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Minimally Invasive Transapical Aortic Valve Implantation and the Risk of Acute Kidney Injury
Justus T. Strauch, MD, Maximilian P. Scherner, MD, Peter L. Haldenwang, MD, Roman Pfister, MD, Elmar W. Kuhn, MD, Navid Madershahian, MD, Parwis Rahmanian, MD, Jens Wippermann, MD, and Thorsten Wahlers, MD Departments of Cardiothoracic Surgery and Cardiology, University Hospital of Cologne, Cologne, Germany
Background. The new technique of minimally invasive transapical aortic valve implantation (TAP-AVI) deals with high-risk patients and despite the absence of cardiopulmonary bypass it might lead to renal impairment. The aim of this study was to estimate the risk of the development of acute kidney injury (AKI) after TAP-AVI and to identify possible risk factors with regard to the morbidity and mortality of the patients. Methods. Data of 30 consecutive patients undergoing TAP-AVI were recorded and followed up for 8 weeks. Postoperative AKI has been defined according to RIFLE criteria. Two patients on chronic hemodialysis have been followed up. Results. Of 28 patients, AKI occurred in 16 patients (57%). Statistical analysis revealed no influence on the risk of developing AKI caused by the dose of applicated contrast medium (p ⴝ 0.09), the patient’s age (p ⴝ 0.5), or the existence of diabetes (p ⴝ 0. 16). Analysis concerning the relationship between a preexisting coronary heart
disease and AKI showed a tendency to be associated with a higher risk of the development of AKI (70% preexisting congenital heart disease in the AKI group versus 50%; p ⴝ 0.28). Only a preoperative serum creatinine greater than 1.1 mg/dL was a strong predictor for developing AKI (p < 0.01). Length of stay in the intensive care unit and the complete length of hospital stay revealed no difference with regard to postoperative development of AKI though statistical analysis showed a trend to a higher mortality in the AKI group (27% vs 6%); univariate analysis did not reach statistical significance (p ⴝ 0.13). Conclusions. The TAP-AVI seems to be a feasible procedure for high-risk patients with a clear risk of developing AKI. Patients at risk should be identified and, if indicated, already preoperatively treated in collaboration with the attending nephrologists. (Ann Thorac Surg 2010;89:465–70) © 2010 by The Society of Thoracic Surgeons
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auspicious one because it seems to offer many potential advantages, including the permission of a more precise positioning and placement of the prosthesis as well as an access which has been used before successfully for left ventricular assist devices and apicoaortic conduit implantation [11, 12]. Taken together, preliminary data suggest that the minimally invasive transapical approach is a viable alternative for patients in whom conventional AVR is not feasible or possesses unacceptable risk, and may lead to a significant decrease in perioperative trauma and eventually to a decrease in perioperative risk. Despite these encouraging data this newly developed technique includes the need of fluoroscopy and angiography using a contrast agent to aid positioning of the valve [13], which may, especially in patients with diabetic nephropathy, lead to acute kidney injury (AKI), which is associated with increased morbidity and mortality [14, 15]. Although previous studies established clinical and surgical characteristics associated with increased risk of acute renal failure (ARF) after cardiac surgery (for example, CPB duration, severe hemodilution during CPB reflected by nadir hematocrit, and low oxygen delivery during CPB), which are avoided by the lack of using CPB during transapical aortic valve implantation (TAP-AVI), other fac-
he treatment of choice for patients with symptomatic severe degenerative aortic stenosis, which is the most frequently acquired heart valve lesion, is the surgical aortic valve replacement (AVR) with cardiopulmonary bypass (CBP). Due to the fact that medically managed symptomatic patients have a poor prognosis [1–3], this procedure has become the gold standard therapy for those patients, although many patients with symptomatic severe aortic stenosis have significant comorbidities. However, especially in these patients, AVR with CBP can be associated with an unacceptable perioperative morbidity and mortality [4]. To reduce the risk caused by this procedure several groups developed new strategies using aortic valvuloplasty to avoid invasive surgery and CPB [5–9]. This led to two approaches [10] which have evolved as potential access routes to the aortic valve during recent years: the retrograde arterial approach using the femoral artery and the transapical approach with implantation of the aortic valve through the left ventricular apex by lateral minithoracotomy. Concerning the technique, the transapical route seems to be the most
Accepted for publication Sept 17, 2009. Address correspondence to Dr Strauch, University Hospital of Cologne, Department of Cardiothoracic Surgery, Kerpener Strasse 62, Cologne, 50925, Germany; e-mail: [email protected].
