[Etiology and physiopathology of pulmonary artery hypertensions (PAHT)]

Pulmonary hypertension results from many causes: left cardiac failure, increased pulmonary blood flow, proximal vascular obstruction, decrease of the distal vascular bed (by loss of vessels, narrowing of their luminal diameter, or endoluminal obstruction). A part from passive hemodynamic responses, active processes contribute to pulmonary hypertension by vasomotricity and remodeling of the vascular wall. The biopathology of vasomotor mediators, as well as of endothelial and smooth muscle cell interactions just begins to be understood.