Pharmacological impact on right ventricular remodelling in pulmonary arterial hypertension

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Abstract
The pathophysiologic mechanisms of pulmonary arterial hypertension (PAH) are initiated by the progressive obstructive changes of the pulmonary resistance vessels which lead to the increase of the afterload of the right ventricle (RV) that responds with functional and structural adaptations. The RV remodelling compensates for a variable period of time but ultimately may fail leading to heart failure and death. The depression of myocardial contractility seems to be one of the primary events in the progression of heart failure in a chronically overloaded RV. However, afterload mismatch remains the leading determinant of heart failure in patients with both PAH and chronic thrombo-embolic pulmonary hypertension. Different therapies induce a variable degree of reverse remodelling on the heart changes typical of PAH. The extent of this effect is strictly related to the reduction of RV afterload. The best results are observed in patients who underwent lung transplantation, pulmonary endoarterectomy and in vasoreactive subjects responders to chronic treatment with calcium channel blocking agents. The RV reverse remodelling effects of the new targeted therapies in non-vasoreactive PAH patients appear to be only mild to moderate.