© 2010 by The Society of Thoracic Surgeons Published by Elsevier Inc
0003-4975/10/$36.00 doi:10.1016/j.athoracsur.2009.09.090
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Minimally Invasive Transapical Aortic Valve Implantation and the Risk of Acute Kidney Injury
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Ann Thorac Surg 2010;89:465–70
Material and Methods
Table 1. Patient Demographics
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Variables
Mean (Range)
Total (n) Female Age (years) Body weight (kg) EuroSCORE (points) Logistic EuroSCORE (%) STS score (%) Diabetes mellitus (n) Coronary heart disease (without indication for surgery) (n)
30 19 82.1 (71–88) 70.7 (50–94) 9.6 (6–18) 19.01 (5.1–77.4) 13.6 (3.2–26) 8 19
EuroSCORE ⫽ European system for cardiac operative risk evaluation; STS ⫽ Society of Thoracic Surgeons.
tors such as older age, diabetes mellitus, and congestive heart failure [16, 17] still remain. Additionally the exigency for using contrast agents presents a new risk factor, which is well known for exacerbating the risk of AKI and may play an important role in terms of estimating the potential risk of this procedure, influencing perioperative morbidity and mortality. The impact of AKI (especially with regard to the administration of contrast) on clinical outcomes has been evaluated most extensively in patients undergoing percutaneous coronary intervention and in patients undergoing cardiac surgery. In both it is associated with increased mortality in-hospital as well as after one year [18, 19]. Information on the impact of TAP-AVI is scarce. Two studies reported the need for postoperative renal replacement therapy in a total of 9 of 69 patients [20, 21]. In these reports, renal failure was not defined, preexisting impairment of renal function was not specified, and information of presurgical and postsurgical creatinine levels as an indicator for the glomerular filtration rate (GFR) was missing. The only study with regard to renal function in patients undergoing transcatheter valve replacement with 58 patients mixes up transfemoral (n ⫽ 46) and transapical (n ⫽ 12) valve replacement with no regard to the differences between these approaches [22]. In this context the aim of the present study was to analyze the results of 30 consecutive patients receiving TAP-AVI with respect to presurgical and postsurgical renal function and possible risk factors for AKI, referring to the assumption that this procedure might be feasible especially in patients classified as high risk.
Patient Characteristics and Inclusion Criteria Thirty consecutive patients with severe aortic stenosis and an unacceptable high risk for open heart surgery with CPB because of significant comorbidity were included in this study between February 2008 and January 2009. This retrospective study has been approved and accepted by the local Ethics Committee. The patients accepted for this procedure were selected by a clinical committee consisting of cardiologists and cardiac surgeons of our department, estimating the frailty in combination with the preoperative cardiac status in combination with preexisting comorbidities and therefore the risk profile of the patients individually. For prevention of contrast-induced renal failure all patients received 600 mg of N-acetylcystein on the evening prior to the procedure and two hours after the intervention. We abstained from intravenous hydration due to the restricted cardiac performance of the patients. All patients underwent echocardiography and left heart catheterization prior to TAP-AVI. Left heart catheterization was performed at least 29 days prior to TAP-AVI. Serum creatinine levels were followed up from the day prior to TAP-AVI daily to the eighth postoperative day and have been also recorded after six and twelve weeks after the procedure.
Prosthetic Valve System and Procedure The implanted prosthetic valve system consists of a pericardial xenograft fixed in a ballon expandable stent of stainless steel (SAPIEN THV; Edwards Lifesciences, Irvine, CA). All patients received a 23 mm or 26 mm external diameter prosthesis, depending on their echocardiographically measured annulus diameter. The necessary dispositions have been published previously (13, 15, 19). The injected contrast agent was Accupaque (Amersham Health AG, Wädenswil, Switzerland), an iodine containing and isoosmolar contrast medium (1 mL contains 647 mg iohexol).
Data Collection, Definitions of AKI, and Patient Demographics Data for all patients’ demographics, clinical characteristics, comorbid conditions, medical treatments, laboratory data, angiographic data (including amount and type of contrast used during TAP-AVI), and perioperative and
Table 2. Risk, Injury, Failure, Loss, and End-stage Kidney (RIFLE) Classification Class Risk Injury Failure Loss End-stage kidney disease
Glomerular Filtration Rate Criteria
Urine Output Criteria
Serum creatinine ⫻ 1.5 Serum creatinine ⫻ 2 Serum creatinine ⫻ 3, or serum creatinine ⱖ4 mg/dL with an acute rise ⬎0.5 mg/dL Persistent acute renal failure ⬅ complete loss of kidney function ⬎4 weeks End stage kidney disease ⬎3 months
⬍0.5 mL/kg/hour ⫻ 6 hours ⬍0.5 mL/kg/hour ⫻ 12 hours ⬍0.3 mL/kg/hour ⫻ 24 hours, or anuria ⫻ 12 hours
postoperative events were routinely collected in a computerized database for all patients undergoing TAP-AVI at our institution prospectively. Also, the creatinine levels one day prior to left heart catheterization were collected. We used these existing data for our analysis. Patients’ demographics are demonstrated in Table 1. Preoperative renal dysfunction has been defined as a serum creatinine level greater than 1.1 mg/dL. The incidence of postoperative AKI has been defined according to RIFLE criteria that are based on the worst of either glomerular filtration criteria or urine output criteria (⬍0.5 mL/kg/hour ⫻ 12 hours). RIFLE, an international consensus classification for acute kidney injury defines three grades of severity, risk (class R), injury (class I), and failure (class F) (Table 2). Glomerular filtration criteria are calculated as a defined increase of serum creatinine (serum creatinine ⫻ 2) above the baseline serum creatinine level. Acute kidney injury should be both abrupt (within 1 to 7 days) and sustained (more than 24 hours) [23]. Dialysis therapy was initiated by the attending nephrologists based on the clinical situation rather than any preset criteria. The primary endpoint of this study was renal outcome (development of postoperative AKI according to RIFLE criteria and follow-up of renal function for 8 weeks); secondary endpoints included 30-day mortality, length of intensive care unit stay (ICU-LOS), and length of hospital stay (LOS).
