Although in controls, RCA flow is similar in systole and diastole, in PH there is systolic flow impediment, which is proportional to RV pressure and mass. In patients with severe RV hypertrophy total mean flow is reduced.

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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 0, 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.

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 (Wilcoxon512.8; p,0.001), and patients with chronic thromboembolic pulmonary hypertension (Wilcoxon523.2; p,0.001). Patients with idiopathic pulmonary arterial hypertension suffered more events than patients with chronic thromboembolic pulmonary hypertension (Wilcoxon57.2; 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.

Henkens IR, Mouchaers KT, Vonk-Noordegraaf A, BoonstraA, Swenne CA, Maan AC, Man S, Twisk JW, van der Wall EE, Schalij MJ, Vliegen HW. Improved ECG detection of presence and severity of right ventricular pressure load validated with cardiac magnetic resonance imaging. 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 Ͻ30 days before onset of therapy were compared with ECGs from matched healthy control subjects (n ϭ 144). Conventional ECG criteria for increased RV pressure load were compared with the ventricular gradient. In 38 patients a cardiac magnetic resonance (CMR) study had been performed within 24 h of the ECG. By multivariable analysis, combined use of conventional ECG parameters (rsrЈ or rsRЈ in V1, R/S Ͼ 1 with R Ͼ 0.5 mV in V1, and QRS axis Ͼ90°) 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) ϭ 0.993, SE 0.004 vs. AUC ϭ 0.945, SE 0.021, P Ͻ 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 MODERATELY INCREASED CHRONIC right ventricular (RV) pressure load is hard to detect noninvasively because of the position and mass of the RV (7, 13, 23). Conventional 12-lead ECG parameters of increased RV pressure load lack diagnostic accuracy, precluding their use for screening purposes (3,16,26,31,34), partly because the chest electrodes predominantly overlie the left ventricle (LV) and partly because the 12-lead ECG renders 12 separate one-dimensional projections of the three-dimensional (3-D) cardiac vector in time (25), but not in the least because the RV mass is relatively low compared with the LV mass. This scalar ECG representation hampers the direct appreciation of the ECG as a recording of a 3-D process. However, a synthesized vectorcardiogram can be easily derived mathematically from the ECG, allowing the calculation of electrocardiographic 3-D parameters. One of these parameters is the ventricular gradient (VG), a 3-D measure of ventricular action potential duration (APD) heterogene...