Vavilis Georgios, Evans Marie, Jernberg Tomas, Rück Andreas, Szummer Karolina
Department of Emergency Medicine, Karolinska University Hospital, Huddinge, Department of Medicine, Huddinge, Karolinska Institutet, Stockholm, Sweden.
Renal Medicine, CLINTEC, Karolinska Institutet, Karolinska University Hospital, Stockholm, Stockholm, Sweden.
Open Heart. 2017 Jun 12;4(2):e000554. doi: 10.1136/openhrt-2016-000554. eCollection 2017.
The occurrence of persistent acute kidney injury (pAKI) following transcatheter aortic valve implantation (TAVI) has serious implications.
There were 1540 patients undergoing and surviving TAVI included in the nationwide SWEDEHEART registry between 2008 and 2015. Creatinine was measured at baseline and discharge, and those with baseline estimated glomerular filtration rate (eGFR) <15 mL/min/1.73 m or dialysis were excluded. pAKI was defined by and encompassing theValve Academic Research Consortium-2 (VARC-2) criteria: increase in serum creatinine concentration ≥26.5 μmol/L or increase by ≥50% (1.5×), or start of in-hospital dialysis until hospital discharge. Logistic regression analysis was used to find baseline factors associated with pAKI. Adjusted Cox regression analysis was used to assess the association of pAKI with mortality. Median follow-up was 1.8 years (IQR 0.7-3.0).
pAKI occurred in 6.1% (n=94) of the patients (71.3% male). These patients had higher creatinine level (117±50 vs 100±35 mmol/L, p<0.001), but similar baseline eGFR (59±21 vs 56±23 mL/min/1.73 m, p=0.18) and received higher contrast volume (129 mL ±89 vs 110 mL ±78, p=0.027). On multivariable logistic regression analysis, pAKI was predicted by eGFR (OR 0.88, 95% CI (0.79 to 0.98), p=0.019), male gender (OR 2.68, 95% CI (1.63 to 4.38), p<0.001) and apical access (OR 2.23, 95% CI (1.35 to 3.69), p=0.002), whereas contrast volume/10 mL (OR 1.02, 95% CI (1.00 to 1.05), p=0.052) did not reach statistical significance. Mortality at 1 year/end of follow-up was 10.4%/26.9%. pAKI was associated with a doubled risk of death (HR 2.04, 95% CI (1.49 to 2.81), p<0.001).
Persistent AKI after TAVI occurs in 6.1% and is associated with a doubled long-term mortality. Special efforts to avoid AKI should be taken, especially among vulnerable patients.
经导管主动脉瓣植入术（TAVI）后持续性急性肾损伤（pAKI）的发生具有严重影响。
2008年至2015年间，全国性的瑞典心脏介入登记研究纳入了1540例接受TAVI并存活的患者。在基线和出院时测量肌酐水平，排除基线估计肾小球滤过率（eGFR）<15 mL/min/1.73 m²或正在接受透析的患者。pAKI根据瓣膜学术研究联盟-2（VARC-2）标准定义并涵盖：血清肌酐浓度升高≥26.5 μmol/L或升高≥50%（1.5倍），或住院期间开始透析直至出院。采用逻辑回归分析寻找与pAKI相关的基线因素。采用校正后的Cox回归分析评估pAKI与死亡率的关联。中位随访时间为1.8年（四分位间距0.7 - 3.0年）。
6.1%（n = 94）的患者发生了pAKI（男性占71.3%）。这些患者的肌酐水平较高（117±50 vs 100±35 mmol/L，p<0.001），但基线eGFR相似（59±21 vs 56±23 mL/min/1.73 m²，p = 0.18），且接受的造影剂剂量更高（129 mL ±89 vs 110 mL ±78，p = 0.027）。多变量逻辑回归分析显示，pAKI的预测因素为eGFR（比值比[OR]0.88，95%置信区间CI，p = 0.019）、男性（OR 2.68，95%CI(1.63至4.38)，p<0.001）和心尖入路（OR 2.23，95%CI(1.35至3.69)，p = 0.002），而造影剂剂量/10 mL（OR 1.02，95%CI(1.00至1.05)，p = 0.052）未达到统计学意义。1年/随访结束时的死亡率分别为10.4%/26.9%。pAKI与死亡风险加倍相关（风险比[HR]2.04，95%CI(1.49至2.81)，p<0.001）。
TAVI后持续性AKI的发生率为6.1%，并与长期死亡率加倍相关。应特别努力避免AKI的发生，尤其是在易患患者中。