Results Twenty-nine out of 30 patients received transapical valve implantation as planned; one patient had to receive an AVR with CBP as the previously implanted valve secondary shifted into the ventricle. One patient needed a conversion to sternotomy to overstitch an affected part of the pulmonary artery. The only patient who needed CPB was the one who needed the conversion to conventional AVR; all other patients were treated completely offpump. This patient did not develop AKI and the conversion neither compromised this patient in the early postoperative phase nor does he suffer from any long-term consequences. Mortality risk, as estimated by logistic European system for cardiac operative risk evaluation (EuroSCORE) was 20.09% (SEM ⫾ 3.18). Eleven of the patients received
Fig 1. Changes in serum creatinine levels (n ⫽ 28). (POD ⫽ postoperative day.)
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Fig 2. Preoperative serum creatinine as a strong predictor of the development of acute kidney injury (AKI) (*p ⫽ 0.003).
23 mm prostheses, while 19 patients received prostheses with a diameter of 26 mm.
Serum Creatinine Levels and Development of AKI Two patients had already been afflicted with end-stage renal disease and required dialysis preoperatively as well. These patients survived the intervention without adverse effects. These patients have been excluded from the analysis of developing AKI. Accordingly, 28 patients were available for the analysis of the impact of TAP-AVI on renal function. Of 28 patients, median preoperative creatinine was 1.23 mg/dL (standard error of the mean [SEM] ⫾ 0.14); the median preoperative serum creatinine in the group of patients with a preoperative serum creatinine less than 1.1 mg/dL was 0.85 (SEM ⫾ 0.03). The median preoperative creatinine in patients with preoperatively increased creatinine levels (⬎1.1 mg/dL) was 1.35 (SEM ⫾ 0.07). The individual levels did not differ significantly from the creatinine levels each patient presented prior to left heart catheterization. Due to the fact that left heart catheterization had been performed at least 25 days prior to TAP-AVI, we did not take the application of contrast during catheterization into consideration. Median overall postoperative peak creatinine was 2.1 mg/dL (SEM ⫾ 0.27). Overall postoperative peak creatinine occurred on day 4 (Fig 1). The median serum creatinine at 48 hours postoperatively was 1.63 mg/dL (SEM ⫾ 0.19) with a median increase of 0.42 mg/dL (SEM ⫾ 0.1) in comparison with preoperative levels. Patients who showed preoperatively increased creatinine levels (⬎1.1 mg/dL) showed a median creatinine level of 2.01 mg/dL (SEM ⫾ 0.14) 48 hours postoperatively and a median increase in serum creatinine levels of 0.60 mg/dL (SEM ⫾ 0.17). Patients with a preoperative serum creatinine less than 1.1 mg/dL showed a median creatinine level of 1.1 mg/dL (SEM ⫾ 0.14) and an increase of 0.27 mg/dL (SEM ⫾ 0.12) (Fig 1). Acute kidney injury occurred in 16 patients (57%). Six
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ADULT CARDIAC Fig 3. Upper curve (): changes in serum creatinine levels of patients with a serum creatinine greater than 1.1 mg/dL (n ⫽ 10). Lower curve (⽧): changes in serum creatinine levels of patients with a serum creatinine less than 1.1 mg/dL (n ⫽ 18).
patients (21%) needed temporary postoperative dialysis (37.5% of the AKI group). Ten of the patients (36%) presented preoperative renal dysfunction with a serum creatinine level greater than 1.1 mg/dL. Nine patients with a preoperatively elevated serum creatinine level developed AKI; only one did not suffer from postoperative AKI. Three patients (10%) who presented serum creatinine levels less than 1.1 mg/dL preoperatively developed AKI. Therefore a preoperative serum creatinine greater than 1.1 mg/dL was a strong predictor for developing AKI (p ⬍ 0.01) (Figs 2; 3). Looking at the long-term follow-up, creatinine levels did reach preoperative levels within six weeks after TAP-AVI was performed. Median serum creatinine in the group of patients with a preoperative serum creatinine less than 1.1 mg/dL was 0.85 (SEM ⫾ 0.05) after six weeks and 0.9 (SEM ⫾ 0.1) after 12
Fig 5. Mortality in patients with postsurgical acute kidney injury (AKI) is considerably higher in comparison with patients without postsurgical impairment of renal function, although univariate analysis revealed no statistical significance (p ⫽ 0.13).
