Pulmonary arterial hypertension (PAH) is a rare, progressive disease in which there is a persistent, abnormal increase in pulmonary artery pressure. Symptoms of pulmonary hypertension are nonspecific and mainly associated with progressive right ventricular failure. The diagnosis of PAH is a multistep process and often requires the skillful use of several tests. The gold standard for the diagnosis of PAH is hemodynamic testing. Echocardiography currently plays an important role in the diagnostic algorithm of PAH as it is minimally invasive and readily available. Moreover, many echocardiographic parameters are closely related to pulmonary hemodynamics. It allows assessment of the right heart′s structure and function, estimation of the pressure in the right ventricle, right atrium, and pulmonary trunk, and exclusion of other causes of elevated pulmonary bed pressure. Echocardiographic techniques are constantly evolving, and recently, measurements made using new techniques, especially 3D visualization, have become increasingly important. In echocardiographic assessment, it is crucial to know current guidelines and new reports that organize the methodology and allow standardization of the examination. This review aims to discuss the different echocardiographic techniques used to evaluate patients with PAH.
Pulmonary arterial hypertension (PAH) can develop subsequently to disorganized endothelial cell proliferation within the pulmonary arteriolar layers that provide mechanical limits to the pulmonary vascular bed. Although the actual factor triggering vascular endothelial proliferation remains unknown to date, genetic susceptibility, hypoxia, inflammation, as well as response to drugs and toxins have been proposed as possible contributors. Since inflammation contributes to vascular remodeling, the changed immune response is increasingly considered a plausible cause of this cardiovascular disease. The interaction of a membrane glycoprotein cluster of differentiation 200 (CD200) and its structurally similar receptor (CD200R) plays a crucial role in the modulation of the inflammatory response. Our previous studies have shown that the overexpression of the other negative co-stimulatory molecule (programmed death cell - PD-1) and its ligand-1 (PD-L1) is closely related to iPAH and the presence of Epstein-Barr virus (EBV) reactivation markers. Therefore, we considered it necessary to analyze the different types of PAH in terms of CD200 and CD200R expression and to correlate CD200/CD200R pathway expression with important clinical and laboratory parameters. The CD200/C200R-signaling pathway has not been subject to much research. We included 70 treatment-naïve, newly diagnosed patients with PAH in our study. They were further divided into subsets according to the pulmonary hypertension classification: chronic thromboembolic pulmonary hypertension (CTEPH) subset, pulmonary arterial hypertension associated with congenital heart disease (CHD-PAH), pulmonary arterial hypertension associated with connective tissue disease (CTD-PAH), and idiopathic pulmonary arterial hypertension (iPAH). The control group consisted of 20 healthy volunteers matched for sex and age. The highest percentages of T CD200+CD4+ and T CD200+CD8+ lymphocytes were observed in the group of patients with iPAH and this finding was associated with the presence of EBV DNA in the peripheral blood. Our assessment of the peripheral blood lymphocytes expression of CD200 and CD200R indicates that these molecules act as negative co-stimulators in the induction and persistence of PAH-associated inflammation, especially that of iPAH. Similar results imply that the dysregulation of the CD200/CD200R axis may be involved in the pathogenesis of several immune diseases. Our work suggests that CD200 and CD200R expression may serve to distinguish between PAH cases. Thus, CD200 and CD200R might be useful as markers in managing PAH and should be further investigated.
Background: Tricuspid annular plane systolic excursion (TAPSE) and tricuspid regurgitation velocity (TRV) are two echocardiographic parameters with prognostic value in patients with pulmonary hypertension (PH). When analyzed concurrently as TRV/TAPSE ratio, they allow the ventricular-pulmonary artery coupling (RVPAC) to be assessed. This could better predict the disease severity in patients with PH. Objective: Our study aimed to evaluate the prognostic value of the TRV/TAPSE ratio echocardiographic parameter in adults with precapillary PH. Methods: The study included 39 patients (74% women; average age, 63 years) with precapillary PH: pulmonary arterial hypertension (PAH), and chronic thromboembolic PH (CTEPH). The mean follow-up period was 16,6 ±13,3 months. Twelve patients (31%) died during observation time. We measured TAPSE as a surrogate of RV contractility and TRV reflecting RV afterload, while ventricular–arterial coupling was evaluated by the ratio between these two parameters (TRV/TAPSE). To assess disease progression and the patient's functional capacity, World Health Organization functional class (WHO FC) was determined. Patient physical capacity was also evaluated using the 6-minute walk test (6MWT). The analysis included values of N-terminal prohormone brain natriuretic peptide (NT-proBNP), which were taken routinely during the follow-up visit. Results: The mean calculated TRV/TAPSE ratio was 0.26 ± 0.08 m/s/mm. On comparison of the TRV/TAPSE ratio to the disease prognostic indicators, we observed statistically significant correlation between TRV/TAPSE and the results of WHO FC, 6MWT and NT-proBNP. TRV/TAPSE ratio is thus a good predictor of mortality in PH patients (AUC, 0.781). Patients with a TRV/TAPSE ratio > 0.30 m/s/mm had a shorter survival time with log-rank test p< 0.0001. Additionally, ROC analysis revealed higher AUC for TRV/TAPSE than for TAPSE and TRV alone. Conclusions: TRV/TAPSE is a promising practicable echocardiographic parameter reflecting RVPAC. Moreover, TRV/TAPSE could be viable risk stratification parameter and could have prognostic value in patients with PH.
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