Residual pulmonary hypertension after pulmonary thromboendarterectomy: incidence, pathogenesis and therapeutic options

Abstract

Pulmonary endarterectomy (PEA) remains the gold standard to treat and potentially cure chronic thromboembolic pulmonary hypertension (CTEPH), despite advances in medical and interventional management of CTEPH in the last ten years (1). There is no clear definition of a successful PEA (2). The outcomes after PEA are multifaceted, and should take the different dimensions of the disease into account: besides procedure survival, should the success of PEA be evaluated according to clearance of pulmonary vessels, hemodynamic evolution or symptom improvement? This question is unsolved and the correlation between these endpoints is quite loose. Indeed, a surgeon may achieve a significant flow restoration without reaching a normalization of hemodynamics, especially if pulmonary microvascular disease (PMD) is present. Conversely, an uncompleted revascularization may lead to dramatic clinical improvement, particularly if the dead space ventilation can be improved. Some patients may also present with a significant improvement in hemodynamics with persistence of substantial perfusion defects. However, due to the difficulty and lack of standardization for evaluation of vascular obstruction and the subjectivity and challenge to quantitatively assess clinical improvement, achievement of normal or nearly normal hemodynamics [mean pulmonary artery pressure (mPAP) and/or pulmonary vascular resistance (PVR)] has been pragmatically considered as the best hallmark for PEA success. This point of view has led to present PEA as a potentially curative treatment for CTEPH and the concept of residual pulmonary hypertension (PH) after PEA