weeks. The median creatinine in patients with preoperatively increased creatinine levels (⬎1.1 mg/dL) was 1.43 (SEM ⫾ 0.09) on postoperative day 42 and 1.37 (SEM ⫾ 0.07) on postoperative day 72. None of the patients suffered from an impairment of renal function in comparison with the preoperative status. The median dose of contrast agent used overall was 115 mL (SEM ⫾ 1 2.9), equal to 1.6 mL/kg (SEM ⫾ 0.19) in relation to body weight. The amount of contrast did not differ significantly in the two groups (1.5 mL/kg body weight in patients without impairment in renal function versus 1.7 mL/kg body weight in the patients who developed AKI), and statistical analysis revealed no significant influence on the risk of developing AKI caused by the dose of the applicated contrast medium; neither the absolute dose (p ⫽ 0.09) nor the dose in relation to bodyweight (p ⫽ 0.72). Similar results with regard to the development of AKI showed the univariate analysis concerning the patient’s age (p ⫽ 0.5) and the existence of diabetes (p ⫽ 0.16). Further analysis concerning the relationship between a preexisting coronary heart disease and AKI showed a tendency to be associated with a higher risk of the development of AKI (70% preexisting CHD in the AKI group versus 50%), although the analysis did not reach a statistical significance (p ⫽ 0.28) (Fig 4).
Morbidity and Mortality
Fig 4. Development of acute kidney injury (AKI) in patients with preexisting congenital heart disease (CHD) and patients without CHD. The left bar shows the prevalence of AKI in patients without CHD (50%), the right bar shows the prevalence in patients with preexisting CHD (70%). The analysis showed no statistical significance (p ⫽ 0.28).
Analysis of the postoperative morbidity in terms of ICU-LOS and the complete length of hospital stay revealed no difference between the patients with and the patients without AKI. Patients with AKI had a medium ICU-LOS of 4.4 days (SEM ⫾ 0.7). Patients without AKI had a medium ICU-LOS of 4.1 days (SEM ⫾ 0.6). With regard to the complete hospital stay analysis as well showed no difference between the two groups (AKI: 11.5 days ⫾ 0.8; no AKI: 12.1 days ⫾ 0.8). None of the patients died during the intervention, 4 patients died in the first seven days after the procedure. The cause of death was a postoperative low cardiac output syndrome with multiple organic failure in the following in all cases; 30 day mortality was 13% in all patients and 50% in patients with postoperative need for dialysis. Statistical analysis
showed a trend to a higher mortality in the AKI group but univariate analysis did not reach statistical significance (p ⫽ 0.13) (Fig 5).
Comment Minimally invasive transapical aortic valve implantation is an innovative approach in search of less invasive treatment modalities for high-risk patients with severe aortic valve disease and has been introduced into clinical practice at a few centers recently. The ultimate goal is to reduce the morbidity and mortality of conventional aortic valve replacement while achieving similar good patient outcome. First data suggest that this procedure is safe and reliable with minimal operative risk and good early outcome [5]. In the present study we analyzed the renal outcome of 30 patients undergoing TAP-AVI at a single center. Moreover, two patients on chronic hemodialysis were followed up. According to the available literature, a total of three patients underwent TAP-AVI before without information with regard to outcome or survival of these patients [18, 19]. The TAP-AVI may impair renal function at least transiently in some patients. The AKI occurred in 57% of the patients and 21% required postsurgical renal replacement therapy. Compared with the estimated risk of 4.5% for renal replacement therapy in patients undergoing AVR with CBP [24], 21% is considerably higher but on the other hand the patient population in these studies is not comparable with our high risk patients with a high incidence of severe comorbidities and more frequent chronic kidney disease. To analyze the definite outcome concerning long time restitution of renal function, studies with larger patient populations and longer time follow-up have to be done. Concerning the potential mechanisms of developing AKI after TAPAVI we cannot give valid information or explanation by analyzing our data. One noticeable fact in this context is the frequent occurrence (11 patients of 16 patients with AKI) of elevated serum creatinine levels during the first 48 hours after surgery. Following the current definition of contrast-induced nephropathy (CIN) with an increase in serum creatinine of 44 mol/L (0.5 mg/dL) or a 25% increase from the baseline value 48 hours after intravascular injection of contrast media, or by the requirement of some form of renal replacement therapy [14, 15], these findings might lead to the conclusion of CIN as a major postoperative risk factor after TAP-AVI. On the other hand, there is no significant difference in the amount of contrast concerning the patients with AKI in comparison with the other group. Nevertheless, to clearly attribute these impairments of renal function to the need of contrast more studies have to be done and other risk factors such as intravascular coagulation, systemic inflammatory response syndrome, or atheroembolism have to be excluded. The importance of focussing on renal function may also result from the shown data. Acute kidney injury is, as a recently published analysis of cardiothoracic surgery patients from 2008 shows [25], a significant independent predictor of increased mortality, length of stay, and ventilator days [25]. Although we
