Authors' contributions: ZB, PS and BH planned and supervised the project; BH and AI 13 introduced laser-speckle imaging for studying cerebrocortical microcirculation in mice and 14 optimized the experimental procedures in preliminary experiments; AP, LH, AI and DS 15 performed the experiments; AP, LH, DS and ÉR evaluated the experiments and analyzed the 16 data; AP and ÉR prepared the figures and tables; AP, LH, PS and ZB wrote the manuscript.

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Device infection is a major potential complication following ventricular assist device implantation and can lead to devastating consequences. The treatment options are few and often challenging to implement. The most durable option may require device exchange to obtain adequate source control. Due to the prolonged support times offered by the new left ventricular assist devices (LVADs), there is concern that the number of patients that will eventually require repeated device exchanges for device infection will increase. The benefit of medical antibiotic therapy alone is limited and is frequently unsuccessful. Surgical treatment strategies that improve outcomes by eliminating the infection and by preventing infection recurrence are needed. We report a case of a third-time LVAD exchange (4th device implant) for device infection within eight years of the index implant, and we briefly discuss the role of the greater omentum in the surgical treatment of this complication.

Background: Pericardiectomy for postradiation constrictive pericarditis has been reported to generally have unfavorable outcomes. This study sought to evaluate surgical outcomes in a large cohort of patients undergoing pericardiectomy for radiation-associated pericardial constriction.Methods: A retrospective analysis of all patients (≥18 years) who underwent pericardiectomy for a diagnosis of constrictive pericarditis with a prior history of mediastinal irradiation from June 2002 to June 2019 was conducted. There were 100 patients (mean age 57.2 ± 10.1 years, 49% females) who met the inclusion criteria.Records were reviewed to look at the surgical approach, the extent of resection, early mortality, and late survival.Results: The overall operative mortality was 10.1% (n = 10). The rate of operative mortality decreased over the study period; however, the test of the trend was not statistically significant (p = .062). Hodgkin's disease was the most common malignancy (64%) for which mediastinal radiation had been received. Only 27% of patients had an isolated pericardiectomy, and concomitant pericardiectomy and valve surgery were performed in 46% of patients. Radical resection was performed in 50% of patients, whereas 47% of patients underwent subtotal resection. Prolonged ventilation (26%), atrial fibrillation (21%), and pleural effusion (16%) were the most common postoperative complications. The overall 1, 5-, and 10-years survival was 73.6%, 53.4%, and 32.1%, respectively. Increasing age (hazard ratio, 1.044, 95% confidence interval 1.017-1.073) appeared to have a significant negative effect on overall survival in the univariate model. Conclusion:Pericardiectomy performed for radiation-associated constrictive pericarditis has poor long-term outcomes. The early mortality, though high (~10%), has been showing a decreasing trend in the test of time.

The understanding of cerebral autoregulation has become of notable importance due to the increased incidence of carotid artery stenosis in the elderly population which entails an increased risk of stroke, the 2nd most common cause of mortality worldwide. Many debates, regarding its exact mechanisms, exist in the scientific literature including the role of endothelial and neuronal nitric oxide (NO) synthases (eNOS and nNOS) and prostanoid mediators (PMs). According to our previous observations, eNOS, surprisingly, does not seem to play an important role in the autoregulation of the cerebrocortical blood flow (CoBF) to unilateral common carotid artery occlusion (CAO) (1). In our recent study we aimed to analyze the combined lack of eNOS and nNOS and the role of PMs in cerebrovascular autoregulation by analyzing the changes of CoBF after reducing the cerebral perfusion pressure by unilateral (left) CAO in wild‐type (WT), as well as in eNOS/nNOS double knock‐out (KO) male mice. The role of PMs was tested by indomethacin administration (1 mg/kg, i.p.) and in thromboxane knock‐out (TPR‐KO) male mice. Using the high temporal and spatial resolution of laser‐speckle imaging regional CoBF changes were analyzed after CAO in anesthetized adult male mice. In wild‐type animals CoBF reduction in the left temporal cortex started immediately after CAO, reaching its maximum (−27%) at 6–9 s. Thereafter, CoBF recovered close to the pre‐occlusion level within 30 s indicating the activation of regulatory pathway(s). Interestingly, the frontoparietal cerebrocortical regions also showed CoBF reduction in the left (−17–19%) hemisphere, indicating a stealing effect through pial collateral vessels from the frontoparietal to the more ischemic temporal cortex. Surprisingly, in eNOS/nNOS double KO animals the acute CoBF reduction after CAO was unaltered in all cerebrocortical regions, but the recovery of CoBF was worsened as compared to controls. Indomethacin treatment resulted in a faster recovery in the temporal region, specifically 9–21 s after the occlusion. In TPR‐KO animals, however, the recovery of the CoBF was slightly diminished. These results indicate that (1) the Willis circle alone is not sufficient to provide an immediate compensation for the loss of one carotid artery, (2) the combined lack of eNOS and nNOS impairs only the subacute phase of the recovery after unilateral CAO and (3) indomethacin treatment results in a faster recovery, probably by inhibiting the release of a vasoconstrictor prostanoid, which is not thromboxane A2. Support or Funding Information EFOP‐3.6.3‐VEKOP‐16‐2017‐00009, OTKA K‐125174, OTKA K‐112964, NVKP‐16‐1‐2016‐0042 Adaptation of the cerebrocortical circulation to carotid artery occlusion involves blood flow redistribution between cortical regions and is independent of eNOSA.PolycarpouL.HricisakA.IringD.SafarE.RuisanchezB.HorvathP.SandorZ.BenyoAm J Physiol Heart Circ Physiol311H972H980