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Background: The effects of intraoperative fluid management on the patients with constrictive pericarditis undergoing pericardiectomy remain unclear. This study explored the relationship between intraoperative fluid management and postoperative outcomes in these patients. Methods: We retrospectively studied 92 patients with constrictive pericarditis undergoing pericardiectomy and assigned them to the restrictive group and the liberal group according to the intraoperative total fluid infusion rate. Postoperative outcomes were compared between the two groups. Binary logistic regression analysis was performed to determine the relationship between the intraoperative total fluid infusion rate and postoperative outcomes. Results: There were 46 (50.0%) cases in the restrictive group and 46 (50.0%) cases in the liberal group. Compared with the liberal group, the restrictive group had significantly lower incidences of postoperative complications and cardiac complications (P = 0.005 and P = 0.006, respectively). Binary logistics regression analysis also showed the increased risks of postoperative complications (OR, 3.551; 95% CI, 1.192-10.580; P = 0.023) and cardiac complications (OR, 6.037; 95% CI, 1.472-25.052; P = 0.013) at the liberal group. In addition, the restrictive group had shorter postoperative hospital stay (P = 0.026) in comparison to the liberal group. Conclusion: In patients with constrictive pericarditis undergoing pericardiectomy the intraoperative total fluid infusion rate was significantly associated with postoperative outcomes. Restrictive fluid management strategy was related to the positive effects on enhanced recovery after surgery and could be advised as the preferred intraoperative fluid management policy.
Heart failure is associated with exercise intolerance and sleep- disordered breathing; however, studies in patients with chronic constrictive pericarditis are scarce. The purpose of our study was to assess exercise capacity and sleep in patients with chronic constrictive pericarditis (CCP) undergoing a pericardiectomy.
The risk factors of postoperative outcomes after pericardiectomy in tuberculous constrictive pericarditis have still been unclear. This study aimed to investigate the predictors of postoperative complication and prolonged intensive care unit (ICU) stay in the patients with tuberculous constrictive pericarditis undergoing pericardiectomy.
Constrictive pericarditis (CP) usually presents as a result of chronic fibrous pericardial thickening and calcification of the pericardium which causes reduced cardiac output. Despite the lack of prospective studies comparing the different therapeutic strategies, surgical pericardiectomy is a valuable treatment under most circumstances.
This study aimed to evaluate the outcomes and complications of triple-combination surgery consisting of thoracic duct ligation (TDL), partial pericardiectomy (PPC), and cisterna chyli ablation (CCA) for the treatment of idiopathic chylothorax in dogs. Eleven privately owned dogs with idiopathic chylothorax underwent the triple-combination surgery: TDL and PPC were performed in left recumbency, followed by CCA in dorsal recumbency. Of the 11 dogs, seven were Shiba, two were Afghan hounds, and one each was Borzoi and mixed-breed. TDL and PPC required two intercostal thoracotomies in five dogs, whereas they were performed through a single intercostal incision in the other dogs. None of the dogs showed major intraoperative complications. The median operation time was 190 min (range, 151-234 min). Nine dogs showed no pleural effusion after surgery without medical management. Another dog showed the disappearance of chylous effusion, followed by the pleural accumulation of modified transudate. However, the residual one dog in whom chylothorax did not improve postoperatively died 4 months after the combination surgery. The mortality rate at the conclusion of this study was 9.1%. Although the triple-combination surgery with TDL, PPC, and CCA was complex and required a prolonged operation time, the success rate of resolving chylothorax in our study was comparable to that of open surgery as previously reported. Therefore, this study suggests that such triple-combination surgery can become one of the therapeutic options for the management of canine idiopathic chylothorax.
