Background: Post-infarction left ventricular (LV) pseudoaneurysm is a rare mechanical complication of myocardial infarction that carries a substantial risk of sudden rupture. The purpose of this study was to compare the surgical results of post-infarction LV pseudoaneurysm with those of conservative treatment.Methods: From 2016 to 2021, 22 patients were hospitalized for LV pseudoaneurysm, including 17 cases (77.3%) caused by myocardial infarction. Of the 17 patients, 10 (58.8%) underwent surgical repair, while seven (41.2%) were treated medically. The clinical course, echocardiograph data, and surgical outcomes were analyzed. Survival rates of the surgical and conservative groups were compared.Results: There were no perioperative deaths. Intra-aortic balloon pumping support was required in two (20%) patients. No follow-up mortality was observed in the surgical group and at the last follow-up, all the patients were classified as New York Heart Association class I–II. In the conservative group, there was one (14.3%) hospital death and two (28.6%) additional deaths during follow-up. A significant difference was found in survival between the two groups (P = 0.024).Conclusions: Surgical repair of post-infarction LV pseudoaneurysm can be performed with good results, while conservative treatment carries a significant risk of sudden death. Surgical repair is indicated for every patient diagnosed, even those with a small pseudoaneurysm without symptoms.

Myocardial fibrosis is a pathological feature of doxorubicin-induced chronic cardiotoxicity that severely affects the prognosis of oncology patients. However, the specific cellular and molecular mediators driving doxorubicin-induced cardiac fibrosis, and the relative impact of different cell populations on cardiac fibrosis, remain unclear.This study aimed to explore the mechanism of doxorubicin-induced cardiotoxicity and myocardial fibrosis and to find potential therapeutic targets. Single-cell RNA sequencing was used to analyze the transcriptome of non-cardiomyocytes from normal and doxorubicin-induced chronic cardiotoxicity in mouse model heart tissue.We established a mouse model of doxorubicin-induced cardiotoxicity with a well-defined fibrotic phenotype. Analysis of single-cell sequencing results showed that fibroblasts were the major origin of extracellular matrix in doxorubicin-induced myocardial fibrosis. Further resolution of fibroblast subclusters showed that resting fibroblasts were converted to matrifibrocytes and then to myofibroblasts to participate in the myocardial remodeling process in response to doxorubicin treatment. Ctsb expression was significantly upregulated in fibroblasts after doxorubicin-induced.This study provides a comprehensive map of the non-cardiomyocyte landscape at high resolution, reveals multiple cell populations contributing to pathological remodeling of the cardiac extracellular matrix, and identifies major cellular sources of myofibroblasts and dynamic gene-expression changes in fibroblast activation. Finally, we used this strategy to detect potential therapeutic targets and identified Ctsb as a specific target for fibroblasts in doxorubicin-induced myocardial fibrosis.

Pulmonary artery sarcoma (PAS) is a rare and devastating disease. The diagnosis is often delayed, and optimal treatment remains unclear. The aim of this study is to report our experience in the surgical management of this disease. Between 2000 and 2018, 17 patients underwent operations for PAS at our center. The medical records were retrospectively reviewed to evaluate the clinical characteristics, operative findings, the postoperative outcomes, and the long‐term results. The mean age at operation was 46.0 ± 12.4 years (range, 26–79 years), and eight (47.1%) patients were male. Six patients underwent tumor resection alone, whereas the other 11 patients received pulmonary endarterectomy (PEA). There were two perioperative deaths. Follow‐up was completed for all patients with a mean duration of 23.5 ± 17.6 months (1–52 months). For all 17 patients, the median postoperative survival was 36 months, and estimated cumulative survival rates at 1, 2, 3, and 4 years were 60.0%, 51.4%, 42.9%, and 21.4%, respectively. The mean survival was 37.0 months after PEA and 14.6 months after tumor resection only (p = 0.046). Patients who had no pulmonary hypertension (PH) postoperatively were associated with improved median survival (48 vs. 5 months, p = 0.023). In conclusion, PAS is often mistaken for chronic pulmonary thromboembolism. The prognosis of this very infrequent disease remains poor. Early detection is essential for prompt and best surgical approach, superior to tumor resection alone, and PEA surgery with PH relieved can provide better chance of survival.

