Pulmonary hypertension is an “umbrella term” used for a spectrum of entities resulting in an elevation of the pulmonary arterial pressure. Clinical symptoms include dyspnea and fatigue which in the absence of adequate therapeutic intervention may lead to progressive right heart failure and death. The pathogenesis of pulmonary hypertension is characterized by three major processes including vasoconstriction, vascular remodeling and microthrombotic events. In addition accumulating evidence point to a cytokine driven inflammatory process as a major contributor to the development of pulmonary hypertension.This review summarizes the latest clinical and experimental developments in inflammation associated with pulmonary hypertension with special focus on Interleukin-6, and its role in vascular remodeling in pulmonary hypertension.

Abstract. We present a fully automatic segmentation algorithm for the whole heart (four chambers, left ventricular myocardium and trunks of the aorta, the pulmonary artery and the pulmonary veins) in cardiac MR image volumes with nearly isotropic voxel resolution, based on shape-constrained deformable models. After automatic model initialization and reorientation to the cardiac axes, we apply a multi-stage adaptation scheme with progressively increasing degrees of freedom. Particular attention is paid to the calibration of the MR image intensities. Detailed evaluation results for the various anatomical heart regions are presented on a database of 42 patients. On calibrated images, we obtain an average segmentation error of 0.76mm.

Furian and colleagues report on the results of two randomized controlled trials testing the use of acetazolamide to prevent the adverse effects of altitude on healthy older persons and in people with COPD. They find that acetazolamide decreased the incidence of altitude related adverse health events (primarily hypoxemia) in both populations with no evidence of adverse events.

As a conclusion, the reliability of the CFD simulations was well confirmed. Besides, it was shown that the accuracy of CFD simulations was closely related to the input BCs.

In patients with PAH/CTEPH, very short-term exposure to moderate hypoxia similar to 2600 m altitude or during commercial air travel did not deteriorate hemodynamics. These results encourage studying the response of PAH/CTEPH during daytrips to the mountain or air travel.