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Pulmonary hypertension and the right and left ventricles

Session presentations

  • Pulmonary vascular remodelling: causes, mechanisms and consequences. Presented by R T Schermuly (Giessen, DE) Congres 365
  • Right ventricle in chronic heart failure. Presented by C F Opitz (Berlin, DE) Congres 365
  • Left ventricle in pulmonary hypertension. Presented by R N Naeije (Brussels, BE) Congres 365
  • Pulmonary hypertension in heart failure with preserved ejection fraction. Presented by M Guazzi (San Donato Milanese, IT) Congres 365


This symposium is a joint session of The ESC and the European Respiratory society (ERS). ERS was represented by Marc Humbert from France as chair person and two speakers R.T Schermuly and R.N Naeije.

 
The first presentation of the session, entitled: pulmonary vascular remodeling: causes mechanisms and consequences was given by Dr Ralf Schermuly from Giessen , Germany. He showed that the remodeling affects all layers of the pulmonary vessels and not only the endothelium with changes in the intima, media and adventitia. This structural remodeling leads to an increase in pulmonary vascular resistance (PVR). The causes include an imbalance between vasodilators and vasoconstrictors, abnormal proliferation, reduced apoptosis, abnormal migration, metabolism changes of the cells and inflammation. The consequences over time are a decline in right ventricular function, increase in PVR and decrease in cardiac output. He showed that right ventricular function has prognostic value and therapies aiming at improving or stabilizing right ventricular function are required.

The second presentation entitled: right ventricle in chronic heart failure (CHF) given by Dr Christian Opitz  from Berlin, Germany discussed the importance of RV function in CHF showing that RV ejection fraction is a predictor of mortality in this setting. He stressed the importance of ventricular interactions in CHF. The assessment of RV function should be part of the diagnostic work up in CHF. He concluded that there is an urgent need for studies assessing the role of targeted therapies in CHF pulmonary hypertension.

Robert Naeije from Brussels, Belgium in the third presentation entitled left ventricle in pulmonary hypertension explained that pulmonary hypertension can be a cause of LV failure. This is in relation to ventricular interdependence including systolic and diastolic interactions, but also that changes in inflammatory markers are expressed in both ventricles in experimental models. He also mentioned that asynchrony is a new aspect that requires further evaluation. This has important clinical implications when treating pulmonary hypertension.

Finally, Marco Guazzi from Milan, Italy in a presentation entitled pulmonary hypertension in heart failure with preserved ejection fraction discussed a very important topic in the field of pulmonary hypertension namely patients with increased pulmonary arterial pressure due to diastolic dysfunction of the left ventricle.  He presented the diagnostic work up developed at the last world congress on pulmonary hypertension. The main part of the presentation was dedicated to potential therapies. He stressed the fact that background therapies for LV dysfunction should be first used. The role of targeted therapies is currently being evaluated. He reminded us that endothelin receptor antagonists did not show benefit in heart failure with decreased function and that the nitric oxide pathway may be more interesting in HF patients. He presented results from his center using sildenafil and mentioned the ongoing RELAX trial assessing the effect of PDE5 inhibition in this setting, whose results should be available soon.

In conclusion, this session emphasized the role of the right ventricle in pulmonary hypertension as well as the importance of the ventricular interdependence and the continuum of the right ventricle – pulmonary vascular-bed-post pulmonary vascular bed and left heart.

References


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Pulmonary hypertension and the right and left ventricles

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.