(1) Background: Prostacyclin analogues (epoprostenol, treprostinil, and iloprost) induce vasodilation in pulmonary arterial hypertension (PAH) but also inhibit platelet function. (2) Objectives: We assessed platelet function in PAH patients treated with prostacyclin analogues and not receiving prostacyclin analogues. (3) Methods: Venous blood was collected from 42 patients treated with prostacyclin analogues (49.5 ± 15.9 years, 81% female) and 38 patients not receiving prostacyclin analogues (55.5 ± 15.6 years, 74% female). Platelet reactivity was analyzed by impedance aggregometry using arachidonic acid (AA; 0.5 mM), adenosine diphosphate (ADP; 6.5 µM), and thrombin receptor-activating peptide (TRAP; 32 µM) as agonists. In a subset of patients, concentrations of extracellular vesicles (EVs) from all platelets (CD61⁺), activated platelets (CD61⁺/CD62P⁺), leukocytes (CD45⁺), and endothelial cells (CD146⁺) were analyzed by flow cytometry. Platelet-rich thrombus formation was measured using a whole blood perfusion system. (4) Results: Compared to controls, PAH patients treated with prostacyclin analogues had lower platelet reactivity in response to AA and ADP (p = 0.01 for both), lower concentrations of platelet and leukocyte EVs (p ≤ 0.04), delayed thrombus formation (p ≤ 0.003), and decreased thrombus size (p = 0.008). Epoprostenol did not affect platelet reactivity but decreased the concentrations of platelet and leukocyte EVs (p ≤ 0.04). Treprostinil decreased platelet reactivity in response to AA and ADP (p ≤ 0.02) but had no effect on the concentrations of EVs. All prostacyclin analogues delayed thrombus formation and decreased thrombus size (p ≤ 0.04). (5) Conclusions: PAH patients treated with prostacyclin analogues had impaired platelet reactivity, EV release, and thrombus formation, compared to patients not receiving prostacyclin analogues.

Background: In this study, we aimed to assess the efficacy and safety of balloon pulmonary angioplasty (BPA) in patients with technically inoperable distal-type chronic thromboembolic pulmonary hypertension (d-CTEPH) and technically operable proximal-type disease (p-CTEPH) by analyzing the results of BPA treatment in two collaborating CTEPH referral centers. Methods and results: We assessed hemodynamic results, functional efficacy, complication and survival rate after BPA treatment in 70 CTEPH patients (median age 64 years; (interquartile range (IQR): 52–73 years)), of whom 16 (median age 73 years; (QR 62–82 years)) were in the p-CTEPH subgroup. Altogether, 377 BPA procedures were performed, resulting in significant (p < 0.001) improvement in mean pulmonary artery pressure (mPAP 48.6 ± 10 vs. 31.3 ± 8.6 mmHg), pulmonary vascular resistance (694 ± 296 vs. 333 ± 162 dynes*s*cm⁻⁵), six-minute walk test (365 ± 142 vs. 433 ± 120 metres) and N-terminal pro B-type natriuretic peptide (1307 (510–3294) vs. 206 (83–531) pg/mL). The rate of improvement did not differ between the sub-groups. Lung injury episodes and severe hemoptysis were similarly infrequent in d-CTEPH and p-CTEPH (6.4% vs. 5%; p = 0.55 and 1.0% vs. 2.5; p = 0.24, respectively). There was no significant difference between the sub-groups regarding survival (p = 0.53 by log-rank test). Conclusion: BPA may be beneficial in patients with p-CTEPH who cannot undergo pulmonary endarterectomy (PEA). Larger long-term studies are needed to better define the efficacy, safety, and optimal BPA procedural standards in this population.

Pulmonary hypertension (PH) is a serious hemodynamic condition, characterized by increased pulmonary vascular resistance (PVR), leading to right heart failure (HF) and death when not properly treated. The prognosis of PH depends on etiology, hemodynamic and biochemical parameters, as well as on response to specific treatment. Biomarkers appear to be useful noninvasive tools, providing information about the disease severity, treatment response, and prognosis. However, given the complexity of PH, it is impossible for a single biomarker to be adequate for the broad assessment of patients with different types of PH. The search for novel emerging biomarkers is still ongoing, resulting in a few potential biomarkers mirroring numerous pathophysiological courses. In this review, markers related to HF, myocardial remodeling, inflammation, hypoxia and tissue damage, and endothelial and pulmonary smooth muscle cell dysfunction are discussed in terms of diagnosis and prognosis. Extracellular vesicles and other markers with complex backgrounds are also reviewed. In conclusion, although many promising biomarkers have been identified and studied in recent years, there are still insufficient data on the application of multimarker strategies for monitoring and risk stratification in PH patients.