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could not show any difference concerning length of ICU or hospital stay, we could show a considerable higher mortality in patients with AKI after TAP-AVI, although analysis did not reach statistical significance. With regard to preoperative risk assessment we could show that impaired preoperative renal function defined as a serum creatinine greater than 1.1 mg/dLl, is a significant indicator for postsurgical AKI and should be taken into consideration while assessing the patients for this procedure. We could not show any correlation between other known risk factors for AKI such as older age or diabetes mellitus [18, 19]. Furthermore, there has been no statistically significant coherency concerning the dose of applicated contrast and postsurgical outcome. Although the question of dose-related nephrotoxicity by using contrast agent in different clinical procedures is still discussed [25], there is no evidence from our data to suggest any dose-related nephrotoxicity. The prevalence of congenital heart disease (CHD) in patients undergoing TAP-AVI emerged as another possible risk factor for AKI. Although we could only show a light trend towards an increased risk, the most likely explanation is the more prominent generalized atherosclerosis in these patients. In this context we have to name the limitations of this study. We are aware of the fact that the studied number of patients is small, especially with regard to the possibilities of statistical analysis. On the other hand the surgical procedure is relatively new and deals with a collective of high-risk patients not comparable with other published studies of renal function after cardiac surgery. In conclusion, TAP-AVI seems to be a feasible procedure for high-risk patients with an adjustable but clear risk of developing AKI. In spite of the promising results concerning the surgical outcome one should have in mind that, especially in the selected collective of high risk patients with a high incidence of comorbidities, the risk of AKI is not a negligible factor for the valuation of this procedure. Although it is not arguable that the detraction of the renal function is of minor importance in comparison with the risk of a conventional open heart surgery with CPB, or rather to the risk of a complete avoidance of surgical treatment, the risk of a postprocedural AKI should be incorporated as a not uncommonly appearing complication. To reduce the risk of AKI and to achieve an optimal treatment of a possibly occurring AKI, and therewith to aim the goal of establishing a procedure with a reduced perioperative risk especially in polymorbid patients, further studies with a larger patient population need to be done to identify risk factors for the development of AKI; patients at risk for AKI (eg, those with elevated preoperative creatinine levels and contingently those with accompanying CHD) should be identified and treated in collaboration with the attending nephrologists. Furthermore preventive strategies, especially for the patients with high risk for AKI, deserve consideration; for example, the prevention of contrast-induced tubular necrosis by using N-acetylcystein or sodium bicarbonate, the possibility of careful intravenous hydration with respect
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to and based on the individual cardiac performance of the patients, as well as the controversially discussed option of immediate dialysis after surgery [26, 27]. Considering the present data, further studies need to be done to scrutinize the incidence of AKI after TAP-AVI, its influence of perioperative morbidity and mortality, and the effectiveness of preoperative prophylaxis, particularly because of the high-risk profile of this patient population.
References 1. Ross JJ, Braunwald E. Aortic stenosis. Circulation 1968;38: 61–7. 2. Bonow RO, Carabello B, de Leon AC, et al. ACC/AHA Guidelines for the Management of Patients With Valvular Heart Disease. Executive Summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients With Valvular Heart Disease). J Heart Valve Dis 1998;7:672–707. 3. Otto CM, Mickel MC, Kennedy JW, et al. Three-year outcome after balloon aortic valvuloplasty. Insights into prognosis of valvular aortic stenosis. Circulation 1994;89:642–50. 4. Ye J, Cheung A, Lichtenstein SV, et al. Six-month outcome of transapical transcatheter aortic valve implantation in the initial seven patients. Eur J Cardiothorac Surg 2007;31:16 –21. 5. Andersen HR, Knudsen LL, Hasenkam JM. Transluminal implantation of artificial heart valves. Description of a new expandable aortic valve and initial results with implantation by catheter technique in closed chest pigs. Eur Heart J 1992;13:704 – 8. 6. Cribier A, Eltchaninoff H, Bash A, et al. Trans-catheter implantation of balloon-expandable prosthetic heart valves, early results in an animal model. Circulation 2001;104(suppl 2):II552. 7. Boudjemline Y, Bonhoeffer P. Steps toward percutaneous aortic valve replacement. Circulation 2002;105:775– 8. 8. Boudjemline Y, Bonhoeffer P. Percutaneous implantation of a valve in the descending aorta in lambs. Eur Heart J 2002;23:1045–9. 9. Webb JG, Munt B, Makkar RR, Naqvi TZ, Dang N. Percutaneous stent-mounted valve for treatment of aortic or pulmonary valve disease. Catheter Cardiovasc Interv 2004;63: 89 –93. 10. Grube E, Laborde JC, Zickmann B, et al. First report on a human percutaneous transluminal implantation of a selfexpanding valve prosthesis for interventional treatment of aortic valve stenosis. Catheter Cardiovasc Interv 2005;66: 465–9. 11. Beyersdorf F. Transapical transcatheter aortic valve implantation. Eur J Cardiothorac Surg 2007;31:7– 8.
