Study protocol
Postprocedural pulmonary complications, pneumonia, Stroke, neurological deficit, hemorrhage, annular calcification, Pneumonia, AKI, myocardial injury, acute kidney injury, infarction
PNEUMONIA, STROKE, CONDUCTION DISTURBANCE, HEMORRHAGE, INFARCTION, PNEUMONIA, KIDNEY DISEASE, DISEASE, EDWARDS, CONDUCTION ABNORMALITIES
The routine monitoring techniques of our institution for patients under general anesthesia were applied, except FBefore inducing anesthesia, all participants were preoxygenated for 3 min using an anesthesia machine (Primus; Drägerwerk, Lubeck, Germany) with FThe TAVI was conducted in accordance with the standard procedures in our institution. Using a transfemoral approach, a balloon-expandable Sapien III valve (Edwards Lifesciences, Irvine, CA, USA), self-expandable Evolut Pro or R valve (Medtronic, Minneapolis, MN, USA), or Lotus valve (Boston Scientific, Natick, MA, USA) was implanted at the diseased aortic valve. The valve was chosen by the heart team based on the size and structure of the native valve and sinus, heights of the coronary artery openings, and considerations regarding future coronary access, the risk of conduction disturbances, and annular calcification. The iliofemoral arteries were accessed under fluoroscopic guidance and closed percutaneously using Perclose ProGlide vascular suture-mediated closure devices (Abbott Vascular Devices, Redwood City, CA, USA). Before the procedure, the patients were given loading doses of dual antiplatelet agents: acetylsalicylic acid and clopidogrel (both 300 mg). During the procedure, the patients were heparinized with unfractionated heparin to achieve an activated clotting time >250 s. At completion of the valve implantation, the effects of heparin were reversed by protamine infusion.During the procedure, arterial blood gas analysis (ABGA) was performed at four time points: baseline (before anesthesia induction, T1), after inducing general anesthesia (T2), after valve implantation (T3), and at the end of the procedure (T4). ABGA was performed using a GEM® Premier 3000 device (Model 5700; Instrumentation Laboratory, Lexington, MA, USA). Oxygenation variables, including PaOTwo serum cardiac biomarkers of myocardial injury, high-sensitivity cTnI (hs-cTnI) and CK-MB, were measured at baseline (before the procedure) and 1, 4, 8, 24, 48, and 72 h after TAVI. hs-cTnI was measured using an Abbott Architect Plus Analyzer (i2000SR; Flex, San Jose, CA, USA), which has a limit of detection of 0.0011 μg/L and limit of blank of 0.0007–0.0013 μg/L. An hs-cTnI concentration ≥99Postprocedural acute kidney injury (AKI) was determined based on the serum creatinine level and urine output according to the Kidney Disease: Improving Global Outcomes Clinical Practice Guidelines criteria for AKI [The postprocedural development of new conduction abnormalities and incidence of permanent pacemaker insertion was assessed. Stroke was defined as an acute episode of a focal or global neurological deficit as a result of hemorrhage or infarction, based on the Valve Academic Research Consortium-2 (VARC-2) definition [Postprocedural pulmonary complications, including reintubation, prolonged mechanical ventilation, and pneumonia, occurred within 7 days following the procedure or until discharge were assessed. Prolonged mechanical ventilation was defined as requirement of mechanical ventilation for more than 12 h after procedure. Pneumonia was defined using the Centers for Disease Control and Prevention (CDC) criteria [