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(Circulation. 2008;118:2120-2121.)
© 2008 American Heart Association, Inc.

Editorial

Exercise-Induced Pulmonary Arterial Hypertension

A New Addition to the Spectrum of Pulmonary Vascular Diseases

Ronald J. Oudiz, MD; Lewis J. Rubin, MD

From the LA Biomedical Research Institute at Harbor–UCLA, Torrance, Calif (R.J.O.); and the University of California, San Diego, La Jolla (L.J.R.).

Correspondence to Lewis J. Rubin, MD, University of California, San Diego, 9300 Campus Point Dr, M/C 7381, La Jolla, CA 92037–1300. E-mail ljrubin@ucsd.edu

Key Words: Editorials • diagnosis • dyspnea • hypertension, pulmonary • pulmonary heart disease

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Although the complex molecular mechanisms responsible for the vasculopathy of pulmonary artery hypertension (PAH) have only recently begun to be unraveled, it has been recognized for decades that the most significant determinant of both symptoms and survival in PAH is the degree of cardiac impairment that results from the increased right ventricular afterload.¹ Exertional dyspnea, the most frequent presenting symptom of PAH,^2,3 results from several physiological impairments that are measurable with cardiopulmonary exercise testing and are indicative of impaired right ventricular output during physical activity: (1) an inability to increase O₂ transport to tissues during exercise, measured as a decrease in peak O₂ compared with normal; (2) premature lactic acidosis, measured as a decrease in the anaerobic threshold, increasing CO₂ output and ventilatory drive; and (3) underperfusion of ventilated lung, measured as a high E/CO₂ at the anaerobic threshold.⁴ Unfortunately, exertional dyspnea is a nonspecific complaint, and a definitive diagnosis of PAH is often delayed until signs and symptoms indicative of more advanced degrees of right heart functional impairment are present.

Article p 2183

In this issue of Circulation, Tolle and colleagues⁵ postulated that mild pulmonary vascular disease, when resting hemodynamics are not substantially abnormal, could be identified by unmasking the impairment in right ventricular function with exercise. They found that, although patients with evidence of PAH at rest had both severe hemodynamic abnormalities and impaired cardiopulmonary gas exchange during exercise, a population of patients with symptoms but relatively normal resting hemodynamics could be identified who manifested . . . [Full Text of this Article]