P ulmonary hypertension (PH) is confirmed by the presence of elevated mean pulmonary arterial pressure (mPAP). The sixth World Symposium revised PH definition recommends a mPAP >20 mmHg on supine right heart catheterization (RHC) during resting conditions. 1 However, mPAP in isolation is not accurate enough to characterise the underlying disease. PH can be caused by various conditions, each with specific management strategies and outcomes, including cardiac output increase, hyperviscosity, pulmonary vascular disease, left-to-right cardiac shunts, and elevation of pulmonary arterial wedge pressure (PAWP) in left heart disease (LHD). 2 PH is hemodynamically classified into pre and postcapillary based on a PAWP threshold value of 15 mmHg (measured at end-expiration) and pulmonary vascular resistance (PVR) of 3 Wood units (WU). Precapillary PH is defined by the concomitant presence of mPAP >20 mmHg, PAWP ≤15 mmHg, and PVR ≥3 WU. Postcapillary PH is classified into two distinct pathophysiological and hemodynamic phenotypes: isolated postcapillary PH (IpcPH, mPAP >20 mmHg, PAWP >15 mmHg, PVR <3 WU) and combined post-and precapillary PH (CpcPH, mPAP >20 mmHg, PAWP >15 mmHg, PVR >3 WU). PH-LHD is the most common form of PH and is often correlated with LHD severity and prognosis. 2 Additional factors can aggravate PH-LHD, including atrial fibrillation, microvascular dysfunction, chronic congestion, pulmonary disease, and right ventricular dysfunction. The CpcPH phenotype-occurring in approximately 13% of PH-LHD patients-features profound exercise intolerance, impaired right heart-pulmonary circulation coupling reserve, heightened ventricular interdependence, and greater increase in extra-vascular lung water during exercise than IpcPH, and portends poor prognosis. 3,4 However, while IpcPH is unfavourable for pulmonary arterial hypertension-targeted drug therapies, preliminary data suggested CpcPH may be responsive. 1 Determinants and