Objectives Right ventricular (RV) function is identified as a key determinant of the outcome in patients with pulmonary hypertension (PH). Several studies have assessed the role of peak global longitudinal RV strain in PH patients; however, less emphasis was given to the RV regional longitudinal strain. The aim of this study was to evaluate the regional RV systolic strain in PH patients and investigate the relationship of these parameters with the severity of PH. Methods RV regional longitudinal peak systolic strain (LPSS) and strain rate (LPSSR) were measured using speckle tracking echocardiography on 100 patients with PH who underwent right heart catheterization, and 29 control subjects. Severe PH was identified by a decreased cardiac index (CI) (<2.0 L/min/m2). Results LPSS and LPSSR of the RV free wall were significantly lower in PH patients than control subjects, especially when comparing the basal and mid regions (P < .001). When comparing severe PH and nonsevere PH, basal and mid LPSS and LPSSR were significantly lower (P < .001). RV free wall mid LPSSR correlated with CI (r = −.703, P < .001). In the multiple logistic regression analysis, mid LPSSR was identified as an independent predictor of severe PH (odds ratio 1.82; 95% confidential interval 1.39–2.40; P < .001). In the receiver operating characteristics curve analysis, a cutoff value of mid LPSSR of −0.92 s−1 predicted severe PH, with a sensitivity and specificity of 75.0% and 93.7%, respectively (AUC = 0.889, P < .001). Conclusions RV free wall mid longitudinal peak systolic strain rate may be useful for the detection of severely impaired RV performance in PH.

Several echocardiographic methods to estimate pulmonary vascular resistance (PVR) have been proposed. So far, most studies have focused on relatively low PVR in patients with a nonspecific type of pulmonary hypertension. We aimed to clarify the clinical usefulness of a new echocardiographic index for evaluating markedly elevated PVR in chronic thromboembolic pulmonary hypertension (CTEPH). We studied 127 CTEPH patients. We estimated the systolic and mean pulmonary artery pressure using echocardiography (sPAP Echo , mPAP Echo ) and measured the left ventricular internal diameter at end diastole (LVIDd). sPAP Echo /LVIDd and mPAP Echo /LVIDd were then correlated with invasive PVR. Using receiver operating characteristic curve analysis, a cutoff value for the index was generated to identify patients with PVR > 1000 dyn·s·cm −5 . We analyzed pre‐ and postoperative hemodynamics and echocardiographic data in 49 patients who underwent pulmonary endarterectomy (PEA). In this study, mPAP Echo /LVIDd moderately correlated with PVR ( r = 0.51, p < 0.0001). There was a better correlation between PVR and sPAP Echo /LVIDd ( r = 0.61, p < 0.0001). sPAP Echo /LVIDd ≥ 1.94 had an 77.1% sensitivity and 75.4% specificity to determine PVR > 1000 dyn·s·cm −5 (area under curve = 0.804, p < 0.0001, 95% confidence interval [CI], 0.66–0.90). DeLong's method showed there was a statistically significant difference between sPAP Echo /LVIDd with tricuspid regurgitation velocity 2 /velocity–time integral of the right ventricular outflow tract (difference between areas 0.14, 95% CI, 0.00–0.27). The sPAP Echo /LVIDd and mPAP Echo /LVIDd significantly decreased after PEA (both p < 0.0001). The sPAP Echo /LVIDd and mPAP Echo /LVIDd reduction rate (ΔsPAP Echo /LVIDd and ΔmPAP Echo /LVIDd) was significantly correlated with PVR reduction rate (ΔPVR), respectively ( r = 0.58, p < 0.01; r = 0.69, p < 0.05). In conclusion, the index of sPAP Echo /LVIDd could be a simpler and reliable method in estimating CTEPH with markedly elevated PVR and also be a convenient method of estimating PVR both before and after PEA.