Abstract 466 Incidence and Predictors of Acute kidney injury in patients undergoing primary PCI for STEMI

Background:
Acute kidney injury (AKI) is a known complication of ST-elevation myocardial infarction (STEMI) with an adverse impact on short- and long-term prognosis. It is diagnosed in 15-20% of STEMI patients. While AKI frequently occurs as a consequence of cardiogenic shock, limited data exists regarding AKI in STEMI patients undergoing primary PCI (pPCI) without cardiogenic shock. We therefore analyzed incidence and predictors of AKI in patients with STEMI undergoing pPCI without concomitant cardiogenic shock following pPCI.

Methods:
We retrospectively assessed patients referred to our institution with STEMI from 1/2015 to 9/2021 that were treated with pPCI. Patients presenting in cardiogenic shock after resuscitation were excluded. We defined AKI according to AKIN criteria with an increase of ≥0.3mg/dl creatinine within the first 72 hours or an increase of ≥1.5 fold within 72 hours after pPCI. Patients were additionally categorized into AKIN stage 1 (≥0.3mg/dl increase/1.5-1.9-fold increase), stage 2 (2.0-2.9-fold increase) or stage 3 (≥3-fold increase, creatinine ≥4mg/dl or acute increase of ≥0.5mg/dl).

Results:
Of the 565 patients analyzed, AKI was diagnosed in 7.4% (42/565). Patients with STEMI lacking signs of cardiogenic shock, who developed subsequent AKI had more often a history of CABG (12% vs. 2%, p<0.001), former stroke/TIA (14% vs. 4%, p=0.003) and known renal insufficiency stadium stage ≥3 (26% vs. 6%, p<0.001). Pain to First Medical Contact (FMC) was longer in patients who developed AKI afterwards (843±1617min vs 455±1245min, p=0.044), whereas FMC-Door and Door-Balloon times did not differ. Neither culprit lesion (p=0.534) nor prevalence of stent thrombosis (AKI 4.8% vs. No-AKI 6.9%; p=0.955) or coronary dissection (AKI 2% vs. No-AKI 1%; p=0.955) differed. PPCI was performed less frequent via radial access in patients with subsequent AKI (50% vs. 70%, p=0.004). Thrombectomy and GPIIbIIIa inhibitors were used equally in both groups. Final TIMI flow <3 was more frequent in the AKI group (19% vs. 8%, p=0.011). There was no higher number of patients treated for MVD within the same session (p=0.315), neither was a difference in the amount of contrast medium used (p=0.278). The first creatinine drawn after admission was significantly higher in the AKI group (0.93±0.24mg/dl vs. 1.26±0.76mg/dl, p<0.001), whereas there were no differences in the first drawn creatinkinase (p=0.236) and in the maximum creatinkinase (p=0.848). Intra-hospital death (AKI 0% vs. No-AKI 1.5%, p=0.420), vasopressor therapy (AKI 7.1% vs. No-AKI 2.7%, p=0.103) and mechanical ventilation (AKI 4.8% vs. no-AKI 1.3%, p=0.088) were rare and did not differ. Patients with AKI showed an overall longer hospital stay (6±3days vs. 9±6days, p<0.001). In the binary regression analysis only the first creatinine value after admission (OR 9.640 (95% CI 1.973-47.109), p<0.001) and final TIMI flow <III (OR 3.104 (95%CI 1.182-8.147), p=0.021) were predictive for AKI.

Conclusion:
After exclusion of patients with concomitant cardiogenic shock, the number of patients with STEMI treated with pPCI developing AKI is only 7.4%. The first creatinine drawn after admission and a TIMI flow <III were independent predictors for AKI in these patients. Gender, Pain to FMC and the access route might have an influence on the severity of subsequent AKI in these patients. AKI in STEMI patients without concomitant cardiogenic shock was not associated with higher intra-hospital mortality.