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12. Siegenthaler MP, Martin J, van de Loo A, et al. Implantation of the permanent Jarvik-2000 left ventricular assist device: a single-center experience. J Am Coll Cardiol 2002;39:1764 –72. 13. Lichtenstein SV, Cheung A, Ye J, et al. Transapical transcatheter aortic valve implantation in humans: initial clinical experience. Circulation 2006;114:591– 6. 14. Thomsen HS, Morcos SK, Barrett BJ. Contrast-induced nephropathy: the wheel has turned 360 degrees. Acta Radiol 2008;49:646 –57. 15. Ranucci M, Ballotta A, Kunkl A, et al. Influence of the timing of cardiac catheterization and the amount of contrast media on acute renal failure after cardiac surgery. Am J Cardiol 2008;101:1112– 8. 16. Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol 2004;44:1393–9. 17. Walther T, Falk V, Kempfert J, et al. Transapical minimally invasive aortic valve implantation; the initial 50 patients. Eur J Cardiothorac Surg 2008;33:983– 8. 18. Wong GT, Irwin MG. Contrast-induced nephropathy. Br J Anaesth 2007;99:474 – 83. 19. Falvo A, Horst HM, Rubinfeld I, et al. Acute renal failure in cardiothoracic surgery patients: what is the best definition of this common and potent predictor of increased morbidity and mortality. Am J Surg 2008;196:379 – 83. 20. Walther T, Simon P, Dewey T, et al. Transapical minimally invasive aortic valve implantation: multicenter experience. Circulation 2007;116:1240 –5. 21. Walther T, Falk V, Borger MA, et al. Minimally invasive transapical beating heart aortic valve implantation-proof of concept. Eur J Cardiothorac Surg 2007;31:9 –15. 22. Aregger F, Wenaweser P, Hellige GJ. Risk of acute kidney injury in patients with severe aortic valve stenosis undergoing transcatheter valve replacement. Nephrol Dial Transplant 2009;24:2175–9. 23. Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P, Acute Dialysis Quality Initiative workgroup. Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care 2004;8:R204 – R212. 24. Gummert JF, Bucerius J, Walther T, et al. Requirement for renal replacement therapy in patients undergoing cardiac surgery. Thorac Cardiovasc Surg 2004;52:70 – 6. 25. Rosovsky M, Rusinek H. Dose-related nephrotoxicity. Radiology 2006;240:614. 26. Lee PT, Chou KJ, Liu CP, et al. Renal protection for coronary angiography in advanced renal failure patients by prophylactic hemodialysis. A randomized controlled trial. J Am Coll Cardiol 2007;50:1015–20. 27. Vogt B, Ferrari P, Schönholzer C, et al. Prophylactic hemodialysis after radiocontrast media in patients with renal insufficiency is potentially harmful. Am J Med 2001;111: 692– 8.
Background. The new technique of minimally invasive transapical aortic valve implantation (TAP-AVI) deals with high-risk patients and despite the absence of cardiopulmonary bypass it might lead to renal impairment. The aim of this study was to estimate the risk of the development of acute kidney injury (AKI) after TAP-AVI and to identify possible risk factors with regard to the morbidity and mortality of the patients. Methods. Data of 30 consecutive patients undergoing TAP-AVI were recorded and followed up for 8 weeks. Postoperative AKI has been defined according to RIFLE criteria. Two patients on chronic hemodialysis have been followed up. Results. Of 28 patients, AKI occurred in 16 patients (57%). Statistical analysis revealed no influence on the risk of developing AKI caused by the dose of applicated contrast medium (p ⴝ 0.09), the patient’s age (p ⴝ 0.5), or the existence of diabetes (p ⴝ 0. 16). Analysis concerning the relationship between a preexisting coronary heart
disease and AKI showed a tendency to be associated with a higher risk of the development of AKI (70% preexisting congenital heart disease in the AKI group versus 50%; p ⴝ 0.28). Only a preoperative serum creatinine greater than 1.1 mg/dL was a strong predictor for developing AKI (p < 0.01). Length of stay in the intensive care unit and the complete length of hospital stay revealed no difference with regard to postoperative development of AKI though statistical analysis showed a trend to a higher mortality in the AKI group (27% vs 6%); univariate analysis did not reach statistical significance (p ⴝ 0.13). Conclusions. The TAP-AVI seems to be a feasible procedure for high-risk patients with a clear risk of developing AKI. Patients at risk should be identified and, if indicated, already preoperatively treated in collaboration with the attending nephrologists. (Ann Thorac Surg 2010;89:465–70) © 2010 by The Society of Thoracic Surgeons
