Corrigendum to: 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases [Eur Heart Journal (2014) 35, 2873–2926,doi:10.1093/eurheartj/ehu281]. In Table 3, the radiation for MRI is “0” and not “-“. The corrected table is shown below.

Exercise stress tests have been used for the diagnosis of pulmonary hypertension, but with variable protocols and uncertain limits of normal. The pulmonary hemodynamic response to progressively increased workload and during recovery was investigated by Doppler echocardiography in 25 healthy volunteers aged from 19 to 62 yrs (mean 36). Mean pulmonary artery pressure (mPAP) was estimated from the maximum velocity of tricuspid regurgitation. Cardiac output (Q) was calculated from the aortic velocity-time integral. Slopes and extrapolated pressure intercepts of mPAP-Q plots were calculated after Poon's adjustment for individual variability. A pulmonary vascular distensibility index α was calculated from each mPAP-Q plot. mPAP increased from 14 ± 3 to 30 ± 7 mmHg (mean ± SD), and decreased to 19 ± 4 after 5 min recovery. The slope of mPAP-Q was 1.37 ± 0.65 mmHg.min.L-1 with an extrapolated pressure intercept of 8.2 ± 3.6 mmHg and an α of 0.017 ± 0.018 mmHg-1. These results agree with those of previous invasive studies. Multipoint mPAP-Q plots were best described by a linear approximation. We conclude that exercise echocardiography of the pulmonary circulation is feasible and provides realistic resistance and compliance estimations. Measurements during recovery are unreliable because of rapid return to baseline.

The purpose of this study was to clarify whether changes in cardiopulmonary haemodynamics induced by pharmacological therapy correlate with exercise capacity and clinical events in patients with pulmonary arterial hypertension.16 randomised trials including 2353 patients, followed up for 16.4¡10.6 weeks, measuring cardiopulmonary haemodynamics by right heart catheterisation and reporting clinical events were included. Meta-analysis and meta-regression analysis were performed to assess the effects of treatments on clinical events and the relationship between haemodynamic changes (pulmonary artery pressure, pulmonary vascular resistance, cardiac index and right atrial pressure) and clinical events.Treatments significantly reduced all-cause death (OR 0.5, 95% CI 0.3-0.7; p,0.01), hospitalisation for pulmonary arterial hypertension (OR 0.4, 95% CI 0.2-0.7; p,0.01), initiation of rescue therapy (OR 0.3, 95% CI 0.2-0.6; p,0.01) and the composite outcome (OR 0.3, 95% CI 0.3-0.5; p,0.01). No relationship was found between changes of haemodynamic parameters and clinical events, whereas changes of cardiac index and pulmonary vascular resistance significantly correlated with changes in the 6-min walking distance (r50. 64, p50.03; r5 -0.55, p50.04, respectively).In patients with pulmonary arterial hypertension, improvements of cardiopulmonary haemodynamics observed in randomised clinical trials correlate with exercise capacity changes but do not predict clinical events in a short-term follow-up. @ERSpublications In PAH, cardiopulmonary haemodynamic improvements correlate with exercise capacity changes but not with clinical events

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