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Review
. 2015 Nov;109(11):1381-90.
doi: 10.1016/j.rmed.2015.06.005. Epub 2015 Jun 12.

The Role of Pulmonary Arterial Stiffness in COPD

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Free PMC article
Review

The Role of Pulmonary Arterial Stiffness in COPD

Jonathan R Weir-McCall et al. Respir Med. .
Free PMC article

Abstract

COPD is the second most common cause of pulmonary hypertension, and is a common complication of severe COPD with significant implications for both quality of life and mortality. However, the use of a rigid diagnostic threshold of a mean pulmonary arterial pressure (mPAP) of ≥25 mHg when considering the impact of the pulmonary vasculature on symptoms and disease is misleading. Even minimal exertion causes oxygen desaturation and elevations in mPAP, with right ventricular hypertrophy and dilatation present in patients with mild to moderate COPD with pressures below the threshold for diagnosis of pulmonary hypertension. This has significant implications, with right ventricular dysfunction associated with poorer exercise capability and increased mortality independent of pulmonary function tests. The compliance of the pulmonary artery (PA) is a key component in decoupling the right ventricle from the pulmonary bed, allowing the right ventricle to work at maximum efficiency and protecting the microcirculation from large pressure gradients. PA stiffness increases with the severity of COPD, and correlates well with the presence of exercise induced pulmonary hypertension. A curvilinear relationship exists between PA distensibility and mPAP and pulmonary vascular resistance (PVR) with marked loss of distensibility before a rapid rise in mPAP and PVR occurs with resultant right ventricular failure. This combination of features suggests PA stiffness as a promising biomarker for early detection of pulmonary vascular disease, and to play a role in right ventricular failure in COPD. Early detection would open this up as a potential therapeutic target before end stage arterial remodelling occurs.

Keywords: Chronic obstructive; Hypertension; Pulmonary; Pulmonary disease; Pulmonary heart disease; Vascular capacitance; Vascular resistance.

Figures

Fig. 1
Fig. 1
Calculation of EA:EES in the right ventricle and pulmonary artery. Ventricular end systolic pressure-volume is linear and characterised by the slope Ees and is generated by measuring pressure-volume loops under gradated preload and afterload conditions. Reproduced from Wang et al., 2011 . Ea = Arterial elastance; Ees = Ventricular elastance.
Fig. 2
Fig. 2
Measurement of PWV using MRI: The location of the two phase contrast planes are delineated on the left image with the distance between them measured. The two separate waveforms are traced on the right relative to the triggering R-wave used to start image acquisition. The time between the waves arriving at the two consecutive locations can then be measured allowing calculation of the speed of the pulse wave.

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