What is the clinical evidence from this study?

Study design: Cohort. Population: Systemic sclerosis without manifest pulmonary arterial hypertension (n=70). Intervention: Right atrial stiffness vs. Lower right atrial stiffness. Primary outcome: All-cause mortality (HR 2.460, 95% CI 1.005-6.021, p=0.049).

June 5, 2022Open Access

Prognostic value of right atrial stiffness in systemic sclerosis

ÁNÁgnes NógrádiUniversity of Pecs ZVZsuzsanna VargaUniversity Hospital of Zurich MHMáté HajduUniversity of Pecs

Key Result

Right atrial stiffness independently predicted all-cause mortality in systemic sclerosis patients without pulmonary arterial hypertension (HR 2.460), providing incremental prognostic value.

Study Design

Type

Cohort (n=70)

Multicenter

Structured PICO

Does echocardiographic measurement of right atrial stiffness predict all-cause mortality in systemic sclerosis patients without manifest pulmonary arterial hypertension?

Population

70 predominantly female (90%) patients with systemic sclerosis without manifest pulmonary arterial hypertension, mean age 57 years, followed for a mean of 4.7 years.

Exposure

Echocardiographic measurement of right atrial (RA) stiffness (calculated as ratio of TriE/e' to reservoir strain using 2D speckle tracking).

Outcome

All-cause mortality after 5 years.hard clinical

Right atrial stiffness is an independent predictor of all-cause mortality in systemic sclerosis patients without pulmonary arterial hypertension, offering incremental prognostic value over RV longitudinal systolic function.

Main Result

Hazard Ratio: 2.46 (95% CI 1.005–6.021)

p-value: p=0.049

Limitations

Relatively low number of participants and events.
Used software developed for left ventricular strain analysis because dedicated atrial strain software was not available.
Right ventricular strain analysis was not performed.

Abstract

OBJECTIVES: We hypothesised that right atrial (RA) size and mechanics may have prognostic role in systemic sclerosis (SSc) patients without manifest pulmonary arterial hypertension (PAH), thus we aimed to investigate the prognostic power of RA volume, strain and stiffness parameters alone and when added to the echocardiographic marker of RV longitudinal systolic function. METHODS: Seventy SSc patients (57±12 years) were enrolled into our follow-up study. They underwent standard echocardiographic and tissue Doppler measurements at baseline. In addition to maximal RA volume index, RA reservoir, conduit and contractile strain were measured with 2D speckle tracking technique. RA stiffness was calculated as ratio of TriE/e' to reservoir strain. Survival was assessed after 5 years. All-cause mortality was chosen as outcome. Sequential χ2 analysis was used to evaluate the incremental prognostic benefit of adding RA volume, strain or stiffness to tricuspid S (TriS). RESULTS: During the follow-up period of 4.7±0.9 years, 6 patients (8.6%) died. When added to TriS in sequential Cox model, RA stiffness significantly improved the diagnostic performance of the model (Δχ2= 3.950; p=0.047) and remained independent predictor of the outcome (HR 2.460 (1.005-6.021); p=0.049). Vmax index and strain parameters did not show incremental prognostic value over TriS. Using ROC analysis, RA stiffness ≥0.156 was the best predictor of mortality (sensitivity=83.3%, specificity =89.1%, AUC=0.859). CONCLUSIONS: RA stiffness is associated with all-cause mortality in SSc patients without PAH independent of and incremental to the RV longitudinal systolic function. It may be proposed as non-invasive marker for identifying patients with high mortality risk.

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