Right ventricular failure (RVF) is often caused by increased afterload and disrupted coupling between the right ventricle (RV) and the pulmonary arteries (PAs). After a phase of adaptive hypertrophy, pressure-overloaded RVs evolve towards maladaptive hypertrophy and finally ventricular dilatation, with reduced stroke volume and systemic congestion. In this article, we review the concept of RV-PA coupling, which depicts the interaction between RV contractility and afterload, as well as the invasive and non-invasive techniques for its assessment. The current principles of RVF management based on pathophysiology and underlying etiology are subsequently discussed. Treatment strategies remain a challenge and range from fluid management and afterload reduction in moderate RVF to vasopressor therapy, inotropic support and, occasionally, mechanical circulatory support in severe RVF.

Risk stratification in pulmonary arterial hypertension (PAH) is crucial in assessing patient prognosis. It serves a prominent role in everyday patient care and can be determined using several validated risk assessment scores worldwide. The recently published 2022 European Society of Cardiology (ESC)/European Respiratory Society (ERS) guidelines underline the importance of risk stratification not only at baseline but also during follow-up. Achieving a low-risk status has now become the therapeutic goal, emphasising the importance of personalised therapy. The application of these guidelines is also important in determining the timing for lung transplantation referral. In this review, we summarise the most relevant prognostic factors of PAH as well as the parameters used in PAH risk scores and their evolution in the guidelines over the last decade. Finally, we describe the central role that risk stratification plays in the current guidelines not only in European countries but also in Asian countries.

Background: precapillary pulmonary hypertension (PH, PcPH) is now defined as a mean pulmonary artery pressure (mPAP) > 20 mmHg, a pulmonary artery wedge pressure (PAWP) ≤ 15 mmHg and a pulmonary vascular resistance (PVR) > 2 WU. For PVR calculation, the measurement of cardiac output (CO) is necessary. It is generally measured using thermodilution. However, recent data showed that the agreement with direct Fick method, historically the gold standard, is less than previously reported. We aimed to create a mathematical model that calculated the probability of being classified differently (PcPH or unclassified PH) if CO measured by direct Fick was used instead of thermodilution for any individual patients with a mPAP > 20 mmHg and a PAWP ≤ 15 mmHg. Methods: The model is based on Bland and Altman analysis with a normally distributed difference of cardiac output, fixed 1.96 standard deviation of bias, bias and physiological cardiac output limits. Results: Following a literature review of the studies comparing CO measured with direct Fick and thermodilution, we fixed the 1.96 standard deviation of bias at 2 L/min, bias at 0 L/min and physiological resting CO limits between 1.3 L/min and 10.2 L/min. Conclusions: This model can help the clinician to evaluate the potential benefit of measuring CO using direct Fick during the diagnostic work-up and its utility in confirming or ruling out a diagnosis of PcPH in any given patient with a mPAP > 20 mmHg and a PAWP ≤ 15 mmHg.