Right ventricle’s road to recovery: remodelling after chronic thromboembolic pulmonary hypertension intervention
Right heart failure is the most common cause of mortality in patients with pulmonary arterial hypertension.1 This includes chronic thromboembolic pulmonary hypertension (CTEPH), which through obstruction of the pulmonary arteries increases afterload on the right ventricle (RV), ultimately resulting in RV failure. Histopathologically, it is also associated with microvascular changes, with smooth muscle hypertrophy, and intimal fibrosis, which cause stiffening, reduced compliance and increased resistance, placing increased afterload on the RV.2 Current therapeutic options for CTEPH include medical therapy, pulmonary endarterectomy (PEA), and balloon pulmonary angioplasty (BPA), and a combination of these therapies is often applied to effectively target both the anatomical larger vessel, as well as the microvascular components of the disease. PEA is the definitive management in surgical candidates with proximal, and therefore surgically amenable disease, and although highly invasive, carr
