Surgical management of cardiac tamponade: Is left anterior minithoracotomy really safe and effective?

Objective: Cardiac tamponade is a life-threatening clinical entity that requires an emergency treatment. Cardiac tamponade can be caused both by benign and malignant diseases. A variety of methods have been described for the treatment of these cases from needle-guided pericardiocentesis, balloon-based techniques to surgical pericardiotomy. The Authors report their experience in surgical management of cardiac tamponade and an exhaustive review of literature. Methods: This study involved 61 patients (37 males and 24 females) with an average age of 61.80 ± 16.32 years. All patients underwent emergency surgery due to the presence of cardiac tamponade. Results: Cardiac tamponade was caused by a benign disease in 57.40% of patients. In cancer patients group, lung cancer, breast cancer and malignant pleural mesothelioma were the most common neoplasms (17-27, 87%). The average preoperative size of pericardial effusion at M-2D echocardiography was 30.15 ± 5.87 mm. Postoperative complications were observed in 11 patients (18%). The reoperation rate was 3.3% (2 patients) due to relapsed cardiac tamponade. 30-day mortality rate was 3.3%. Overall cumulative survival was 29.9 ± 20.1 months. Twenty-nine patients (47.5%) died during the follow up period. By dividing the population into two groups, group B (benign) and group M (malignant), there was a statistically significant difference (P<0.001) in terms of survival. Conclusion: In conclusions, anterior minithoracotomy for surgical treatment of cardiac tamponade has to be held into account in patients both with benign diseases and malignancies. Keywords: Cardiac tamponade, Minithoracotomy, Pericardial malignancies, Overall surviva

Mechanisms of endothelial cell dysfunction in cystic fibrosis

Although cystic fibrosis (CF) patients exhibit signs of endothelial perturbation, the functions of the cystic fibrosis conductance regulator (CFTR) in vascular endothelial cells (EC) are poorly defined. We sought to uncover biological activities of endothelial CFTR, relevant for vascular homeostasis and inflammation. We examined cells from human umbilical cords (HUVEC) and pulmonary artery isolated from non-cystic fibrosis (PAEC) and CF human lungs (CF-PAEC), under static conditions or physiological shear. CFTR activity, clearly detected in HUVEC and PAEC, was markedly reduced in CF-PAEC. CFTR blockade increased endothelial permeability to macromolecules and reduced trans‑endothelial electrical resistance (TEER). Consistent with this, CF-PAEC displayed lower TEER compared to PAEC. Under shear, CFTR blockade reduced VE-cadherin and p120 catenin membrane expression and triggered the formation of paxillin- and vinculin-enriched membrane blebs that evolved in shrinking of the cell body and disruption of cell-cell contacts. These changes were accompanied by enhanced release of microvesicles, which displayed reduced capability to stimulate proliferation in recipient EC. CFTR blockade also suppressed insulin-induced NO generation by EC, likely by inhibiting eNOS and AKT phosphorylation, whereas it enhanced IL-8 release. Remarkably, phosphodiesterase inhibitors in combination with a β2 adrenergic receptor agonist corrected functional and morphological changes triggered by CFTR dysfunction in EC. Our results uncover regulatory functions of CFTR in EC, suggesting a physiological role of CFTR in the maintenance EC homeostasis and its involvement in pathogenetic aspects of CF. Moreover, our findings open avenues for novel pharmacology to control endothelial dysfunction and its consequences in CF

Conventional vs. extended D2 lymphadenectomy in gastric cancer patients: less is more?—more or less

n/

Surgical management of cardiac tamponade: Is left anterior minithoracotomy really safe and effective?

Objective: Cardiac tamponade is a life-threatening clinical entity that requires an emergency treatment. Cardiac tamponade can be caused both by benign and malignant diseases. A variety of methods have been described for the treatment of these cases from needle-guided pericardiocentesis, balloon-based techniques to surgical pericardiotomy. The Authors report their experience in surgical management of cardiac tamponade and an exhaustive review of literature. Methods: This study involved 61 patients (37 males and 24 females) with an average age of 61.80 ± 16.32 years. All patients underwent emergency surgery due to the presence of cardiac tamponade. Results: Cardiac tamponade was caused by a benign disease in 57.40% of patients. In cancer patients group, lung cancer, breast cancer and malignant pleural mesothelioma were the most common neoplasms (17-27, 87%). The average preoperative size of pericardial effusion at M-2D echocardiography was 30.15 ± 5.87 mm. Postoperative complications were observed in 11 patients (18%). The reoperation rate was 3.3% (2 patients) due to relapsed cardiac tamponade. 30-day mortality rate was 3.3%. Overall cumulative survival was 29.9 ± 20.1 months. Twenty-nine patients (47.5%) died during the follow up period. By dividing the population into two groups, group B (benign) and group M (malignant), there was a statistically significant difference (P < 0.001) in terms of survival. Conclusion: In conclusions, anterior minithoracotomy for surgical treatment of cardiac tamponade has to be held into account in patients both with benign diseases and malignancies

Establishment and long-term culture of human cystic fibrosis endothelial cells

Endothelial cell (EC) dysfunction has been reported in cystic fibrosis (CF) patients. Thus, the availability of CF EC is paramount to uncover mechanisms of endothelial dysfunction in CF. Using collagenase digestion, we isolated cells from small fragments of pulmonary artery dissected from non-CF lobes or explanted CF lungs. These cells were a heterogeneous mixture, containing variable percentages of EC. To obtain virtually pure pulmonary artery endothelial cells (PAEC), we developed an easy, inexpensive, and reliable method, based on the differential adhesion time of pulmonary artery cells collected after collagenase digestion. With this method, we obtained up to 95% pure non-CF and CF-PAEC. Moreover, we also succeed at immortalizing both PAEC and CF-PAEC, which remained viable and with unchanged phenotype and proliferation rate over the 30th passage. These cells recapitulated cystic fibrosis transmembrane conductance regulator expression and functions of the parental cells. Thus, we isolated for the first time endothelial cells from CF patients, providing a valuable tool to define the emerging role of EC in CF lung and vascular disease