Premium
Impella support and acute kidney injury during high‐risk percutaneous coronary intervention: The Global cVAD Renal Protection Study
Author(s) -
Flaherty Michael P.,
Moses Jeffrey W.,
Westenfeld Ralf,
Palacios Igor,
O'Neill William W.,
Schreiber Theodore L.,
Lim Michael J.,
Kaki Amir,
Ghiu Ioana,
Mehran Roxanna
Publication year - 2020
Publication title -
catheterization and cardiovascular interventions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.988
H-Index - 116
eISSN - 1522-726X
pISSN - 1522-1946
DOI - 10.1002/ccd.28400
Subject(s) - medicine , impella , acute kidney injury , percutaneous coronary intervention , conventional pci , odds ratio , kidney disease , hemodialysis , cardiology , renal replacement therapy , incidence (geometry) , renal function , surgery , myocardial infarction , cardiogenic shock , physics , optics
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 m 2 ) 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.