Is it Necessary to Define New Hemodynamic Indexes of Pulmonary Hypertension?

Rev Esp Cardiol 2003;56(11):1041-2 1041 Idiopathic pulmonary hypertension is a syndrome characterized by dyspnea, fatigue, chest pain, syncope, and an increase in pulmonary vascular resistance with no identifiable cause. In most cases it can course asymptomatically for years, increasing vascular resistance and remodeling the vascular tree. Pulmonary hypertension is often found in other disorders which present the same symptomatology, pathology and response to treatment as the idiopathic form. These disorders are associated with collagen disease, congenital cardiopathy with left-right shunts, anorexigen use or human immunodeficiency virus (HIV) carrier status. Following the Evian Meeting,1 these types of pulmonary hypertension have been grouped, along with the idiopathic form, under the heading of pulmonary artery hypertension (PAH). The conclusions from this meeting were presented recently at the 3rd World Symposium on Pulmonary Hypertension, held in Venice in June 2003. Pulmonary hypertension is diagnosed when mean pulmonary artery pressure is more than 25 mm Hg at rest or higher than 30 mm Hg during exercise. Symptoms appear when mean pulmonary artery pressure exceeds 30–40 mm Hg. Above this figure, cardiac output begins to decrease progressively. However, in daily clinical practice effort tolerance or heart failure symptoms are not associated with the hemodynamic severity of PAH. Thus, new hemodynamic definitions of PAH are needed to help us understand this discrepancey. These definitions should include pressure-volume curves, analysis of the beat-to-beat curve or detailed analysis of pulmonary vascular resistance after pulmonary arED I TO R I A L