The 2nd International Conference on Drug Discovery & Therapy: Dubai, February 1 - 4, 2010


Invited Speaker

New Concepts in the Invasive Evaluation of Remodelling of the Right Ventricle and Pulmonary Vasculature in Pulmonary Arterial Hypertension: Future Targets for Drug Evaluation
Enric Domingo
Spain

Pulmonary arterial hypertension is a rare fatal disease defined as a sustained elevation of pulmonary arterial pressure to more than 25 mmHg at rest, with a mean pulmonary-capillary wedge pressure and left ventricular end-diastolic pressure of less than 15 mmHg at rest. Histopathology of PAH is founded on structural modifications on the vascular wall of small pulmonary arteries characterized by thickening of all its layers . These changes, named as vascular remodelling, include vascular proliferation, fibrosis, and vessel obstruction. In clinical practice the diagnosis of Pulmonary Hypertension relies on measurements of pulmonary vascular pressure and cardiac output, and calculation of pulmonary vascular resistances. Direct evaluation of pulmonary vascular structure is not routinely performed in pulmonary hypertension since current imaging techniques are limited and since little is known about the relationship between structural changes and functional characteristics of the pulmonary vasculature. Intravascular ultrasound studies in patients with pulmonary hypertension have shown a thicker middle layer, increased wall-thickness ratio and diminished pulsatility than in control patients. Optical Coherence Tomography , a new high resolution imaging modality that has proven its superiority over IVUS for the detection and characterization of coronary atherosclerotic plaque composition, may potentially be a useful technique for the in vivo study of the pulmonary arterial wall. In addition the analysis of the pressure-volume curves of the right ventricle will help to better evaluate the effect of drugs on the intrinsic load independent contractility of this ventricle. This would allow the in vivo study of right ventricular and pulmonary artery remodelling in PAH.
















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