Personal ViewMildly elevated pulmonary artery systolic pressure on echocardiography: bridging the gap in current guidelines
Introduction
Pulmonary hypertension is a common and highly morbid condition associated with decreased survival. Defined as mean pulmonary artery pressure (mPAP) of more than 20 mm Hg measured with right heart catheterisation,1 based on the upper limit of normal pulmonary artery pressure in healthy individuals at rest and the increased risks associated with mPAP of more than 20 mm Hg, pulmonary hypertension is present in more than three-quarters of patients who undergo clinically indicated right heart catheterisation procedures.2, 3 However, pulmonary artery systolic pressure (PASP) can also be estimated (ePASP) noninvasively using echocardiography with adequate reliability. Indeed, ePASP is a standard assessment in contemporary echocardiography, and can be measured on about two-thirds of all echocardiograms.4, 5 Elevated ePASP of more than 30 mm Hg is associated with substantial increases in morbidity and mortality, and frequently occurs alongside metabolic and cardiopulmonary comorbidities.6 Current guidelines for the diagnosis and management of pulmonary hypertension7 outline assessment and referral approaches to identify subgroups of patients with pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH),1 which are relatively rare diseases. However, approaches to management for the high numbers of patients with elevated ePASP who do not have underlying severe pulmonary vascular disease such as PAH, especially those with underlying cardiopulmonary and metabolic comorbidities, are not well established.
In this Personal View, we evaluate ePASP as a marker for increased risk for morbidity and mortality and propose a multidisciplinary approach to the assessment and management of elevated ePASP and aggressive risk-reduction strategies in the context of an understanding of underlying pathophysiology and comorbidities.
Section snippets
Assessment of risk
Echocardiography can be used to obtain ePASP by measuring the tricuspid regurgitation velocity (TRV) doppler signal. Specifically, ePASP is determined by calculating the estimated trans-tricuspid regurgitation gradient (equivalent to 4 × TRV2) and adding the estimated right atrial pressure based on the size of the inferior vena cava and collapsibility with sniff (ie, a sharp forceful inhalation through the nose).7 Values of ePASP or PASP, measured with echocardiography or right heart
Management strategies
In contemporary guidelines for diagnosis and management of pulmonary hypertension in symptomatic patients, TRV measured on echocardiography, in addition to other clinical characteristics (figure 2), has an important role in the algorithm for identification of patients with PAH and CTEPH, the two groups of patients with pulmonary hypertension for which there are well proven therapeutic interventions.7 However, a substantial gap in recommendations exists for the management of patients with
Conclusions and future directions
Current data show that patients with an ePASP of more than 30 mm Hg are at risk for increased morbidity and mortality, which might relate to multiple underlying comorbidities, elevated pressure within the pulmonary circulation, and the consequent effects on the heart. While we do not advocate screening the general population for increased PASP, this is a common high-risk finding on clinical echocardiograms that often receives inadequate attention. Clinicians should be aware of the adverse
Declaration of interests
BAM reports grants and personal fees from Actelion, outside the submitted work. In addition, BAM is a co-inventor on a US patent for endothelin B receptor cysteine405, a redox-sensitive, functional cysteinyl thiol that regulates pulmonary vascular nitric oxide formation (9,605,047), and on US provisional patent applications for the following: platelet cell surface NEDD9, a mediator of pulmonary arterial thrombosis (PCT/US2019/059890); a risk-stratification score for patients with exercise
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