Tamponada serca jako powikłanie implantacji elektrod o aktywnej fiksacji

W pracy zaprezentowano dwa przypadki wystąpienia wczesnej tamponady serca po udanej implantacji stymulatora serca oraz kardiowertera-defibrylatora z użyciem elektrod o aktywnej fiksacji. W obu przypadkach po zabiegu implantacji w badaniu echokardiograficznym ujawniono istotną ilość płynu w worku osierdziowym. U jednej pacjentki nie wykazano perforacji wolnej ściany mięśnia sercowego, wykonano perikardiotomię z następowym 24-godzinnym drenażem worka osierdziowego bez repozycji elektrod. U drugiej chorej wykonano nakłucie worka osierdziowego z drenażem osierdzia, a po potwierdzeniu perforacji wolnej ściany prawej komory, elektrodę reponowano przeznaczyniowo z worka osierdziowego do przegrody międzykomorowej w warunkach kardiochirurgicznej sali operacyjnej. W niniejszej pracy przeanalizowano możliwe mechanizmy powstania i terapii tamponady serca po implantacji elektrod o aktywnej fiksacji, uwzględniając dane z piśmiennictwa. (Folia Cardiologica Excerpta 2012; 7, 2: 110-114

Enhanced antiplatelet effect of enteric- -coated acetylsalicylic acid in co-administration with pantoprazole

Background. Proton pump inhibitors (PPI) are recommended for patients receiving antiplatelet therapy. Several studies have revealed that PPI may attenuate the antiplatelet effect of ASA. However, our pilot study has indicated a positive interaction between pantoprazole and enteric-coated aspirin. The aim of the current study was to confirm that pantoprazole enhances the antiplatelet effect ofenteric-coated aspirin in patients with acute coronary syndrome (ACS) treated with dual antiplatelettherapy. Moreover, the influence of CYP2C19 polymorphism on the antiplatelet effect of aspirinwas assessed.Material and methods. Ninety three consecutive ACS patients were prospectively enrolled in a randomized, crossover, open-labeled study. Forty four patients were given orally 40 mg of pantoprazole for the initial fourdays while the remaining forty nine were treated with pantoprazole from the 5th to the 8th day of hospitalization. Blood samples were collected at 6.00 a.m., 10.00 a.m., 2.00 p.m., and 7.00 p.m. on the 4th and 8th daysof hospitalization. Aggregation in response to arachidonic acid was assessed by impedance aggregometry.Results. Lower mean platelet aggregation on pantoprazole was observed on the 8th day of hospitalization(p = 0.03). A cross-time analysis of platelet aggregation demonstrated statistical significance at two hoursand six hours after co-administration of pantoprazole and antiplatelet agents, with the highest absolutedifference observed two hours after drugs ingestion. No significant differences in aggregation betweenstudy groups were observed on the 4th day of hospitalization. No influence of CYP2C19 polymorphismon the antiplatelet effect of aspirin was observed.Conclusions. Co-administration of pantoprazole enhances the antiplatelet effect of enteric-coated aspirinin patients with ACS.Background. Proton pump inhibitors (PPI) are recommended for patients receiving antiplatelet therapy.Several studies have revealed that PPI may attenuate the antiplatelet effect of ASA. However, our pilot study has indicated a positive interaction between pantoprazole and enteric-coated aspirin.The aim of the current study was to confirm that pantoprazole enhances the antiplatelet effect ofenteric-coated aspirin in patients with acute coronary syndrome (ACS) treated with dual antiplatelettherapy. Moreover, the influence of CYP2C19 polymorphism on the antiplatelet effect of aspirinwas assessed.Material and methods. Ninety three consecutive ACS patients were prospectively enrolled in a randomized, crossover, open-labeled study. Forty four patients were given orally 40 mg of pantoprazole for the initial fourdays while the remaining forty nine were treated with pantoprazole from the 5th to the 8th day of hospitalization. Blood samples were collected at 6.00 a.m., 10.00 a.m., 2.00 p.m., and 7.00 p.m. on the 4th and 8th daysof hospitalization. Aggregation in response to arachidonic acid was assessed by impedance aggregometry.Results. Lower mean platelet aggregation on pantoprazole was observed on the 8th day of hospitalization(p = 0.03). A cross-time analysis of platelet aggregation demonstrated statistical significance at two hoursand six hours after co-administration of pantoprazole and antiplatelet agents, with the highest absolutedifference observed two hours after drugs ingestion. No significant differences in aggregation betweenstudy groups were observed on the 4th day of hospitalization. No influence of CYP2C19 polymorphismon the antiplatelet effect of aspirin was observed.Conclusions. Co-administration of pantoprazole enhances the antiplatelet effect of enteric-coated aspirinin patients with ACS

CdS-decorated porous anodic SnOxSnO_x photoanodes with enhanced performance under visible light

Electrochemically generated nanoporous tin oxide films have already been studied as photoanodes in photoelectrochemical water splitting systems. However, up to now, the most significant drawback of such materials was their relatively wide band gap (ca. 3.0 eV), which limits their effective performance in the UV light range. Therefore, here, we present for the first time an effective strategy for sensitization of porous anodic SnO(x) films with another narrow band gap semiconductor. Nanoporous tin oxide layers were obtained by simple one-step anodic oxidation of metallic Sn in 1 M NaOH followed by further surface decoration with CdS by the successive ionic layer adsorption and reaction (SILAR) method. It was found that the nanoporous morphology of as-anodized SnO(x) is still preserved after CdS deposition. Such SnO(x)/CdS photoanodes exhibited enhanced photoelectrochemical activity in the visible range compared to unmodified SnO(x). However, the thermal treatment at 200 °C before the SILAR process was found to be a key factor responsible for the optimal photoresponse of the material