Background: The presence of constrictive pericarditis (CP) in conjunction with tricuspid regurgitation (TR) and the worsening of TR following pericardiectomy are associated with a reduction in patient survival. The purpose of this study was to investigate the prevalence of tuberculous CP in conjunction with TR, the incidence of worsening regurgitation following pericardiectomy, and the analysis of associated factors. Methods: Seventy-five consecutive patients who underwent pericardiectomy for tuberculous CP at the institution between January 2021 and December 2023 were retrospectively analyzed. Their clinical, imaging, and hemodynamic characteristics were analyzed. Results: Among the 75 patients with tuberculous CP, 29 patients (38.7%) had mild or greater TR preoperatively and 27 patients (36%) had worsening TR after pericardiectomy. In patients with worsening TR, the pericardial thickness of the right ventricular (RV) lateral wall was significantly thickened preoperatively, and there was a reduction in the tricuspid annular plane systolic excursion (TAPSE), right ventricle S’ tissue Doppler velocity (S’), and right ventricle fractional area change (FAC) postoperatively. The preoperative inferior vena cava diameter and the postoperative right atrial and RV basal diameters were significantly larger in patients with worsening TR compared with patients with non-worsening TR, whereas the TAPSE, S’, and FAC were significantly lower before and after the surgery (P < .05). The FAC [OR = 0.354; 95% CI (0.165-0.761), P = .008] and pericardial thickness of the RV lateral wall [OR = 1.887; 95% CI (1.206-2.953), P = .005] were independently associated with worsening TR. Conclusion: Patients with tuberculous CP often have coexisting TR, and pericardiectomy can lead to worsening TR. The pericardial thickness of the RV lateral wall and FAC are independently associated with worsening TR following pericardiectomy.

To the Editor, The authors 1 are thanked for their interest and valuable comments on the article "Tricuspid Regurgitation in Tuberculous Constrictive Pericarditis Underwent Pericardiectomy." 2 Tuberculosis infection is the main cause of constrictive pericarditis (CP) in developing countries, accounting for approximately 38%-83% of all CP cases. Currently, pericardiectomy is the only effective treatment for CP. 3 Studies have shown that both CP combined with tricuspid regurgitation (TR) and worsening TR due to pericardiectomy reduce long-term survival. This phenomenon that deserves attention in the preoperative evaluation by surgeons. 4-7 There is no consensus on the mechanism of coexisting TR in CP. It is believed that TR is secondary to the structural and functional remodeling of the patient's right atrium and right ventricle during the pathological processes of CP and that the patient's combination of underlying diseases, such as arrhythmia, pacemaker implantation, and chronic lung disease, is an important influencing factor. In tuberculous CP, the presence of inflammatory factors that damage the valvular apparatus deserves further research and discussion. In CP, worsening TR is associated with right ventricular systolic dysfunction. Meanwhile, impaired right ventricular systolic function complicates the treatment of pericardiectomy and reduces long-term patient survival. This makes a detailed assessment of right ventricular morphology and function particularly important. Currently, echocardiographic assessment of right ventricular systolic function is mainly based on right ventricular fractional area change, tricuspid annular plane systolic excursion, and right ventricular S' tissue Doppler velocity, as mentioned in the article, but it can be considered using speckle tracking imaging, 3-dimensional echocardiography or even magnetic resonance imaging to assess right ventricular morphology, local myocardial function, and degree of fibrosis in detail. Thank you again for agreeing with the viewpoint of the article. For tuberculosis CP, we will prospectively study the patients through various aspects, including clinical, blood biochemical, multimodal imaging, and prognostic aspects, to understand the mechanism of worsening TR and the factors and extent of right ventricular myocardial injury. This will provide more information for surgical strategies and improve the long-term prognosis of patients.