Introduction: Hypertensive nephropathy is characterized by glomerular and tubulointerstitial damage, but we know little about changes in cell-specific gene expression in the early stages of hypertensive kidney injury, which usually has no obvious pathological changes. Methods: We performed unbiased single-cell RNA sequencing of rat kidney samples from hypertensive kidney injury to generate 10,602 single-cell transcriptomes from 2 control and 2 early stage hypertensive kidney injury samples. Results: All major cell types of the kidney were represented in the final dataset. Side-by-side comparisons showed that cell type-specific changes in gene expression are critical for functional impairment of glomeruli and tubules and activation of immune cells. In particular, we found a significantly reduced gene expression profile of maintaining vascular integrity in glomerular cells of hypertensive kidney injury. Meanwhile, the expression of genes associated with oxidative stress injury and fibrosis in the renal tubules and collecting ducts was elevated, but the degree of tubular cells response to injury differed between parts. We also found a signature of immune cell infiltration in hypertensive kidney injury. Conclusion: Exploring the changes of gene expression in hypertension-injured kidneys may be helpful to identify the early biomarkers and signal pathways of this disease. Our data provide rich resources for understanding the pathogenesis of hypertensive renal injury and formulating effective treatment strategies.

Background and Aims: While surgical left atrial appendage occlusion (SLAAO) reduces stroke in atrial fibrillation (AF) patients, its efficacy in patients without pre-operative AF but with CHA₂DS₂-VASc ≥2 remains uncertain despite their high post-operative AF risk (15–54%). The aim of this study was to evaluate whether prophylactic SLAAO reduces post-operative thrombo-embolic events in valvular surgery patients. Methods: The OPINION was a multicentre, open-label, randomized, superiority trial conducted at three cardiac surgery centres in China. Eligible non-AF patients with CHA₂DS₂-VASc ≥2 and an indication for valve repair or replacement due to mitral or aortic valve lesions were randomly assigned (1:1) to undergo SLAAO (intervention arm) or not undergo SLAAO (control arm) during surgery. The primary outcome was a composite of ischaemic stroke, transient ischaemic attack (TIA), or cardiovascular mortality assessed at 1 year. The primary analysis was done in the intention-to-treat population. Results: Between April 2021 and June 2024, a total of 2157 patients were enrolled and randomized. After exclusion of 39 patients who withdrew informed consent, 2118 participants were included in the intention-to-treat population (1062 in the SLAAO group and 1056 in the control group). Baseline characteristics were well-balanced between the SLAAO group and control group (mean age 55.5 [11.4] vs 55.6 [11.5] years, P = .65; female 32.9% vs 32.3%, P = .78; CHA2DS2-VASc score 2.88 [0.98] vs 2.87 [0.96], P = .83; median EuroSCORE II 1.58% [1.42%] vs 1.56% [1.28%], P = .74). The 1-year primary endpoint occurred in 73 (6.9%) patients in the SLAAO group and in 87 (8.2%) patients in the control group (hazard ratio 0.83; 95% confidence interval 0.61–1.14; P = .25). Conclusions: For valvular surgery patients with CHA₂DS₂-VASc scores ≥2 but no pre-operative AF, routine prophylactic left atrial appendage closure did not significantly reduce the incidence of the primary composite endpoint (ischaemic stroke, TIA, and cardiovascular mortality) at 1-year follow-up. Trial Registration: ChiCTR.org registry ChiCTR2100042238

Background: The definitive treatment for chronic thromboembolic pulmonary hypertension (CTEPH) is pulmonary endarterectomy (PEA), which has good long‐term outcomes. However, after surgery, a quarter of the patients still have residual pulmonary hypertension (RPH). In pulmonary hemodynamics, there are no unified criteria for RPH, even though the level may affect long‐term survival.Methods: Between March 1997 and December 2021, 253 CTEPH patients were treated at our center with PEA. Patients were evaluated retrospectively and classified into early (1997–2014) and late (2015–2021) groups. The clinical characteristics and perioperative outcomes of the two groups were compared, and risk factor analysis for RPH and long‐term survival for all cases was performed.Results: There was no statistically significant difference in demographics between the two groups. However, the Early Group had a significantly higher rate of perioperative death (9.8% vs. 1.2%, p = .001), RPH (48.8% vs. 14.0%, p < .001), and reperfusion pulmonary edema (18.3% vs. 2.9%, p < .001). The median follow‐up time was 66.0 months, and overall survival rates at 5, 10, 15, and 18 years after PEA were 91.2%, 83.9%, 64.5%, and 46.0%, respectively. Age and postoperative systolic pulmonary artery pressure (sPAP) were independently related to long‐term outcomes in the multivariate Cox analyses. Patients with postoperative sPAP less than 46 mm Hg had a higher chance of survival.Conclusions: PEA improved CTEPH hemodynamics immediately and had a positive effect on long‐term survival. Patients with postoperative sPAP ≥ 46 mm Hg indicate clinically significant RPH and have a lower long‐term survival rate.