title: The Critical Role of Pulmonary Arterial Compliance in Pulmonary Hypertension.
abstract: The normal pulmonary circulation is a low-pressure, high-compliance system. Pulmonary arterial compliance decreases in the presence of pulmonary hypertension because of increased extracellular matrix/collagen deposition in the pulmonary arteries. Loss of pulmonary arterial compliance has been consistently shown to be a predictor of increased mortality in patients with pulmonary hypertension, even more so than pulmonary vascular resistance in some studies. Decreased pulmonary arterial compliance causes premature reflection of waves from the distal pulmonary vasculature, leading to increased pulsatile right ventricular afterload and eventually right ventricular failure. Evidence suggests that decreased pulmonary arterial compliance is a cause rather than a consequence of distal small vessel proliferative vasculopathy. Pulmonary arterial compliance decreases early in the disease process even when pulmonary artery pressure and pulmonary vascular resistance are normal, potentially enabling early diagnosis of pulmonary vascular disease, especially in high-risk populations. With the recognition of the prognostic importance of pulmonary arterial compliance, its impact on right ventricular function, and its contributory role in the development and progression of distal small-vessel proliferative vasculopathy, pulmonary arterial compliance is an attractive target for the treatment of pulmonary hypertension.
authors: 1 Division of Cardiovascular Medicine, University of Minnesota Medical School, Minneapolis, Minnesota; and.
authors: Thenappan
authors: T
authors: Thenappan
authors: 1 Division of Cardiovascular Medicine, University of Minnesota Medical School, Minneapolis, Minnesota; and.
authors: Kurt W
authors: KW
authors: Prins
authors: 1 Division of Cardiovascular Medicine, University of Minnesota Medical School, Minneapolis, Minnesota; and.
authors: Marc R
authors: MR
authors: Pritzker
authors: 2 Aria CV, Inc., St. Paul, Minnesota.
authors: John
authors: J
authors: Scandurra
authors: 2 Aria CV, Inc., St. Paul, Minnesota.
authors: Karl
authors: K
authors: Volmers
authors: 1 Division of Cardiovascular Medicine, University of Minnesota Medical School, Minneapolis, Minnesota; and.
authors: E Kenneth
authors: EK
authors: Weir
mesh_terms: D003187:Compliance / Q000502:physiology; D006333:Heart Failure; D006801:Humans; D006976:Hypertension, Pulmonary / Q000503:physiopathology*; D009389:Neovascularization, Pathologic / Q000503:physiopathology; D011379:Prognosis; D011651:Pulmonary Artery / Q000503:physiopathology*; D011652:Pulmonary Circulation / Q000502:physiology*; D059289:Vascular Stiffness / Q000502:physiology*; D018497:Ventricular Dysfunction, Right / Q000503:physiopathology*
keywords: heart failure; impedance; resistance; right ventricle; stiffness