Foreword: right ventricular function and pulmonary hypertension
1 Heart Failure and Pulmonary Hypertension Unit, Hospital Universitario 12 de Octubre, Madrid, Spain
2 Department of Chest Medicine, Institute of Tuberculosis and Lung Diseases, Warsaw, Poland
* Corresponding author. E-mail address: mangomezs{at}telefonica.net
The last decade has been a period of great advances in the field of pulmonary arterial hypertension (PAH). Many randomized clinical trials have assessed the efficacy of emerging medications developed to modify the fatal course of this disease. All those clinical investigation has been devoted to improve the exercise tolerance by acting on the pulmonary arterioles.
Although PAH is a disease of pulmonary vessels, it predominantly affects the right ventricle (RV). Indeed, mortality as well as signs and symptoms of pulmonary hypertension can be explained by RV failure. This is why the prognostic staging of PAH can be done by analysing the morphology and function of the right heart and also why we can expect RV protection and support to be beneficial even if the progression of pulmonary vascular changes cannot be controlled totally.
Before designing and testing the therapeutic interventions that could target the RV function, it seems appropriate to review the existing knowledge on its physiopathology and clinical aspects related to PAH.
In this supplement, Robert Naeije and Sandrine Huez summarize the state-of-the-art concerning physiological concepts about the determinants of RV function in rest and exercise. The exercise stress test for non-invasive diagnosis of pulmonary hypertension may be particularly useful for the detection of early disease. Further studies are needed to confirm the right ventriculo-arterial decoupling.
Jean-Luc Vachiery reviews the importance of exercise echocardiography as an important diagnosis tool in the assessment and management of the disease. New echocardiographic techniques such as tissue-Doppler imaging, strain, and strain-rate analysis may provide further insights in the understanding of RV dysfunction.
Neurohormonal activation and sympathetic system stimulation, followed by activation of the renin, angiotensin, and aldosteron system could be considered as important mechanisms in the pathophysiology and consequently as management targets in congestive heart failure. However, the evidence related to the presence and clinical significance of neurohormonal activation in isolated RV failure is very limited. Adam Torbicki and Marcin Kurzyna review the existing evidence, current recommendations, and potential future directions in this interesting area.
Effective targeting of the RV requires efficient and reliable follow-up markers. According to Anna Fijalkowska from the same team, humoral biomarkers such as brain natriuretic peptide, NT-proBNP, and troponin originating from RV cardiac myocytes may be considered useful for the assessment and monitoring of RV dysfunction.
Gerhard-Paul Diller gives us an overview of the pathophysiology of Eisenmenger syndrome and discusses the potential explanations for the remarkable resilience of the RV in this setting.
Gerry Coghlan offers a practical review of current and emerging clinical tools useful to evaluate RV function.
Since RV failure in pulmonary hypertension is the result of the complex interaction between geometry, structure, function, perfusion, and metabolism, MRI and nuclear techniques are particularly promising to study RV function in pulmonary hypertension. All these aspects are discussed by Anton Vonk Noordegraaf.
Right ventricular function is a main determinant of long-term prognosis. Irene Lang reviews the therapeutic goals to preserve or ameliorate RV function, including the present surgical strategies such as pulmonary endarterectomy, lung transplantation, closure of shunt lesions, and explore future possibilities such as resynchronization therapy. Nazzareno Galié summarizes the different therapies that can reverse the RV remodelling.
Stefan Janssens focuses particularly on the underlying mechanisms that govern the transition from a pressure-overloaded hypertrophic, normocontractile RV to the dysfunctional and failing RV in various pathological conditions. He reviews the concepts of RV remodelling, at a cellular level trying to understand the mechanisms. They also stress the need for translational research, specifically targeted towards unravelling key molecular events that determine RV remodelling.
There is scanty information about the cell and molecular changes occurring in the compromised RV. Sheila G. Haworth emphasizes the need to understand the cellular and biochemical response to an elevated pulmonary vascular resistance if we are to develop therapeutic strategies to improve RV function.
The overall message from this Workshop and from the articles in this supplement is to consider all the important aspects of RV function in PAH. The ability to provide better ways of applying those scientific messages should help advance our knowledge of this intriguing and devastating disease.
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 Top Acknowledgements |
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This supplement is based on the Workshop titled, ‘Right Ventricular Function and Pulmonary Hypertension’, held on 2 September 2006, in Barcelona. Speakers at the meeting covered a variety of topics to the diagnosis and management of the RV failure in PAH. The meeting was an official activity of the Pulmonary Circulation and Right Ventricular Function Working Group from ESC. The Workshop and the publication were supported by an unrestricted educational grant from Bayer ScheringPharmaAG.
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