Clin Res Cardiol (2022). https://doi.org/10.1007/s00392-022-02002-5
Incidence and Predictors of Acute kidney injury in patients undergoing primary PCI for STEMI
N. Schacher¹, P. Buetow¹, S. Khater¹, P. Ferstl¹, M. Tröbs¹, M. Marwan¹, S. Achenbach¹, L. Gaede¹
¹Med. Klinik 2 - Kardiologie, Angiologie, Universitätsklinikum Erlangen, Erlangen;
Background: Acute kidney injury (AKI) is a known complication of ST-elevation myocardial infarction (STEMI) with an adverse impact on short- and long-term prognosis. It is diagnosed in 15-20% of STEMI patients. While AKI frequently occurs as a consequence of cardiogenic shock, limited data exists regarding AKI in STEMI patients undergoing primary PCI (pPCI) without cardiogenic shock. We therefore analyzed incidence and predictors of AKI in patients with STEMI undergoing pPCI without concomitant cardiogenic shock following pPCI. Methods: We retrospectively assessed patients referred to our institution with STEMI from 1/2015 to 9/2021 that were treated with pPCI. Patients presenting in cardiogenic shock after resuscitation were excluded. We defined AKI according to AKIN criteria with an increase of ≥0.3mg/dl creatinine within the first 72 hours or an increase of ≥1.5 fold within 72 hours after pPCI. Patients were additionally categorized into AKIN stage 1 (≥0.3mg/dl increase/1.5-1.9-fold increase), stage 2 (2.0-2.9-fold increase) or stage 3 (≥3-fold increase, creatinine ≥4mg/dl or acute increase of ≥0.5mg/dl). Results: Of the 565 patients analyzed, AKI was diagnosed in 7.4% (42/565). Patients with STEMI lacking signs of cardiogenic shock, who developed subsequent AKI had more often a history of CABG (12% vs. 2%, p<0.001), former stroke/TIA (14% vs. 4%, p=0.003) and known renal insufficiency stadium stage ≥3 (26% vs. 6%, p<0.001). Pain to First Medical Contact (FMC) was longer in patients who developed AKI afterwards (843±1617min vs 455±1245min, p=0.044), whereas FMC-Door and Door-Balloon times did not differ. Neither culprit lesion (p=0.534) nor prevalence of stent thrombosis (AKI 4.8% vs. No-AKI 6.9%; p=0.955) or coronary dissection (AKI 2% vs. No-AKI 1%; p=0.955) differed. PPCI was performed less frequent via radial access in patients with subsequent AKI (50% vs. 70%, p=0.004). Thrombectomy and GPIIbIIIa inhibitors were used equally in both groups. Final TIMI flow <3 was more frequent in the AKI group (19% vs. 8%, p=0.011). There was no higher number of patients treated for MVD within the same session (p=0.315), neither was a difference in the amount of contrast medium used (p=0.278). The first creatinine drawn after admission was significantly higher in the AKI group (0.93±0.24mg/dl vs. 1.26±0.76mg/dl, p<0.001), whereas there were no differences in the first drawn creatinkinase (p=0.236) and in the maximum creatinkinase (p=0.848). Intra-hospital death (AKI 0% vs. No-AKI 1.5%, p=0.420), vasopressor therapy (AKI 7.1% vs. No-AKI 2.7%, p=0.103) and mechanical ventilation (AKI 4.8% vs. no-AKI 1.3%, p=0.088) were rare and did not differ. Patients with AKI showed an overall longer hospital stay (6±3days vs. 9±6days, p<0.001). In the binary regression analysis only the first creatinine value after admission (OR 9.640 (95% CI 1.973-47.109), p<0.001) and final TIMI flow <III (OR 3.104 (95%CI 1.182-8.147), p=0.021) were predictive for AKI. Conclusion: After exclusion of patients with concomitant cardiogenic shock, the number of patients with STEMI treated with pPCI developing AKI is only 7.4%. The first creatinine drawn after admission and a TIMI flow <III were independent predictors for AKI in these patients. Gender, Pain to FMC and the access route might have an influence on the severity of subsequent AKI in these patients. AKI in STEMI patients without concomitant cardiogenic shock was not associated with higher intra-hospital mortality.
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