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auspicious one because it seems to offer many potential advantages, including the permission of a more precise positioning and placement of the prosthesis as well as an access which has been used before successfully for left ventricular assist devices and apicoaortic conduit implantation [11, 12]. Taken together, preliminary data suggest that the minimally invasive transapical approach is a viable alternative for patients in whom conventional AVR is not feasible or possesses unacceptable risk, and may lead to a significant decrease in perioperative trauma and eventually to a decrease in perioperative risk. Despite these encouraging data this newly developed technique includes the need of fluoroscopy and angiography using a contrast agent to aid positioning of the valve [13], which may, especially in patients with diabetic nephropathy, lead to acute kidney injury (AKI), which is associated with increased morbidity and mortality [14, 15]. Although previous studies established clinical and surgical characteristics associated with increased risk of acute renal failure (ARF) after cardiac surgery (for example, CPB duration, severe hemodilution during CPB reflected by nadir hematocrit, and low oxygen delivery during CPB), which are avoided by the lack of using CPB during transapical aortic valve implantation (TAP-AVI), other fac-
he treatment of choice for patients with symptomatic severe degenerative aortic stenosis, which is the most frequently acquired heart valve lesion, is the surgical aortic valve replacement (AVR) with cardiopulmonary bypass (CBP). Due to the fact that medically managed symptomatic patients have a poor prognosis [1–3], this procedure has become the gold standard therapy for those patients, although many patients with symptomatic severe aortic stenosis have significant comorbidities. However, especially in these patients, AVR with CBP can be associated with an unacceptable perioperative morbidity and mortality [4]. To reduce the risk caused by this procedure several groups developed new strategies using aortic valvuloplasty to avoid invasive surgery and CPB [5–9]. This led to two approaches [10] which have evolved as potential access routes to the aortic valve during recent years: the retrograde arterial approach using the femoral artery and the transapical approach with implantation of the aortic valve through the left ventricular apex by lateral minithoracotomy. Concerning the technique, the transapical route seems to be the most
Accepted for publication Sept 17, 2009. Address correspondence to Dr Strauch, University Hospital of Cologne, Department of Cardiothoracic Surgery, Kerpener Strasse 62, Cologne, 50925, Germany; e-mail: [email protected].
© 2010 by The Society of Thoracic Surgeons Published by Elsevier Inc
0003-4975/10/$36.00 doi:10.1016/j.athoracsur.2009.09.090
ADULT CARDIAC
Minimally Invasive Transapical Aortic Valve Implantation and the Risk of Acute Kidney Injury
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Ann Thorac Surg 2010;89:465–70
Material and Methods
Table 1. Patient Demographics
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Variables
Mean (Range)
Total (n) Female Age (years) Body weight (kg) EuroSCORE (points) Logistic EuroSCORE (%) STS score (%) Diabetes mellitus (n) Coronary heart disease (without indication for surgery) (n)
30 19 82.1 (71–88) 70.7 (50–94) 9.6 (6–18) 19.01 (5.1–77.4) 13.6 (3.2–26) 8 19
EuroSCORE ⫽ European system for cardiac operative risk evaluation; STS ⫽ Society of Thoracic Surgeons.
tors such as older age, diabetes mellitus, and congestive heart failure [16, 17] still remain. Additionally the exigency for using contrast agents presents a new risk factor, which is well known for exacerbating the risk of AKI and may play an important role in terms of estimating the potential risk of this procedure, influencing perioperative morbidity and mortality. The impact of AKI (especially with regard to the administration of contrast) on clinical outcomes has been evaluated most extensively in patients undergoing percutaneous coronary intervention and in patients undergoing cardiac surgery. In both it is associated with increased mortality in-hospital as well as after one year [18, 19]. Information on the impact of TAP-AVI is scarce. Two studies reported the need for postoperative renal replacement therapy in a total of 9 of 69 patients [20, 21]. In these reports, renal failure was not defined, preexisting impairment of renal function was not specified, and information of presurgical and postsurgical creatinine levels as an indicator for the glomerular filtration rate (GFR) was missing. The only study with regard to renal function in patients undergoing transcatheter valve replacement with 58 patients mixes up transfemoral (n ⫽ 46) and transapical (n ⫽ 12) valve replacement with no regard to the differences between these approaches [22]. In this context the aim of the present study was to analyze the results of 30 consecutive patients receiving TAP-AVI with respect to presurgical and postsurgical renal function and possible risk factors for AKI, referring to the assumption that this procedure might be feasible especially in patients classified as high risk.
