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(Circulation. 2008;118:2183-2189.)
© 2008 American Heart Association, Inc.

Vascular Medicine

Exercise-Induced Pulmonary Arterial Hypertension

James J. Tolle, MD; Aaron B. Waxman, MD, PhD; Teresa L. Van Horn, BA; Paul P. Pappagianopoulos, MEd; David M. Systrom, MD

From the Pulmonary and Critical Care Unit, Medical Services, Massachusetts General Hospital, Harvard Medical School, Boston, Mass.

Correspondence to James J. Tolle, MD, Pulmonary and Critical Care Unit, BUL 1-148, Massachusetts General Hospital, 55 Fruit St, Boston, MA 02114. E-mail jjtolle{at}yahoo.com

Received October 29, 2007; accepted September 5, 2008.

Background— The clinical relevance of exercise-induced pulmonary arterial hypertension (PAH) is uncertain, and its existence has never been well studied by direct measurements of central hemodynamics. Using invasive cardiopulmonary exercise testing, we hypothesized that exercise-induced PAH represents a symptomatic stage of PAH, physiologically intermediate between resting pulmonary arterial hypertension and normal.

Methods and Results— A total of 406 consecutive clinically indicated cardiopulmonary exercise tests with radial and pulmonary arterial catheters and radionuclide ventriculographic scanning were analyzed. The invasive hemodynamic phenotype of exercise-induced PAH (n=78) was compared with resting PAH (n=15) and normals (n=16). Log-log plots of mean pulmonary artery pressure versus oxygen uptake (O₂) were obtained, and a "join-point" for a least residual sum of squares for 2 straight-line segments (slopes m1, m2) was determined; m2<m1="plateau," and m2>m1="takeoff" pattern. At maximum exercise, O₂ (55.8±20.3% versus 66.5±16.3% versus 91.7±13.7% predicted) was lowest in resting PAH, intermediate in exercise-induced PAH, and highest in normals, whereas mean pulmonary artery pressure (48.4±11.1 versus 36.6±5.7 versus 27.4+3.7 mm Hg) and pulmonary vascular resistance (294±158 versus 161±60 versus 62±20 dyne · s · cm^–5, respectively; P<0.05) followed an opposite pattern. An exercise-induced PAH plateau (n=32) was associated with lower O₂max (60.6±15.1% versus 72.0±16.1% predicted) and maximum cardiac output (78.2±17.1% versus 87.8±18.3% predicted) and a higher resting pulmonary vascular resistance (247±101 versus 199±56 dyne · s · cm^–5; P<0.05) than takeoff (n=40). The plateau pattern was most common in resting PAH, and the takeoff pattern was present in nearly all normals.

Conclusions— Exercise-induced PAH is an early, mild, and clinically relevant phase of the PAH spectrum.

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CLINICAL PERSPECTIVE

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