
A simpler noninvasive method of predicting markedly elevated pulmonary vascular resistance in patients with chronic thromboembolic pulmonary hypertension
Author(s) -
Zhai YaNan,
Li AiLi,
Tao XinCao,
Xie WanMu,
Gao Qian,
Zhang Yu,
Chen AiHong,
Lei JiePing,
Zhai ZhenGuo
Publication year - 2022
Publication title -
pulmonary circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.791
H-Index - 40
ISSN - 2045-8940
DOI - 10.1002/pul2.12102
Subject(s) - medicine , cardiology , vascular resistance , pulmonary hypertension , pulmonary artery , receiver operating characteristic , hemodynamics , diastole , confidence interval , blood pressure
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.