The 2026 annual meeting of the European Society of Cardiology (ESC) ran from August 28 through August 31 in Munich, Germany. The ESC Congress 2026 brought together cardiologists from around the world for the four-day experience. 

Today, we are showcasing some of the abstracts presented at the conference focusing on primary/essential hypertension. Some descriptions and conclusions were edited for clarity and brevity. To view all the abstracts presented at the 2026 ESC Congress, view the event’s abstract archive. 

Pulmonary Hypertension Abstracts from ESC Congress 2026

Clinical and Morphological Profiles in Different Hemodynamic Types of Pulmonary Hypertension in Patients with Mitral Valve Disease and Predictors of Persistent Pulmonary Hypertension Post-Surgery

  • Description: To identify the main differences in patients undergoing surgical correction of acquired mitral valve disease, depending on the type of pulmonary hypertension before surgery; to identify factors associated with the persistent pulmonary hypertension and its type one year after surgical correction of mitral valve disease.
  • Conclusion: Patients with mitral valve disease and combined post/precapillary pulmonary hypertension are characterized by more pronounced disturbances in right ventricle-pulmonary artery coupling, elevated levels of myocardial strain markers, severe changes in pulmonary circulation hemodynamics with arteriolization of venules and a higher prevalence of pandemic arterial thrombosis. For the first time, potentially modifiable factors have been identified as making the greatest impact on the pulmonary hypertension dynamics one year after surgery.

AA–LTB4–ROS Axis Drives Macrophage Extracellular Trap Formation and Endothelial Injury in Smoking‑Induced Pulmonary Hypertension

  • Description: Smoking-associated pulmonary hypertension is characterized by chronic pulmonary vascular inflammation, endothelial dysfunction, and vascular remodeling. Growing evidence suggests that macrophage dysregulation and lipid metabolic signaling, particularly arachidonic acid–derived leukotriene B4, play a critical role in driving endothelial injury. Despite this, the mechanistic link between cigarette smoke exposure, macrophage extracellular trap formation, and subsequent endothelial dysfunction remains poorly defined.
  • Conclusion: Cigarette smoke induces arachidonic acid metabolic remodeling in macrophages, activating an LTB4–NOX2–ROS–PAD2–MET axis that promotes endothelial injury and pulmonary vascular remodeling. Targeting macrophage lipid metabolism and macrophage extracellular trap formation may provide a promising therapeutic avenue for smoking-associated pulmonary hypertension.

Post-Capillary Pulmonary Hypertension: Impact of the Current ESC/ERS Updated PVR Cutoff on Pulmonary Vascular Disease and RV Arterial Coupling

  • Description: Robust data demonstrate a continuum of clinical risk associated with pulmonary vascular resistance in patients with elevated mean pulmonary arterial pressure beyond the pulmonary arterial occlusion pressure, leading to an update and revision of the pulmonary vascular resistance cutoff to 2 WU.
  • Conclusion: Pulmonary vascular resistance cutoff >2 WU increases the prevalence of the precapillary component of pulmonary hypertension related to left heart disease. This is linked to pulmonary vascular disease severity and the development of RVA uncoupling. A pulmonary vascular resistance >5 WU was associated with prognostic cutoff values ​​in the alpha and pulmonary arterial capacitance, leading to right ventricular-arterial coupling uncoupling. A more detailed multiparametric assessment of the RV-PA functional unit may be important for phenotyping and tailoring specific vasodilator treatment to patients with pulmonary hypertension related to left heart disease.

Prognostic Value of Composite Hemodynamic Indices in Congenital Heart Disease-Associated Pulmonary Hypertension: Insights From a National Multicenter Prospective Registry Study

  • Description: In congenital heart disease-associated pulmonary arterial hypertension, right heart catheterisation is essential, but conventional haemodynamic indices from the ESC simplified four-strata model have limited prognostic value. Whether composite indices—PVRI, effective arterial elastance (Ea), pulmonary arterial compliance (PAC), and cardiac power output (CPO)—confer incremental value remains unknown.
  • Conclusion: Composite RHC-derived haemodynamic indices (PVRI, Ea, PAC, and CPO) independently predict all-cause mortality and meaningfully improve risk reclassification beyond the ESC simplified four-strata risk model in congenital heart disease-associated pulmonary arterial hypertension, whereas conventional indices provide limited incremental value. The identification of a haemodynamic–nutritional coupling axis opens a mechanistically informed avenue for integrated haemodynamic and nutritional intervention strategies in congenital heart disease-associated pulmonary arterial hypertension. 

Crucial Role of TRPV2 in the Development of Hypoxia-Induced Pulmonary Hypertension

  • Description: Sustained hypoxia induces pulmonary vasoconstriction, leading to adverse pulmonary vascular remodeling and pulmonary hypertension. However, the precise mechanism by which vasoconstriction leads to vascular remodeling remains to be elucidated.
  • Conclusion: Transient receptor potential cation channel subfamily V member 2 plays a crucial role in the development of hypoxia-induced PH along with an inappropriate increase of pulmonary artery smooth muscle cells. The results indicate that transient receptor potential cation channel subfamily V member 2 is a novel therapeutic target for treatment of hypoxia-induced pulmonary hypertension.

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