Early left atrial dysfunction in idiopathic pulmonary fibrosis patients without chronic right heart failure

No data are actually available regarding the left atrial (LA) functional assessment by two-dimensional speckle tracking echocardiography (2D-STE) in early-stage idiopathic pulmonary fibrosis (IPF). The primary end-point of our study was to assess whether global LA peak strain (GLAPS), measured by 2D-STE analysis, may detect early alterations in LA function in IPF patients without right heart failure (RHF). Between September 2017 and January 2019, 50 consecutive IPF patients (73.8 ± 6.8 years, 36 males) without chronic RHF and 30 controls matched by age, sex and cardiovascular risk factors, were enrolled in an observational retrospective case–control study. All patients underwent a complete echocardiographic study implemented with 2D-STE analysis. GLAPS, left ventricular (LV) global longitudinal strain (GLS), right atrial (RA) reservoir strain (GSA+) and right ventricular (RV)-GLS were obtained in each patient. LVFP were significantly increased in IPF patients in comparison to controls (average E/e′ ratio 14.4 ± 3.0 vs 9.6 ± 1.5, p < 0.0001), while LV-GLS was slightly reduced in IPF patients compared to controls (19.4 ± 3.6% vs 21.0 ± 2.2%, p = 0.03).Moreover, GLAPS was significantly impaired in IPF patients in comparison to controls (18.4 ± 3.7% vs 28.4 ± 5.6%, p < 0.0001).Finally, the two groups of patients did not show any statistically significant difference in both RA-GSA + (23.9 ± 3.7% vs 24.5 ± 4.0%, p = 0.49) and RV-GLS (− 22.6 ± 3.3% vs − 23.5 ± 3.0%, p = 0.22). Notably, LV-GLS was strongly inversely correlated both with RV/LV basal diameter ratio and TRV in IPF patients (r = − 0.87 and − 0.82, respectively) but not in controls (r = − 0.29 and − 0.27, respectively). This finding highlights a likely process of ventricular interdependence in non-advanced IPF, with consequent LV diastolic dysfunction and secondary impairment in LV-GLS and GLAPS. Early LA reservoir dysfunction in IPF patients may be secondary to LV diastolic dysfunction induced by ventricular interdependence and may develop before RV diastolic and systolic dysfunction.