Michael P Flaherty1, Jeffrey W Moses2, Ralf Westenfeld3, Igor Palacios4, William W O'Neill5, Theodore L Schreiber6, Michael J Lim7, Amir Kaki8, Ioana Ghiu9, Roxanna Mehran10. 1. Division of Cardiology, Baptist Health-Heart and Vascular Center, Louisville, Kentucky. 2. Division of Cardiology, Columbia University Medical Center, New York, New York. 3. Division of Cardiology, University Hospital Düsseldorf, Düsseldorf, Germany. 4. Division of Cardiology, Massachusetts General Hospital, Boston, Massachusetts. 5. Division of Cardiology, Henry Ford Hospital, Detroit, Michigan. 6. Division of Cardiology, St. John's McComb Hospital, Wayne State University, Detroit, Michigan. 7. Division of Cardiology, St. Louis University, St. Louis, Missouri. 8. Division of Cardiology, St. John's Hospital, Wayne State University, Detroit, Michigan. 9. Division of Cardiology, Abiomed Inc., Danvers, Massachusetts. 10. Division of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York.
Abstract
BACKGROUND: Protection against acute kidney injury (AKI) has been reported with the use of Impella during high-risk percutaneous coronary intervention (HR-PCI). We sought to evaluate this finding by determining the occurrence of AKI during Impella-supported HR-PCI in patients from the Global cVAD Study and compare this incidence with their calculated AKI risk at baseline. METHODS AND RESULTS: In this prospective, multicenter study, we enrolled 314 consecutive patients. We included 223 patients that underwent nonemergent HR-PCI supported with Impella 2.5 or Impella CP and excluded those requiring hemodialysis prior to HR-PCI (19) and those with insufficient data (72). The primary outcome was AKI postprocedurally at 48 hr versus the predicted risk of AKI according to Mehran risk score. Logistic regression analysis determined predictors of AKI. Overall, 4.9% (11) of Impella-supported patients developed AKI (exclusively stage 1) at 48 hr versus a predicted rate of 21.9%, representing a 77.6% lower AKI rate (p < .0001). In this study, no Impella-supported patients required renal replacement therapy. Estimated glomerular filtration rate (ml/min/1.73 m2 ) alone predicted AKI (adjusted odds ratio [AOR]: 4.915; 95% confidence intervals [CI]: 1.02-23.53, p = .046), and increasing contrast had insignificant effects on AKI during high-risk PCI (AOR: 1.15; 95% CI: 0.87-1.51, p = .332). In patients not protected from AKI, the postprocedure incidence of AKI was not significantly greater and did not correlate with chronic kidney disease severity. CONCLUSION: The incidence of AKI was lower during HR-PCI than expected from current risk models. Although further exploration of this finding is warranted, these data support a new protective strategy against AKI during HR-PCI.
BACKGROUND: Protection against acute kidney injury (AKI) has been reported with the use of Impella during high-risk percutaneous coronary intervention (HR-PCI). We sought to evaluate this finding by determining the occurrence of AKI during Impella-supported HR-PCI in patients from the Global cVAD Study and compare this incidence with their calculated AKI risk at baseline. METHODS AND RESULTS: In this prospective, multicenter study, we enrolled 314 consecutive patients. We included 223 patients that underwent nonemergent HR-PCI supported with Impella 2.5 or Impella CP and excluded those requiring hemodialysis prior to HR-PCI (19) and those with insufficient data (72). The primary outcome was AKI postprocedurally at 48 hr versus the predicted risk of AKI according to Mehran risk score. Logistic regression analysis determined predictors of AKI. Overall, 4.9% (11) of Impella-supported patients developed AKI (exclusively stage 1) at 48 hr versus a predicted rate of 21.9%, representing a 77.6% lower AKI rate (p < .0001). In this study, no Impella-supported patients required renal replacement therapy. Estimated glomerular filtration rate (ml/min/1.73 m2 ) alone predicted AKI (adjusted odds ratio [AOR]: 4.915; 95% confidence intervals [CI]: 1.02-23.53, p = .046), and increasing contrast had insignificant effects on AKI during high-risk PCI (AOR: 1.15; 95% CI: 0.87-1.51, p = .332). In patients not protected from AKI, the postprocedure incidence of AKI was not significantly greater and did not correlate with chronic kidney disease severity. CONCLUSION: The incidence of AKI was lower during HR-PCI than expected from current risk models. Although further exploration of this finding is warranted, these data support a new protective strategy against AKI during HR-PCI.
Authors: Vandan D Upadhyaya; Abbas Alshami; Ishan Patel; Steven Douedi; Amy Quinlan; Tresy Thomas; Joni Prentice; Dawn Calderon; Arif Asif; Shuvendu Sen; Aditya Mehra; Mohammad A Hossain Journal: J Clin Med Res Date: 2021-05-25