A b s t r a c t Background and aim:To assess the safety and efficacy of a refined balloon pulmonary angioplasty (BPA) strategy in patients with chronic thromboembolic pulmonary hypertension (CTEPH).Methods: There were 157 BPA sessions performed in 56 CTEPH patients (47 non-operable, nine after pulmonary endarterectomy; aged 58.6 ± 17.9 years; 28 females) with severely impaired pulmonary haemodynamics (mean pulmonary artery pressure [mPAP]: 51.3 ± 12.2 mm Hg, pulmonary vascular resistance [PVR]: 10.1 ± 3.9 Wood Units). The first 50 sessions aimed to recanalise chronic occlusions and prevent reocclusion with aggressive anticoagulation. The next 107 sessions aimed to relieve "web" and "ring" lesions using reduced tip load guidewires and less intensive anticoagulation.Results: There was significant reduction in haemoptysis (22% vs. 7%, p = 0.01), vessel injury (30% vs. 13%, p = 0.01), and reperfusion pulmonary injuries (22% vs. 4%, p = 0.01) after changing the BPA strategy. Mortality at 14 days was also reduced (6% vs. 0%; p = 0.05). The cumulative survival rate was 94.6% at 24 months after the first BPA, which was more favourable than medically treated historic controls. In the 31 patients with > 3 BPA sessions, there was significant reduction of PVR (10.3 ± 3.7 vs. 5.9 ± 2.8 Wood Units; p = 0.01), mPAP (50.7 ± 10.8 vs. 35.6 ± 9.3 mm Hg; p = 0.01) and improvement in World Health Organisation functional class (3.19 ± 0.48 vs. 1.97 ± 0.80; p < 0.001).Conclusions: Balloon pulmonary angioplasty improves haemodynamics and outcome but requires refined strategy to limit early complication rate.

Outcomes of COVID-19 in patients vaccinated and unvaccinated against SARS-CoV-2 and suffering from pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension

INTRODUCTION Balloon pulmonary angioplasty (BPA) is a treatment option for a patient with chronic thromboembolic pulmonary hypertension. OBJECTIVES We aimed to investigate the evolution of electrocardiographic (ECG) markers of right ventricular hypertrophy (RVH) after BPA. PATIENTS AND METHODS Standard 12-lead ECG was performed in 41 patients with chronic thromboembolic pulmonary hypertension before the first BPA and after completion of treatment. RESULTS In the whole study group, the percentage change in the pulmonary vascular resistance (PVR) after BPA correlated with the percentage change in the values of the following ECG parameters (P <0.05): axis of the QRS (rho = 0.530) and T wave (rho = 0.372); P wave in leads II (rho = 0.340) and III (rho = 0.430); S wave in lead V 5 (rho = 0.634); R/S ratio in lead V 5 (rho =-0.636); S wave in lead V 6 (rho = 0.508); S wave in lead I (rho = 0.496). Then, the group was divided into 2 subgroups: group A, defined as a drop in PVR greater than the median value (49%) for the whole study population; and group B, defined as a drop in PVR below the median value. In group A, the following parameters changed after BPA: T-wave axis (P <0.001), P wave in lead II (P <0.001), S wave in lead V 5 (P <0.001), R/S ratio in lead V 5 (P <0.001). In group B, despite some hemodynamic and functional improvement, there were no differences in ECG markers of RVH after BPA. CONCLUSIONS An improvement in RVH parameters can be observed on ECG after a hemodynamically effective BPA.

