Polycarpou, Andreas

Abstract Objectives Type B aortic dissection (TBAD) is rare in patients aged ≤30 years, and data on this population remain limited. This study aimed to characterize the underlying aetiology, and outcomes of invasively treated young patients with TBAD, with a focus on the impact of heritable thoracic aortic disease (HTAD). Methods A retrospective multicentre analysis was conducted across 19 international aortic centres, including 139 patients aged ≤30 years with TBAD. Patients with chronic TBAD (n = 42) were excluded for the final analysis. The cohort was classified as uncomplicated (n = 86) or complicated (n = 53) TBAD. Clinical, radiologic, intraoperative, and postoperative data were collected using standardized forms. Outcomes were compared between subgroups defined by TBAD complexity, HTAD status, and surgical strategy. Kaplan-Meier and Andersen-Gill analyses were used for survival and recurrent aortic intervention, respectively. Results Mean follow-up time was 6.5 years. HTAD was identified in 57% of patients. Most presented with uncomplicated TBAD (62%), while high-risk uncomplicated cases were uncommon. Endovascular repair was predominant in complicated TBAD, while open repair was more frequent in uncomplicated cases. Early mortality was low (n = 3), and mid-term survival was excellent across all subgroups. HTAD was a significant predictor of recurrent aortic interventions (HR = 3.3, P = .004). No significant differences were observed in survival or reintervention rates between uncomplicated and complicated TBAD or between operative strategies. Conclusions In young patients, TBAD predominantly occurs in the context of HTAD. Both open and endovascular repair are associated with excellent early outcomes and mid-term survival. However, HTAD remains a significant predictor of recurrent aortic interventions.

Carotid artery stenosis (CAS) affects approximately 5–7.5% of older adults and is recognized as a significant risk factor for vascular cognitive impairment (VCI). The impact of CAS on cerebral blood flow (CBF) within the ipsilateral hemisphere relies on the adaptive capabilities of the cerebral microcirculation. In this study, we aimed to test the hypothesis that the impaired availability of nitric oxide (NO) compromises CBF homeostasis after unilateral carotid artery occlusion (CAO). To investigate this, three mouse models exhibiting compromised production of NO were tested: NOS1 knockout, NOS1/3 double knockout, and mice treated with the NO synthesis inhibitor L-NAME. Regional CBF changes following CAO were evaluated using laser-speckle contrast imaging (LSCI). Our findings demonstrated that NOS1 knockout, NOS1/3 double knockout, and L-NAME-treated mice exhibited impaired CBF adaptation to CAO. Furthermore, genetic deficiency of one or two NO synthase isoforms increased the tortuosity of pial collaterals connecting the frontoparietal and temporal regions. In conclusion, our study highlights the significant contribution of NO production to the functional adaptation of cerebrocortical microcirculation to unilateral CAO. We propose that impaired bioavailability of NO contributes to the impaired CBF homeostasis by altering inter- and intrahemispheric blood flow redistribution after unilateral disruption of carotid artery flow.

Abstract OBJECTIVES The prevalence and aetiology of acute aortic dissection type A (AADA) in patients ≤30 years is unknown. The aims of this clinical study were to determine the prevalence and potential aetiology of AADA in surgically treated patients ≤30 years and to evaluate the respective postoperative outcomes in this selective group of patients in a large multicentre study. METHODS Retrospective data collection was performed at 16 participating international aortic institutions. All patients ≤30 years at the time of dissection onset were included. The postoperative results were analysed with regard to connective tissue disease (CTD). RESULTS The overall prevalence of AADA ≤30 years was 1.8% (139 out of 7914 patients), including 51 (36.7%) patients who were retrospectively diagnosed with CTD. Cumulative postoperative mortality was 8.6%, 2.2% and 1.4%. Actuarial survival was 80% at 10 years postoperatively. Non-CTD patients (n = 88) had a significantly higher incidence of arterial hypertension (46.6% vs 9.8%; P < 0.001) while AADA affected the aortic root (P < 0.001) and arch (P = 0.029) significantly more often in the CTD group. A positive family history of aortic disease was present in 9.4% of the study cohort (n = 13). CONCLUSIONS The prevalence of AADA in surgically treated patients ≤30 years is <2% with CTD and arterial hypertension as the 2 most prevalent triggers of AADA. Open surgery may be performed with good early results and excellent mid- to long-term outcomes.

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 post-radiation 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 (≥18years) 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 surgical approach, 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 trend was not statistically significant (P=0.062). Hodgkin’s disease was the most common malignancy (64%) for which mediastinal radiation had been received. Only 27% patients had an isolated pericardiectomy, and concomitant pericardiectomy and valve surgery was performed in 46% patients. Radical resection was performed in 50% patients, whereas 47% patients underwent a subtotal resection. Prolonged ventilation (26%), atrial fibrillation (21%) and pleural effusion (16%) were the most common post-operative complications. The overall 1,5- and 10-years survival was 73.6%, 53.4% and 32.1% respectively. Increasing age (HR 1.044, 95%CI 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) . 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 A 2 . Support or Funding Information EFOP‐3.6.3‐VEKOP‐16‐2017‐00009, OTKA K‐125174, OTKA K‐112964, NVKP‐16‐1‐2016‐0042