Tuberculous pericarditis (TP) can progress to tuberculous constrictive pericarditis (TB-CP), a life-threatening fibrotic syndrome. However, the cellular architecture and intercellular circuits that link granulomatous inflammation to pericardial fibrosis remain poorly defined. We performed single-cell RNA sequencing (scRNA-seq) on 81,634 cells from surgically resected pericardium of six patients with TB-CP and three normal controls. Ligand-receptor and trajectory analyses were integrated with spatial transcriptomics, histology, immunohistochemistry, and multiplex immunofluorescence to map cell states, signalling pathways, and immune-stromal niches in situ. We generated an integrated single-cell and spatial atlas of the human pericardium in TB-CP, delineating 14 major cell types and heterogeneous transcriptional programmes associated with granuloma formation, vascular remodelling, and fibrotic activation. Spatial mapping revealed MMP9⁺ macrophage-rich granulomatous cores surrounded by infiltrating CCL19⁺ fibroblasts and T cells. In parallel, S100A4⁺ endothelial cells displayed endothelial-to-mesenchymal transition-like programmes and trajectories converging on ACTA2⁺ myofibroblasts, supported by immune cell-derived TGF-β and VEGF signalling. Ligand-receptor analysis and spatial co-localisation suggested macrophages may act as hubs that couple immune activation to endothelial reprogramming, fibroblast activation, and T-cell recruitment within fibrotic lesions. This human atlas defines the cellular landscape and key intercellular circuits underlying the immunopathogenesis of TB-CP. Our findings show that a spatially organised immune-endothelial-fibroblast network is associated with pericardial fibrosis and nominate VEGF/TGF-β pathways and associated cell states as potential biomarkers and therapeutic targets. National Natural Science Foundation of China (82270486 to F.X.); Science and Technology Bureau of Sichuan Province (2021YFS0051, 2024YFFK0209 to Y.W.; 2024NSFC0646 to F.X.).

Background/Objectives: Tuberculous constrictive pericarditis (TCP) is characterized by “backward failure” and systemic venous congestion, leading to secondary multi-organ dysfunction. The Model for End-Stage Liver Disease (MELD) 3.0 score assesses liver, renal, and nutritional status, yet its prognostic utility in TCP remains undefined. This study aimed to evaluate the preoperative MELD 3.0 score as a predictor of time to discharge in patients undergoing pericardiectomy for TCP. Methods: We analyzed 190 patients undergoing pericardiectomy for TCP between 2018 and 2024. The association between preoperative MELD 3.0 scores and time to discharge (ICU, postoperative, and total) was assessed using Fine–Gray competing risks regression to account for in-hospital mortality. Models were adjusted for age, albumin, and anti-tuberculosis therapy. Results: Each unit increase in MELD 3.0 was associated with higher operative mortality (OR 1.21, p = 0.013). In multivariable analysis, a high MELD 3.0 score (>median 9.6) was independently associated with a lower probability of discharge (i.e., delayed discharge) for total hospital stay (subdistribution hazard ratio [sHR] 0.606, 95% CI 0.453–0.811), postoperative stay (sHR 0.665), and ICU stay (sHR 0.658). Preoperative albumin was also a strong predictor of faster discharge. Conclusions: The preoperative MELD 3.0 score independently predicts delayed hospital discharge after pericardiectomy for TCP, even when accounting for mortality risk. It serves as a pragmatic tool for quantifying the systemic burden of congestion and stratifying perioperative risk.

Objective: New-onset persistent left bundle branch block (LBBB) following transcatheter aortic valve replacement (TAVR) is an independent predictor of long-term cardiovascular mortality in patients. The aim of this study is to evaluate the impact of new-onset LBBB on early cardiac reverse remodeling and clinical outcomes after TAVR. Methods: A retrospective analysis was performed on 101 patients who underwent successful TAVR for severe aortic stenosis between March 2021 and October 2024 at our institution. Echocardiographic variables indicative of cardiac remodeling were analysed preoperatively and at one and six months after TAVR. Furthermore, the clinical outcomes of the patients were monitored during the follow-up period. Result: Of the 101 patients who underwent TAVR, 28 (27.7%) had new-onset LBBB. Transcatheter heart valve(THV) implantation depth was an influential factor for new LBBB, which was more prevalent in patients with thinner interventricular septal thickness preoperatively. At the six-month follow-up, the new-LBBB group showed an increase in left ventricular diameter and left ventricular mass index and a reduction in left ventricular ejection fraction compared with the preoperative period. Mitral regurgitation in the no-LBBB group was significantly reduced at 1 month postoperatively. In contrast, mitral regurgitation in new-LBBB group was reduced at one month postoperatively, but worsened at six months.There was no significant difference in rehospitalization rates within 6 months postoperatively between patients with or without LBBB. Conclusions: New-onset persistent LBBB after TAVR did not affect short-term rehospitalization, but may adversely affect early postoperative reversal of cardiac remodeling.