Background Galectin-3 (Gal-3) is a proinflammatory, profibrotic molecule implicated in the pathogenesis of heart failure. The role of Gal-3 in patients with chronic constrictive pericarditis (CCP) is not clear. Objective The aim of this study was to assess plasma Gal-3 in patients with CCP and correlate it with clinical, functional and histologic parameters. Methods We prospectively evaluated 25 symptomatic patients with CCP referred for pericardiectomy and 21 healthy controls. Patients underwent clinical assessment, Gal-3 and B-type natriuretic peptide (BNP) measurements, echocardiography, cardiac magnetic resonance imaging and cardiopulmonary exercise test (CPET) at baseline. Six months after pericardiectomy CPET was repeated. An alpha error < 5% was considered statistically significant, with a confidence interval of 95%. Results Twenty-five patients with a median age of 45 years were included. Etiology was mainly idiopathic (n = 19, 76%); and 14 (56%) patients had NYHA functional class III/IV. Median BNP and Gal-3 were 143 (89-209) pg/dL and 14.8 (9.7-17.2) ng/mL, respectively. Gal-3 levels were not significantly higher in CCP patients than in control (p = 0.22). There were no significant correlations of Gal-3 with BNP, echocardiographic and cardiac magnetic resonance measures and histological findings. After pericardiectomy, it was found a statistically significant correlation between Gal-3 and the CPTE measures test duration (r = -0.79; p < 0.001) and exercise time (r = -0.79; p < 0.001). Conclusions Patients with CCP had normal levels of Gal-3 as compared to the controls. Gal-3 did not correlate with morphological and functional measures before pericardiectomy. However, the associations between Gal-3 and exercise intolerance after pericardiectomy may suggest a role of Gal-3 in prognosis prediction after pericardiectomy. (Arq Bras Cardiol. 2020; 114(4):683-689).
Idiopathic pericarditis (IP) and pericardial mesothelioma (PM) are causes of pericardial effusion in dogs. Pericardiectomy can be a definitive treatment in the case of idiopathic pericardial effusion or a short-term intervention for mesothelioma. The aim of the present study was to investigate which histopathologic parameters are correlated with clinical outcomes in a cohort of dogs that underwent pericardiectomy. The histopathological findings of 22 IPs and 5 PMs were compared with clinical and survival data and the immunohistochemical characterization of immune cells (CD3, CD79α, Iba1). In IP, the mesothelium was lost in 20 cases, reactive in 9, atypical in 3, and mesothelial papillary hyperplasia (MPH) was observed in 4 cases. Numerous macrophages were found in both IPs and PMs especially at the superficial layer of the pericardium. T lymphocytes were observed in mild to moderate numbers and were more numerous than B lymphocytes in both IPs and PMs. MPH was correlated with the quantity of lymphoplasmacytic infiltrate in the superficial layer, inversely related to the thickness of the pericardium, and associated with a longer overall survival. Pericardial fibrosis was present in 19 out of 22 IPs and in all mesotheliomas and was correlated with increased time from initial presentation and pericardiectomy and lymphoplasmacytic infiltrate in the deep zone. Pericardial thickness was correlated with the amount of lymphoplasmacytic and macrophagic infiltrate in the deep zone. Mesothelioma was associated with an increased number of pericardiocentesis procedures before pericardiectomy and with the presence of macrophages in the superficial pericardial layer, edema, fibrin, and hemorrhage. Disease-free interval and overall survival were significantly shorter in patients with mesothelioma compared with IP.
Inflammatory responses play a critical role in left ventricular remodeling after acute myocardial infarction (AMI). NR4A3, a member of the NR4A orphan nucleus receptor family, has recently emerged as a therapeutic target for treatment of inflammation. This aim of this study is to explore the therapeutic effect of NR4A3 in cardiac remodeling post AMI. Male C57BL/6 mice were administered with lentiviral over-expression of NR4A3 (lenti-NR4A3) or empty vector (lenti-con) 7 days before coronary artery ligation. H9c2 cardiomyocytes deprived of serum were used to mimic ischemic conditions in vivo. Lenti-NR4A3 treatment significantly repressed neutrophil infiltration in the myocardium, reduced infarct size, and attenuated the reduction of left ventricular function after AMI. Furthermore, NR4A3 over-expression inhibited the NF-κB (IκB) signaling by decreasing IκBα phosphorylation and by inhibiting the translocation of p65 to the nucleus. Meanwhile, NR4A3 over-expression also increases the activity of JAK2-STAT3 signaling in mouse hearts after AMI. The inhibitory effect of NR4A3 on NF-κB activation was almost completely abolished by the JAK2 inhibitor AG490, indicating that NR4A3 prevented serum deprivation induced NF-κB activation in a STAT3 dependent manner. These findings provide novel evidence that NR4A3 could inhibit post-AMI inflammation responses via JAK2-STAT3/NF-κB signaling and may well be a therapeutic target for cardiac remodeling after AMI.
