This meta-analysis confirmed that USAT significantly reduced PAMP, RV/LV ratio and CT obstruction scores with similar death rates and a lower risk of major bleeding compared with patients with PE undergoing systemic thrombolytic treatment.
We present our single-center results on ultrasound-assisted thrombolysis (USAT) in patients with pulmonary embolism (PE) at intermediate high risk (IHR) and high risk (HR). Our study consisted of 75 patients with PE who underwent USAT (60 at IHR and 15 at HR). The median time delay from symptoms to USAT was 5 days. Ultrasound-assisted thrombolysis resulted in improvements in tricuspid annular plane systolic excursion; pulmonary artery (PA) systolic and mean pressures; Qanadli score; right to left ventricle diameter ratio and right to left atrial diameter ratio; and diameters of main, right, and left PA regardless of the baseline risk status ( P < .0001 for all). Death was documented in 4 patients, and major and minor bleeding were noted in 2 and 5 of the patients, respectively. No PE-related event was noted during postdischarge follow-up period of median 310 days. Our study revealed that USAT facilitates the resolution of PA thrombotic burden, recovery of pulmonary hemodynamics, and right heart functions with acceptable rates of procedure-related complications in patients with PE, irrespective of the IHR or HR status.
Different Doppler echocardiography (DE) models have been proposed for estimation of mean pulmonary arterial pressures (PAMP) from tricuspid regurgitation (TR) jet velocity. We aimed to compare four TR-derived DE models in predicting the PAMP measured by right heart catheterization (RHC) in different groups of precapillary pulmonary hypertension (PH). A total of 287 patients with hemodynamically pre-capillary PH were enrolled (mean age = 51 ± 17.4 years, 59.9% female). All patients underwent DE before RHC (< 3 h) and four formulae (F) were used for TR-derived PAMP estimation (PAMP-DE). These were as follows: F1 = Chemla (0.61 × systolic pulmonary artery pressure [PASP] + 2); F2 = Friedberg (0.69 × PASP − 0.22), F3 = Aduen (0.70 × PASP); and F4 = Bech-Hanssen (0.65 × PASP − 1.2). The PASP and PAMP (mmHg) measured by RHC were 89.1 ± 30.4 and 55.8 ± 20.8, respectively. In the overall PH group, DE estimates for PASP (r = 0.59, P = 0.001) and PAMP (r = 0.56, P = 0.001 for all) showed significant correlations with corresponding RHC measures. Concordance was noted between Chemla and Bech-Hanssen, and Aduen and Bech-Hanssen. The Bland–Altman plot showed that Chemla and Bech-Hanssen overestimated and Friedberg and Aduen underestimated PAMP-RHC measures. Paired-t test showed significant systematic biases for Aduen and Bech-Hanssen while Passing-Bablok non-parametric analysis revealed significant systematic biases all four PAMP-DE estimates. There was poor agreement between PAMP-RHC measures and PAMP-DE deciles (Kappa values were 0.112, 0.097, 0.095, and 0.121, respectively). This study showed a poor agreement between PAMP-DE estimates by four TR-derived formulae and PAMP-RHC in patients with PH, regardless of the etiology. However, these results can not be fully extrapolated to a normal population and did not address the reliability of DE estimates for PH screening procedures.
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