of controls did not change over time. In MCT rats, ECG changes were already present on day 14 but more explicit on day 25: increased RV electromotive forces decreased mean QRS-vector magnitude and changed QRS-axis orientation. Important changes in action potential duration distribution and repolarization sequence were reflected by a decreased spatial ventricular gradient magnitude and increased QRS-T spatial angle. On day 25, LV-to-RV fractional shortening ratio was increased, and RV hypertrophy was found, but not on day 14. In conclusion, developing PAH is characterized by early ECG changes preceding RV hypertrophy, whereas severe PAH is marked by profound ECG changes associated with anatomical and functional changes in the RV. Three-dimensional ECG analysis appears to be very sensitive to early changes in RV afterload. fight ventricular hypertrophy; monocrotaline; electrocardiogram

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]

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]

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]

Vitamin K antagonists are advised in pulmonary arterial hypertension patients despite a lack of safety data. We reviewed major bleeding in three classes of pulmonary hypertension patients, all receiving vitamin K antagonists. Bleeding event rates were 5.4 per 100 patient-years for patients with idiopathic pulmonary arterial hypertension, 19 per 100 patient-years for connective tissue disease related pulmonary arterial hypertension patients and 2.4 per 100 patient-years for chronic thromboembolic pulmonary hypertension patients. Life tables analysis showed that event-free survival was worse in patients with connective tissue disease related pulmonary hypertension than in patients with idiopathic pulmonary arterial hypertension (Wilcoxon=12.8; p<0.001), and patients with chronic thromboembolic pulmonary hypertension (Wilcoxon=23.2; p<0.001). Patients with idiopathic pulmonary arterial hypertension suffered more events than patients with chronic thromboembolic pulmonary hypertension (Wilcoxon=7.2; p<0.01). Major bleeding was independent of age, sex, target international normalised ratio (INR) range, documented INR, vitamin K antagonist type, or right atrial pressure, but was associated with use of prostacyclin analogues. Major bleeding risk during vitamin K antagonist therapy differs among groups of patients with pulmonary hypertension. Further research regarding optimal anticoagulant therapy is needed, as well as risk-benefit analyses for pulmonary hypertension patients with a higher bleeding propensity.

A 62-year-old man with a history of significant alcohol consumption presented with atypical neurological symptoms. Bacterial meningitis, caused by Streptococcus pneumoniae, was diagnosed with a 24-hour delay. Despite antibiotic treatment, the patient developed heart failure and multiple organ failure. He also had endocarditis with insufficient mitral and aortic valves. Subsequently, we found signs of a pulmonary infection. Because of an unsustainable haemodynamic situation, double heart valve replacement was considered necessary, despite the extremely high surgical risk and the extracardial infection foci showed by leukocyte scintigraphy. The patient died shortly after surgery. The triad of meningitis, pneumonia and endocarditis caused by Streptococcus pneumoniae is called the Austrian syndrome. This syndrome is rare and often has a serious course. It is strongly associated with asplenia, functional asplenia or hyposplenism, as occurs with alcohol abuse. Early recognition and a combination of antibiotic and surgical treatment is essential.