Abstract Background The diagnostic pathway of pulmonary hypertension (PH) is complex and requires several parameters. Differential diagnosis between left heart disease (group 2) and pulmonary disease (group 3) as PH etiology is also challenging. The latest European guidelines recommend a comprehensive echocardiographic evaluation for suspected PH, and the use of several basic echocardiographic indices to assess cardiac etiology of PH. Speckle tracking echocardiography (STE) has emerged as a more sensitive technique to evaluate myocardial performance in different clinical settings and is recommended for the diagnosis of HFpEF. Purpose Our ai was to assess the potential value of STE to predict left heart disease in patients presenting with dyspnoea and PH. Methods Consecutive outpatients with dyspnoea with efforts and subsequent diagnosis of PH were retrospectively enrolled. Inclusion criteria were New York heart association (NYHA) class≥II, LV ejection fraction≥50%, echocardiographic evidence of systolic pulmonary artery pressure≥35 mmHg and tricuspid regurgitant velocity≥2.8 ms, known diagnosis of PH with relative etiology (heart failure with preserved ejection fraction, HFpEF or lung diseases i.e. sarcoidosis, idiopathic pulmonary fibrosis, chronic obstructive lung disease). Patients underwent clinical, biohumoral and echocardiographic evaluation, STE was performed offline. Primary endpoint was the prediction of HFpEF. Results Overall, 145 patients were enrolled (80 with HFpEF, 65 with lung disease). Mean age was 75±12 years, 53% were female. Patients with HFpEF were older (77±10 vs. 68±14 years, p<0.0001) and had higher LA volume (93±37 vs. 64±31 ml, p<0.0001), E/E’ by tissue Doppler imaging (TDI) (15±5 vs. 9±3, p<0.0001), mitral regurgitation (MR) grading (p=0.002), lower tricuspid regurgitation (TR) grading (p=0.004). Regarding STE, patients with HFpEF had lower peak atrial longitudinal strain (PALS) (15 ± 8 vs. 24 ± 11%, p<0.0001) and LV global longitudinal strain (-13 ± 9 vs. -17 ± 6%, p=0.009). LA stiffness, calculated as the ratio between E/E’ and PALS, an index of LA dysfunction and fibrosis, was higher in patients with HFpEF (median LA stiffness = 1.09 [CI = 0.64-1.73] 0. Vs.0.35 [CI = 0.20-0.59], p<0.0001). With ROC curves, both E/E’ and global PALS provided a good prediction for HFpEF (AUC 0.73 and 0.79 respectively), but LA stiffness significantly enhanced the predictive power (AUC = 0.83) with an optimal cutoff value ≥0.53. With multivariate analysis including age, LA volume, LV GLS, LA stiffness, mitral and tricuspid regurgitation grade, LA stiffness≥0.53 (RR = 19.14, CI 5.86-62.55) was the only independent predictor of HFpEF in our cohort of patients with PH (Fig.1). Conclusions STE may aid differential diagnosis of etiology between left heart disease and pulmonary disease in patients with PH. The combination of TDI E/E’ and PALS to calculate LA stiffness offers the most accurate prediction of PH with cardiac etiology.
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