(1) Background: Pulmonary embolism (PE) is the third most frequent acute cardiovascular condition worldwide. PE response teams (PERTs) have been created to facilitate treatment implementation in PE patients. Here, we report on the 5-year experience of PERT operating in Warsaw, Poland, with regard to the characteristics and outcomes of the consulted patients. (2) Methods: Patients diagnosed with PE between September 2017 and December 2021 were included in the study. Clinical and treatment data were obtained from medical records. Patient outcomes were assessed in-hospital, at a 1- and 12-month follow-up. (3) Results: There were 235 PERT activations. The risk of early mortality was low in 51 patients (21.8%), intermediate–low in 83 (35.3%), intermediate–high in 80 (34.0%) and high in 21 (8.9%) patients. Anticoagulation alone was the most frequently administered treatment in all patient subgroups (altogether 84.7%). Systemic thrombolysis (47.6%) and interventional therapy (52%) were the prevailing treatment options in high-risk patients. The in-hospital mortality was 6.4%. The adverse events during 1-year follow-up included five deaths, two recurrent VTE and two minor bleeding events. (4) Conclusions: Our initial 5-year experience showed that the activity of the local PERT facilitated patient-tailored decision making and the access to advanced therapies, with subsequent low overall mortality and treatment complication rates, confirming the benefits of PERT implementation.

Background: The remodeling of the right heart in patients with chronic pulmonary hypertension (cPH) is associated with the appearance of electrocardiographic (ECG) abnormalities. We investigated the resolution of ECG markers of right ventricular hypertrophy (RVH) caused by acute and long‐term hemodynamic improvement.Methods: Twenty‐nine (29) patients with chronic thromboembolic pulmonary hypertension (CTEPH) and seven patients with pulmonary arterial hypertension (PAH) were included in the analysis. Patients with CTEPH achieved a significant long‐term hemodynamic improvement following the treatment with balloon pulmonary angioplasty (BPA); all the patients with PAH reported significant acute hemodynamic relief after a single inhalation of iloprost, fulfilling the criteria of responder. Standard 12‐lead ECG was performed before and after intervention.Results: The interval between baseline and control ECG in CTEPH and PAH groups was 28 (IQR: 17–36) months and 15 min (IQR: 11–17), respectively. Despite similar hemodynamic improvement in both groups, only the CTEPH group presented significant changes in most analyzed ECG parameters: T‐wave axis (p = .002), QRS‐wave axis (p = .012), P‐wave amplitude (p < .001) and duration in II (p = .049), R‐wave amplitude in V₁ (p = .017), R:S ratio in V₁ (p = .046), S‐wave amplitude in V₅ (p = .004), R‐wave amplitude in V₅ (p = .044), R:S ratio in V₅ (p = .004), S‐wave amplitude in V₆ (p = .026), R‐wave amplitude in V₆ (p = .01), and R‐wave amplitude in aVR (p = .031). In patients with PAH, significant differences were found only for P wave in II (duration: p = .035; amplitude: p = .043) and QRS axis (p = .018).Conclusions: The effective treatment of cPH ensures improvement in ECG parameters of RVH, but it requires extended time.

We present a case of a 67-year-old female with proximal chronic thromboembolic pulmonary hypertension (CTEPH), disqualified from pulmonary endarterectomy due to multiple comorbidities and high risk-to-benefit ratio as assessed by multidisciplinary CTEPH team. She was referred for balloon pulmonary angioplasty (BPA) and underwent three sessions with balloon catheters up to 8 mm diameter. During the second procedure, the elastic recoil phenomenon was observed in the treated post-thrombotic lesion of the right lower lobe artery, which made the balloon angioplasty ineffective. It was decided to implant a self-expanding stent for the prevention of restenosis. The procedure resulted in significant improvement of regional perfusion, as confirmed by control angiography. We feel that it contributed to the significant improvement of hemodynamic parameters and exercise capacity, as assessed three months after the last BPA procedure. In conclusion, pulmonary artery stenting may be an option in proximal CTEPH when elastic recoil phenomenon makes balloon angioplasty of a large vessel ineffective.