Juerg Schmidli

OBJECTIVES: Spinal cord injury is detrimental for patients undergoing open or endovascular thoracoabdominal aortic aneurysm (TAAA) repair. The aim of this survey and of the modified Delphi consensus was to gather information on current practices and standards in neuroprotection in patients undergoing open and endovascular TAAA. METHODS: The Aortic Association conducted an international online survey on neuromonitoring in open and endovascular TAAA repair. In a first round an expert panel put together a survey on different aspects of neuromonitoring. Based on the answers from the first round of the survey, 18 Delphi consensus questions were formulated. RESULTS: A total of 56 physicians completed the survey. Of these, 45 perform open and endovascular TAAA repair, 3 do open TAAA repair and 8 do endovascular TAAA repair. At least 1 neuromonitoring or protection modality is utilized during open TAAA surgery. Cerebrospinal fluid (CSF) drainage was used in 97.9%, near infrared spectroscopy in 70.8% and motor evoked potentials or somatosensory evoked potentials in 60.4%. Three of 53 centres do not utilize any form of neuromonitoring or protection during endovascular TAAA repair: 92.5% use CSF drainage; 35.8%, cerebral or paravertebral near infrared spectroscopy; and 24.5% motor evoked potentials or somatosensory evoked potentials. The utilization of CSF drainage and neuromonitoring varies depending on the extent of the TAAA repair. CONCLUSIONS: The results of this survey and of the Delphi consensus show that there is broad consensus on the importance of protecting the spinal cord to avoid spinal cord injury in patients undergoing open TAAA repair. Those measures are less frequently utilized in patients undergoing endovascular TAAA repair but should be considered, especially in patients who require extensive coverage of the thoracoabdominal aorta.

Large thoracic and thoraco-abdominal aneurysms may compress adjacent mediastinal structures. We present a case of a large thoraco-abdominal aneurysm compressing the left atrium and leading to functional mitral valve stenosis after total aortic arch repair, requiring urgent open thoraco-abdominal aneurysm repair.

In the originally published version of this manuscript, the group author name was incorrect. The group author name should read “Aortic impulse in TEVAR group” instead of “Collaborators”. This error has been corrected online.

Altered lipid metabolism has been shown to be of major importance in a range of metabolic diseases, with particular importance in cardiovascular disease (CVD). As a key metabolic product, altered lipoprotein(a) (Lp(a)) levels may be associated with adverse clinical outcomes in high-risk cardiovascular patients undergoing cardiac surgery. We aimed to investigate the impact of the important metabolite Lp(a) on complications and clinical outcomes in high-risk patients. A prospective observational cohort study was performed. Data were derived from the Bern Perioperative Biobank (ClinicalTrials.gov NCT04767685), and included 192 adult patients undergoing elective cardiac surgery. Blood samples were collected at 24 h preoperatively, before induction of general anaesthesia, upon weaning from cardiopulmonary bypass (CPB), and the first morning after surgery. Clinical endpoints included stroke, myocardial infarction, and mortality within 30 days after surgery or within 1 year. Patients were grouped according to their preoperative Lp(a) levels: 30 mg/dL (n = 71, 37%). The groups with increased vs. normal Lp(a) levels were comparable with regard to preoperative demographics and comorbidities. Median age was 67 years (interquartile range (IQR) 60.0, 73.0), with median body mass index (BMI) of 23.1 kg/m² (23.7, 30.4), and the majority of patients being males (75.5%). Over the observational interval, Lp(a) levels decreased in all types of cardiac surgery after CPB (mean decline of approximately −5 mg/dL). While Lp(a) levels decreased in all patients following CPB, this observation was considerably pronounced in patients undergoing deep hypothermic circulatory arrest (DHCA) (decrease to preoperative Lp(a) levels by −35% (95% CI −68, −1.7), p = 0.039). Increased Lp(a) levels were neither associated with increased rates of perioperative stroke or major adverse events in patients undergoing cardiac surgery, nor with overall mortality in the perioperative period, or at one year after surgery. Other than for cohorts in neurology and cardiology, elevated Lp(a) might not be a risk factor for perioperative events in cardiac surgery.

Patients undergoing cardiac surgery are at increased cardiovascular risk, which includes altered lipid status. However, data on the effect of cardiac surgery and cardiopulmonary bypass (CPB) on plasma levels of key lipids are scarce. We investigated potential effects of CPB on plasma lipid levels and associations with early postoperative clinical outcomes. This is a prospective bio-bank study of patients undergoing elective cardiac surgery at our center January to December 2019. The follow-up period was 1 year after surgery. Blood sampling was performed before induction of general anesthesia, upon weaning from cardiopulmonary bypass (CPB), and on the first day after surgery. Clinical end points included the incidence of postoperative stroke, myocardial infarction, and death of any cause at 30 days after surgery as well as 1-year all-cause mortality. A total of 192 cardiac surgery patients (75% male, median age 67.0 years (interquartile range 60.0–73.0), median BMI 26.1 kg/m² (23.7–30.4)) were included. A significant intraoperative decrease in plasma levels compared with preoperative levels (all p < 0.0001) was observed for total cholesterol (TC) (Cliff’s delta d: 0.75 (0.68–0.82; 95% CI)), LDL-Cholesterol (LDL-C) (d: 0.66 (0.57–0.73)) and HDL-Cholesterol (HDL-C) (d: 0.72 (0.64–0.79)). At 24h after surgery, the plasma levels of LDL-C (d: 0.73 (0.650.79)) and TC (d: 0.77 (0.69–0.82)) continued to decrease compared to preoperative levels, while the plasma levels of HDL-C (d: 0.46 (0.36–0.55)) and TG (d: 0.40 (0.29–0.50)) rebounded, but all remained below the preoperative levels (p < 0.001). Mortality at 30 days was 1.0% (N = 2/192), and 1-year mortality was 3.8% (N = 7/186). Postoperative myocardial infarction occurred in 3.1% of patients (N = 6/192) and postoperative stroke in 5.8% (N = 11/190). Adjusting for age, sex, BMI, and statin therapy, we noted a protective effect of postoperative occurrence of stroke for pre-to-post-operative changes in TC (adjusted odds ratio (OR) 0.29 (0.07–0.90), p = 0.047), in LDL-C (aOR 0.19 (0.03–0.88), p = 0.045), and in HDL-C (aOR 0.01 (0.00–0.78), p = 0.039). No associations were observed between lipid levels and 1-year mortality. In conclusion, cardiac surgery induces a significant sudden drop in levels of key plasma lipids. This effect was pronounced during the operation, and levels remained significantly lowered at 24 h after surgery. The intraoperative drops in LDL-C, TC, and HDL-C were associated with a protective effect against occurrence of postoperative stroke in adjusted models. We demonstrate that the changes in key plasma lipid levels during surgery are strongly correlated, which makes attributing the impact of each lipid to the clinical end points, such as postoperative stroke, a challenging task. Large-scale analyses should investigate additional clinical outcome measures.