Pulmonary hypertension (PH) is a common complication of numerous diseases, including left-sided heart diseases and chronic lung diseases and/or hypoxia, where PH is associated with exercise limitation and a worse prognosis. Other forms of PH include pulmonary arterial hypertension (PAH), chronic thromboembolic PH (CTEPH), and PH with unclear multifactorial mechanisms. Over the past decade, it has been documented that systolic pulmonary artery pressure (sPAP) may help estimate mean pulmonary artery pressure (mPAP) in adults with high accuracy and reasonably good precision (mPAP = 0.61 sPAP + 2 mm Hg). This strong linear relationship between sPAP and mPAP was unexpected from a classic physiologic point of view. Consistent results have been obtained from independent teams using either high-fidelity micromanometer-tipped PA catheters or fluid-filled catheters. Overall, the strong link between sPAP and mPAP has been documented over a wide range of PAPs, heart rate, cardiac output, wedge pressure, and causes of PH, during changes in posture and activity, and irrespective of patient’s sex, age, and BMI. A review of available invasive data confirms that patients with CTEPH and idiopathic PAH matched for their mPAP exhibit essentially similar sPAP. Pressure redundancy may be explained by the dependence of PA compliance upon mPAP. The 25 mm Hg threshold used to define PH accurately corresponds to an sPAP of 38 mm Hg. Although the limits of the echocardiographic estimation of sPAP are widely documented, results from invasive studies may furnish an evidence-based sPAP-derived mPAP value, potentially useful in the multiparameter echocardiographic approach currently used to diagnose and follow patients with PH.