Background: The aim of the study was to assess soluble ST2 (sST2) concentration and its dynamic changes in the periprocedural period in patients with chronic thromboembolic pulmonary hypertension (CTEPH) treated with balloon pulmonary angioplasty (BPA). Methods: We prospectively analyzed 57 procedures of BPA performed in 37 patients with CTEPH. Biomarkers, such as N-terminal pro B-type natriuretic peptide (NT-proBNP), troponin T (TnT), and sST2 were assessed at four time points: Before the BPA procedure, 24 h and 48 h after the procedure, and at the discharge from hospital. Each postprocedural period was assessed for complications. Results: Before the BPA procedure, median sST2 concentration was 26.56 ng/mL (IQR: 16.66–40.83 ng/mL). sST2 concentration was significantly higher 24 h and 48 h after the BPA compared to the baseline measurements (33.31 ng/mL (IQR: 20.81–62.56), p = 0.000 and 27.45 ng/mL (IQR: 17.66–54.45), p = 0.028, respectively). sST2 level 24 h after the BPA procedure was significantly higher in the group with complications compared to the group without complications in the postprocedural period (97.66 ng/mL (IQR: 53.07–126.18) vs. 26.86 ng/mL (IQR: 19.10–40.12), p = 0.000). Conclusions: sST2 concentration in patients with CTEPH treated with BPA changes significantly in the postprocedural period and is significantly higher in the group with complications in postprocedural period.

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.

Effective targeted therapy of pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH) requires regular risk stratification. Among many prognostic parameters, three hemodynamic indices: right atrial pressure, cardiac index, and mixed venous saturation are considered critically important for correct risk classification. All of them are measured invasively and require right heart catheterization (RHC). The study was aimed to verify assumption that a model based on non-invasive parameters is able to predict hemodynamic profile described by the mentioned invasive indices. A group of 330 patients with pulmonary hypertension was used for the selection of the best predictors from the set of 17 functional, biochemical, and echocardiographic parameters. Multivariable logistic regression models for the prediction of low-risk and high-risk profiles were created. The cut-off points were determined and subsequent validation of the models was conducted prospectively on another group of 136 patients. The ROC curve analysis showed the very good discrimination power of the models (AUC 0.80–0.99) in the prediction of the hemodynamic profile in the total validation group and subgroups: PAH and CTEPH. The models indicated the risk profiles with moderate sensitivity (57–60%) and high specificity (87–93%). The method enables estimation of the hemodynamic indices when RHC cannot be performed.

. Conclusion: Efficacy of rescue intrapericardial chemotherapy with cisplatin is independent of parameters of hemodynamic instability and levels of inflammatory markers in recurrent pericardial effusion.Pericardial diseases constitute an infrequent, although very serious clinical problem among oncological patients. They practically always cause deterioration of the patient's quality of life. The increasing amount of pericardial effusion and the resulting cardiac tamponade is a life-threatening condition which requires urgent diagnostics and treatment.The European Society of Cardiology (ESC) Position Paper related to cardio-oncology summarizes the knowledge on acute and chronic pericarditis as the complication resulting from anticancer treatment: some cytotoxic drugs and radiotherapy (1). Experts indicate that pericardial complications in oncology are usually associated with mediastinal tumors occupying the pericardium. The document does not discuss the issue of pericardial effusion as a potential manifestation of malignant tumor progression. The present state of knowledge concerning malignant pericarditis is based on several retrospective studies and descriptions of small groups of patients. This article presents our own prospective experience related to the treatment of patients suffering from recurrent pericardial effusion and hemodynamic instability in the course of malignant disease.The primary purpose of the observation was the assessment of determinants of overall survival of oncological patients subject to emergency pericardiocentesis and intrapericardial chemotherapy with the use of cisplatin due to recurrent symptomatic pericardial effusion and cardiac tamponade.The detailed aims included the identification of factors which could have direct impact on the overall survival of patients, these included among others: complications of pericardiocentesis and cisplatin administered intrapericardially; signs of inflammatory process: pericardial effusion culture test results, fever, white blood cell count; hemodynamic conditions: baseline level of N-terminal pro-B type natriuretic peptide (NTproBNP), volume and duration of pericardial drainage; interval for recurrence pericardial effusion; possibility of further anticancer treatment. 373

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