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The Evolving Landscape of Exercise-Induced Pulmonary Hypertension

  • Adult Congenital Heart Disease (A Bhatt and K Niwa, Section Editors)
  • Published:
Current Treatment Options in Cardiovascular Medicine Aims and scope Submit manuscript

Opinion statement

Normal pulmonary artery pressures at rest, with an exaggerated rise during exercise, characterize exercise-induced pulmonary hypertension. Exercise itself as it relates to this condition is not deleterious, nor does it cause or induce disease. However much like any classical stress test, it is a physiologic probe that aids in disease unmasking. Although more work is required to establish criteria for defining this clinical entity, the phenomenon is real. It remains unknown whether it represents a nascent form of cardiopulmonary disease and whether its genesis predicts fulminant cardiopulmonary disease. Incremental cardiopulmonary exercise testing and the construction of pressure–flow plots to describe the pulmonary vascular response to exercise will be essential in defining this disease. The critical first step remains a consensus definition that will allow for further prospective study focused by a common language.

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Notes

  1. Vascular distensibility has proven to be an important contribution to the dynamic nature of PVR. In fact, experimental models predict pulmonary pressures across varying cardiac outputs by introducing only two additional variables—resting Total Pulmonary Vascular Resistance (R 0) and a distensibility coefficient (α) [55, 56]. Their behavior is governed by the following equation put forth by Linehan [56].

    $$ \mathrm{mPAP} = \frac{{\left[{\left(1+\alpha \cdot \mathrm{LAP}\right)}^5+5\alpha {R}_0\cdot Q\right]}^{\frac{1}{5}}-1}{\alpha } $$

    α has been defined in most terrestrial species to be roughly 2 %, which reflects a 2 % change in vascular diameter per increased mmHg. This plays an important role in the dynamic nature of PVR as rising flows and rising LAPs engorge and dilate pulmonary blood vessels. It has been suggested that α explains nearly all of the the curvilinearity seen in multipoint mPAP-Q plots [13•, 39]. Hence the linear Ohmic understanding of mPAP betrays the true curvilinearity of mPAP in nature. This is all due to the fact that the pulmonary vasculature is not a rigid pipe but a compliant vessel.

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  1. Department of Medicine, Division of Cardiology, Yawkey Center for Outpatient Care, Massachusetts General Hospital, 5th Floor 32 Fruit Street, Boston, MA, 02114, USA

    J. Sawalla Guseh MD

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Guseh, J.S. The Evolving Landscape of Exercise-Induced Pulmonary Hypertension. Curr Treat Options Cardio Med 18, 41 (2016). https://doi.org/10.1007/s11936-016-0459-5

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