Non-invasive monitoring of flow rates within the supplying cannulae of VAV-ECMO and the use of partial occlusion for venous-supplying cannula enable individualized patient management and effective weaning from VAV-ECMO.

Objective: Brucellosis is frequently seen in Mediterranean and Middle East countries, including Turkey. We report the medical and surgical management of 31 cases of native endocarditis. Material and Method: Thirty-one patients were admitted to our clinic with suspected Brucella Endocarditis. The diagnosis was established by either isolation of Brucella species, or the presence of antibodies. Following preoperative antibiotic therapy patients underwent valve replacement with excessive tissue debridment. Patients were followed up with Brucella titers, blood cultures, and echocardiography. Results: On admission all patients were febrile and mostly dyspneic (NYHA Class 3 or 4). The blood tests were normal except for elevated ESR, CRP and serological tests. The aortic valve was involved in 19 patients, mitral valve in 7 patients, and both valves in 5. After serological confirmation of BE, antibiotic therapy was maintained. Twenty-five of the patients received rifampicine, doxycycline, and cotrimaxozole; 2 of them received a combination of rifampicine, streptomycin, and doxycycline; and 4 of them received rifampicine, tetracycline, and cotrimaxozole. Tissue loss in most of the affected leaflets and vegetationswere presenting all patients. Valve replacements were performed with mechanical and biologic prostheses. All the patients were afebrile at discharge but received the antibiotics for 101, 2 ± 16, 9 days. The follow-up was 37, 1 ± 9, 2 months. Discussion: In our retrospective study, combination of adequate medical and surgical therapy resulted in declined morbidity and mortality rate. The valve replacement with aggressive debridement is the most important part of the treatment, which should be supported with efficient preoperative and long term postoperative medical treatment.

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Injury to the donor heart during cold preservation has a negative impact on graft survival before transplantation. This study aims to examine whether doxycycline, known as an MMP-2 inhibitor, has a positive effect on donor heart preservation via its antioxidant action when added to standard preservation solution. Hearts were obtained from 3-month-old male Wistar rats and randomly divided into three groups: hearts stored for 1 h at 4 °C (1) with doxycycline preservation solution (DOX cardioplegia) with low Ca2+; (2) with standard cardioplegia with low Ca2+; and (3) unstored hearts. All hearts were perfused in working mode, arrested at 37 °C, removed from the perfusion system, reattached in Langendorff perfusion system, and converted to working mode for 1 h. At the end of the storage period, hearts preserved in DOX cardioplegia had significantly less weight gain than those preserved in the standard cardioplegia. DOX cardioplegia-induced preservation resulted in significantly higher heart rates and better recovery quality during reperfusion in aortic flow compared to the standard cardioplegia group. Recovery in the left ventricular function and Lambeth Convention Arrhythmia scores during 1 h reperfusion were also significantly better in the DOX cardioplegia group. Biochemical data showed that DOX cardioplegia prevented an increase in MMP-2 activity and blocked apoptosis through increased activity of the pro-survival kinase Akt in the donor heart homogenates. DOX cardioplegia also led to a balanced oxidant/antioxidant level in the heart homogenates. This is the first study to report that cardioplegia solution containing doxycycline provides better cardioprotection via the preservation of heart function, through its role in controlling cellular redox status during static cold storage.

Zn2+‐homoeostasis including free Zn2+ ([Zn2+]i) is regulated through Zn2+‐transporters and their comprehensive understanding may be important due to their contributions to cardiac dysfunction. Herein, we aimed to examine a possible role of Zn2+‐transporters in the development of heart failure (HF) via induction of ER stress. We first showed localizations of ZIP8, ZIP14 and ZnT8 to both sarcolemma and S(E)R in ventricular cardiomyocytes (H9c2 cells) using confocal together with calculated Pearson's coefficients. The expressions of ZIP14 and ZnT8 were significantly increased with decreased ZIP8 level in HF. Moreover, [Zn2+]i was significantly high in doxorubicin‐treated H9c2 cells compared to their controls. We found elevated levels of ER stress markers, GRP78 and CHOP/Gadd153, confirming the existence of ER stress. Furthermore, we measured markedly increased total PKC and PKCα expression and PKCα‐phosphorylation in HF. A PKC inhibition induced significant decrease in expressions of these ER stress markers compared to controls. Interestingly, direct increase in [Zn2+]i using zinc‐ionophore induced significant increase in these markers. On the other hand, when we induced ER stress directly with tunicamycin, we could not observe any effect on expression levels of these Zn2+ transporters. Additionally, increased [Zn2+]i could induce marked activation of PKCα. Moreover, we observed marked decrease in [Zn2+]i under PKC inhibition in H9c2 cells. Overall, our present data suggest possible role of Zn2+ transporters on an intersection pathway with increased [Zn2+]i and PKCα activation and induction of HF, most probably via development of ER stress. Therefore, our present data provide novel information how a well‐controlled [Zn2+]i via Zn2+ transporters and PKCα can be important therapeutic approach in prevention/treatment of HF.