Purulent pericarditis is rarely encountered in the antibiotherapy era, mainly in immunosupressed patients, after cardiac operations, in septicemia. Diagnosis of purulent pericarditis is based upon the analysis of pericardial drainage, obtained through pericardiocentesis or preferably, through a surgical approach. The reported case has following peculiarities: clinical signs of false acute surgical abdomen; altered clinical and biological response to infection; Optimal treatment is early, efficient pericardial drainage, with low risk of tissue contamination and of pericardial constriction; Surgical subxyphoid pericardial drainage is prefered in patients with affected general status. Antero-(lateral) thoracic approach with associated anterior pericardiectomy ensures an efficient pericardial drainage and prevents pericardial constriction, with low risks for pleural contamination.
Occult or overt but delayed cardiac disease after thoracic radiotherapy for Hodgkin's disease may be common. Detailed cardiac evaluation was performed in 108 patients, mean age 46 +/- 6.2 years, with Hodgkin's disease at 175 +/- 43 months after irradiation. The study protocol included clinical examination, graded treadmill exercise test and echocardiography. Some patients with angina pectoris, previous myocardial infarction and an abnormal ECG were studied by thallium-201 scintigraphy, cardiac catheterization and coronary angiography. Cardiac disease was found in 12 patients (11%). Three patients had angina pectoris, one patient had myocardial infarction, two complained of dyspnea on effort and two had congestive heart failure. At catheterization, constrictive pericarditis was diagnosed in four patients; in two additional patients an occult constrictive pericarditis was found. One patient had both mitral and tricuspidal regurgitation and one had mitral regurgitation alone. Eight patients (7.4%) had severe coronary artery disease; four of these had associated constrictive pericarditis. Four patients had a pericardiectomy and another four had undergone coronary artery by-pass graft. Two patients died after operation from persistent pericardial constriction. It is concluded that the incidence of delayed cardiac disease after radiotherapy is relatively high; chronic pericardial disorders and coronary artery disease are the most frequent manifestations of this disease. Standard surgical treatment may be beneficial because of the relative youth of these patients.
Inflammation of the pericardium (pericarditis) is characterized by excruciating chest pain. This systematic literature review summarizes clinical, humanistic, and economic burdens in acute, especially recurrent, pericarditis, with a secondary aim of understanding United States treatment patterns and outcomes. Short-term clinical burden is well characterized, but long-term data are limited. Some studies report healthcare resource utilization and economic impact; none measure health-related quality-of-life. Pericarditis is associated with infrequent but potentially life-threatening complications, including cardiac tamponade (weighted average: 12.7% across 10 studies), constrictive pericarditis (1.84%; 9 studies), and pericardial effusion (54.7%; 16 studies). There are no approved pericarditis treatments; treatment guidelines, when available, are inconsistent on treatment course or duration. Most recommend first-line use of conventional treatments, for example, nonsteroidal antiinflammatory drugs with or without colchicine; however, 15-30% of patients experience recurrence. Second-line therapy may involve conventional therapies plus long-term utilization of corticosteroids, despite safety issues and the difficulty of tapering or discontinuation. Other exploratory therapies (eg, azathioprine, immunoglobulin, methotrexate, anakinra) present steroid-sparing options, but none are supported by robust clinical evidence, and some present tolerability challenges that may impact adherence. Pericardiectomy is occasionally pursued in treatment-refractory patients, although data are limited. This lack of an evidence-based treatment pathway for patients with recurrent disease is reflected in readmission rates, for example, 12.2% at 30 days in 1 US study. Patients with continued recurrence and inadequate treatment response need approved, safe, accessible treatments to resolve pericarditis symptoms and reduce recurrence risk without excessive treatment burden.
We find that cardiac group 2 innate lymphoid cells (ILC2s) are essential for the development of IL-33-induced eosinophilic pericarditis. We show a pathogenic role for ILC2s in cardiac inflammation, in which ILC2s activated by IL-33 drive the development of eosinophilic pericarditis in collaboration with cardiac fibroblasts. ILCs, not T and B cells, are required for the development of pericarditis. ILC2s transferred to the heart of Rag2-/-Il2rg-/- mice restore their susceptibility to eosinophil infiltration. Moreover, ILC2s direct cardiac fibroblasts to produce eotaxin-1. We also find that eosinophils reside in the mediastinal cavity and that eosinophils transferred to the mediastinal cavity of eosinophil-deficient ΔdblGATA1 mice following IL-33 treatment migrate to the heart. Thus, the serous cavities may serve as a reservoir of cardiac-infiltrating eosinophils. In humans, patients with pericarditis show higher amounts of ILCs in pericardial fluid than do healthy controls and patients with other cardiac diseases. We demonstrate that ILCs play a critical role in pericarditis.
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