Background: For patients with high-risk pulmonary artery embolism (PE), catheter-directed therapies pose a viable alternative treatment option to systemic thrombolysis or anticoagulation. Right now, there are multiple devices available which have been proven to be safe and effective in lower-risk settings. There is, however, little data comparing their efficacies in high-risk PE. Methods: We performed a retrospective, single-center study on patients with high-risk PE undergoing catheter interventional treatment. Patients receiving large-bore catheter thrombectomy were compared to patients receiving alternative treatment forms. Results: Of the 20 patients included, 9 received large-bore thrombectomy, and 11 received alternative interventional treatments. While the baseline characteristics were comparable between the two groups, periprocedural and in-hospital mortality tended to be significantly lower with large-bore thrombectomy when compared to other treatment forms (0 vs. 55% and 33 vs. 82%, p = 0.07 and 0.01, respectively). Conclusions: In this small, retrospective study, large-bore thrombectomy was associated with lower mortality as compared to alternative treatment forms. Future prospective research is needed to corroborate these findings.
Left atrial (LA) reservoir strain provides prognostic information in patients with and without heart failure (HF), but might be altered by atrial fibrillation (AF). The aim of the current study was to investigate changes of LA deformation in patients undergoing cardioversion (CV) for first-time diagnosis of AF.We performed 3D-echocardiography and strain analysis before CV (Baseline), after 25 ± 10 days (FU-1) and after 190 ± 20 days (FU-2). LA volumes, reservoir, conduit and active function were measured. In total, 51 patients were included of whom 35 were in SR at FU-1 (12 HF and preserved ejection fraction (HFpEF)), while 16 had ongoing recurrence of AF (9 HFpEF). LA maximum volume was unaffected by cardioversion (Baseline vs. FU-2: 41 ± 11 vs 40 ± 10 ml/m2; p = 0.85). Restored SR led to a significant increase in LA reservoir strain (Baseline vs FU-1: 12.9 ± 6.8 vs 24.6 ± 9.4, p < 0.0001), mediated by restored LA active strain (SR group Baseline vs. FU-1: 0 ± 0 vs. 12.3 ± 5.3%, p < 0.0001), while LA conduit strain remained unchanged (Baseline vs. FU-1: 12.9 ± 6.8 vs 13.1 ± 6.2, p = 0.78). Age-controlled LA active strain remained the only significant predictor of LA reservoir strain on multivariable analysis (β 1.2, CI 1.04-1.4, p < 0.0001). HFpEF patients exhibited a significant increase in LA active (8.2 ± 4.3 vs 12.2 ± 6.6%, p = 0.004) and reservoir strain (18.3 ± 5.7 vs. 22.8 ± 8.8, p = 0.04) between FU-1 and FU-2, associated with improved LV filling (r = 0.77, p = 0.005).Reestablished SR improves LA reservoir strain by restoring LA active strain. Despite prolonged atrial stunning following CV, preserved SR might be of hemodynamic and prognostic benefit in HFpEF.
Venous thromboembolism presenting as deep vein thrombosis or pulmonary embolism (PE) remains to be an important cause of mortality and morbidity worldwide. Despite its significance and incidence, compared to many other cardiovascular conditions there are significant gaps in knowledge in many aspects of it, including its pathophysiology. A rare sequela of PE is chronic thromboembolic pulmonary hypertension (CTEPH). This complication has a poor outcome and data is scarce in this field. Many therapeutic approaches are based solely on clinical expertise, which can be explained by the complex and not fully understood pathobiology of this disease. Over the years, many theories have been proposed regarding its genesis. Although generally acute PE is accepted as a trigger for CTEPH, this condition is multifactorial and cannot be explained by recurring PEs only. By reviewing the current evidence, we have demonstrated that thrombus non-resolution in CTEPH is due to multiple mechanisms and predisposing factors including: inflammation, small-vessel disease, impaired angiogenesis, platelet dysfunction, coagulopathies, malignancy, impaired fibrinolysis, genetics and many other components. Based on the current evidence, we aimed to explain the pathophysiology CTEPH, PE and the connection between these two important diseases. Furthermore, we highlight the negative hemodynamic effects of CTEPH and PE on the right ventricle and its role in further exacerbation of these patients.
Abstract Acute pulmonary embolism is a life-threatening condition caused by the thromboembolic obstruction of pulmonary arteries, which often leads to hemodynamic instability, right ventricular failure, and potentially death. Patients with massive or high-risk PE are particularly vulnerable and may not respond to conventional treatments, necessitating the implementation of mechanical circulatory support. Here, we discuss recent advancements in the diagnosis and multidisciplinary management of patients with high-risk PE and highlight the need for rapid and personalized treatment strategies.
