Right atrial strain is a surrogate of coupling in the right heart

This editorial refers to ‘Balloon pulmonary angioplasty improves right atrial reservoir and conduit functions in chronic thromboembolic pulmonary hypertension’, by Y. Yamasaki et al., pp. 855–862.

There is growing awareness of the importance of the right atrial (RA)–right ventricular (RV) axis in pulmonary hypertension (PH). Invasively measured RA pressure, a surrogate marker of RV stiffness, has been a key predictor of outcome in multiple epidemiological studies of pulmonary arterial hypertension (PAH) across decades.^1–3 This observation has not been made for any form of post-capillary PH⁴ or borderline PH,⁵ suggesting an exclusive functional importance of the RA in pre-capillary PH.

The manuscript by Yamasaki et al.⁶ features novel work as it focuses on right atrial function predicting reverse remodelling in chronic thrombo-embolic pulmonary hypertension (CTEPH). The authors performed cardiac magnetic resonance imaging (CMRI) and right heart catheterization in 29 CTEPH patients prior to and after percutaneous balloon pulmonary angioplasty (BPA) in Japan, where BPA is the primary treatment option for CTEPH. RA phasic function was studied with a CMRI-based feature-tracking algorithm. As a secondary finding of this manuscript, authors obtained excellent BPA results, with a mean pulmonary artery pressure declining from 38.4 ± 10.3 before BPA to 24.4 ± 4.2 mmHg after BPA. Six-minute walk distance improved from 382 ± 87 to 451 ± 94 m, and functional class was significantly improved. BPA has been introduced in Europe after refinement of the original technique⁷ by Japanese interventionists,⁸ providing a new therapeutic option for CTEPH patients who are not suitable candidates for pulmonary endarterectomy (PEA). Although Japanese CTEPH may be different from European CTEPH,⁹ authors’ results resemble haemodynamic outcomes achieved by PEA. To study reverse right heart remodelling in the absence of surgical trauma such as PEA, right atrial strain was measured in the current study and was significantly improved after BPA rising from 32.4% to 42.7%, which is near-normalized when compared with 123 normal individuals in whom mean RA reservoir strain was 44.9 ± 11.6%.¹⁰ Yamasaki et al. observed improvements in RA reservoir and conduit functions after BPA and identified them as sensitive non-invasive markers of reverse vascular remodelling and decreased RV afterload, illustrating that changes of RA strain correlate well with changes of steady components of RV afterload (e.g. change in pulmonary vascular resistance (PVR)). Presumably changes of RA strain will also associate with changes of pulsatile components of afterload, e.g., pulmonary artery compliance, which were, however, not shown in the present work. Correlations were also found with BNP levels, the key biomarker for RV function.

There is accumulating evidence that right atrial imaging, including its size, is of unique importance. The RA is in continuity with the inferior vena cava (IVC), and based on RA diameter and respiratory variation of IVC diameter PAH may be diagnosed.¹¹ In the DETECT study that was designed for early detection of PAH in scleroderma (SSc) patients, most of the SSc patients with newly diagnosed PAH presented with PVR values <3 WU which is below the current revised threshold of PVR for PAH,¹² but RA size was already mildly increased.¹³ The normal direction of flow towards the RV is determined by small pressure differences between central venous- and RA pressure,¹⁴ by RA contraction and the resistance of the RV to diastolic filling (RV end-diastolic stiffness). Advances in CMRI and speckle-tracking echocardiography have led us to understand three functions of the RA: reservoir, (passive) conduit, and (active) contractile. While reservoir and conduit function are captured by peak RA longitudinal strain rate (LSR) and early RA LSR, respectively, RA active contractile strain is measured by RA late LSR. Recent data have demonstrated that RA peak LSR is less of an estimate of RA pressure,^15,16 than it is an estimate of RV diastolic function reflected in RV end-diastolic pressure and end-diastolic elastance, and clinical worsening.¹⁷ A recent study combined CMRI and conductance catheterization to examine RV functional correlates of RA strain including RV-pulmonary vascular coupling in severe PAH.¹⁸ The term coupling defines the energy transfer from the RV to the pulmonary circulation and can be assessed by the ratio between end-systolic elastance (Ees) and arterial elastance (Ea). CMRI-derived right atrial (RA) phasic function was associated primarily with RV diastolic function, and may be an estimate of RV-PA coupling in those patients who have not fallen below the point of uncoupling at an Ees/Ea of 0.805 as was the case in this study.¹⁸

Impaired RA reservoir function (low peak LSR) is correlated with RA size, inferior vena cava (IVC) diameter,¹⁸ and backward flow in the IVC.¹⁹ In addition to tricuspid regurgitation as one of the signs of poor RA–RV coupling, atrial regurgitation occurs mostly during atrial contraction and contributes independently to backwards venous flow, systemic congestion, and subsequent aggravation of clinical signs of right heart failure.¹⁹ As the authors recognize, there is more work to do to decipher the role of vena cava compliance and RA function to better understand IVC-RA coupling, and its potential improvement after BPA, or any other relief of RV afterload.

In summary, data are accumulating that RA strain may be an early and sensitive surrogate for positive or negative right heart remodelling, and coupling. Assessment of RA function delivers sensitive data, and should be part of the management and follow-up of patients with PAH.

Conflict of interest: none declared.

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