Patient Characteristics and Inclusion Criteria Thirty consecutive patients with severe aortic stenosis and an unacceptable high risk for open heart surgery with CPB because of significant comorbidity were included in this study between February 2008 and January 2009. This retrospective study has been approved and accepted by the local Ethics Committee. The patients accepted for this procedure were selected by a clinical committee consisting of cardiologists and cardiac surgeons of our department, estimating the frailty in combination with the preoperative cardiac status in combination with preexisting comorbidities and therefore the risk profile of the patients individually. For prevention of contrast-induced renal failure all patients received 600 mg of N-acetylcystein on the evening prior to the procedure and two hours after the intervention. We abstained from intravenous hydration due to the restricted cardiac performance of the patients. All patients underwent echocardiography and left heart catheterization prior to TAP-AVI. Left heart catheterization was performed at least 29 days prior to TAP-AVI. Serum creatinine levels were followed up from the day prior to TAP-AVI daily to the eighth postoperative day and have been also recorded after six and twelve weeks after the procedure.
Prosthetic Valve System and Procedure The implanted prosthetic valve system consists of a pericardial xenograft fixed in a ballon expandable stent of stainless steel (SAPIEN THV; Edwards Lifesciences, Irvine, CA). All patients received a 23 mm or 26 mm external diameter prosthesis, depending on their echocardiographically measured annulus diameter. The necessary dispositions have been published previously (13, 15, 19). The injected contrast agent was Accupaque (Amersham Health AG, Wädenswil, Switzerland), an iodine containing and isoosmolar contrast medium (1 mL contains 647 mg iohexol).
Data Collection, Definitions of AKI, and Patient Demographics Data for all patients’ demographics, clinical characteristics, comorbid conditions, medical treatments, laboratory data, angiographic data (including amount and type of contrast used during TAP-AVI), and perioperative and
Table 2. Risk, Injury, Failure, Loss, and End-stage Kidney (RIFLE) Classification Class Risk Injury Failure Loss End-stage kidney disease
Glomerular Filtration Rate Criteria
Urine Output Criteria
Serum creatinine ⫻ 1.5 Serum creatinine ⫻ 2 Serum creatinine ⫻ 3, or serum creatinine ⱖ4 mg/dL with an acute rise ⬎0.5 mg/dL Persistent acute renal failure ⬅ complete loss of kidney function ⬎4 weeks End stage kidney disease ⬎3 months
⬍0.5 mL/kg/hour ⫻ 6 hours ⬍0.5 mL/kg/hour ⫻ 12 hours ⬍0.3 mL/kg/hour ⫻ 24 hours, or anuria ⫻ 12 hours
postoperative events were routinely collected in a computerized database for all patients undergoing TAP-AVI at our institution prospectively. Also, the creatinine levels one day prior to left heart catheterization were collected. We used these existing data for our analysis. Patients’ demographics are demonstrated in Table 1. Preoperative renal dysfunction has been defined as a serum creatinine level greater than 1.1 mg/dL. The incidence of postoperative AKI has been defined according to RIFLE criteria that are based on the worst of either glomerular filtration criteria or urine output criteria (⬍0.5 mL/kg/hour ⫻ 12 hours). RIFLE, an international consensus classification for acute kidney injury defines three grades of severity, risk (class R), injury (class I), and failure (class F) (Table 2). Glomerular filtration criteria are calculated as a defined increase of serum creatinine (serum creatinine ⫻ 2) above the baseline serum creatinine level. Acute kidney injury should be both abrupt (within 1 to 7 days) and sustained (more than 24 hours) [23]. Dialysis therapy was initiated by the attending nephrologists based on the clinical situation rather than any preset criteria. The primary endpoint of this study was renal outcome (development of postoperative AKI according to RIFLE criteria and follow-up of renal function for 8 weeks); secondary endpoints included 30-day mortality, length of intensive care unit stay (ICU-LOS), and length of hospital stay (LOS).
Results Twenty-nine out of 30 patients received transapical valve implantation as planned; one patient had to receive an AVR with CBP as the previously implanted valve secondary shifted into the ventricle. One patient needed a conversion to sternotomy to overstitch an affected part of the pulmonary artery. The only patient who needed CPB was the one who needed the conversion to conventional AVR; all other patients were treated completely offpump. This patient did not develop AKI and the conversion neither compromised this patient in the early postoperative phase nor does he suffer from any long-term consequences. Mortality risk, as estimated by logistic European system for cardiac operative risk evaluation (EuroSCORE) was 20.09% (SEM ⫾ 3.18). Eleven of the patients received
Fig 1. Changes in serum creatinine levels (n ⫽ 28). (POD ⫽ postoperative day.)
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Fig 2. Preoperative serum creatinine as a strong predictor of the development of acute kidney injury (AKI) (*p ⫽ 0.003).
23 mm prostheses, while 19 patients received prostheses with a diameter of 26 mm.
Serum Creatinine Levels and Development of AKI Two patients had already been afflicted with end-stage renal disease and required dialysis preoperatively as well. These patients survived the intervention without adverse effects. These patients have been excluded from the analysis of developing AKI. Accordingly, 28 patients were available for the analysis of the impact of TAP-AVI on renal function. Of 28 patients, median preoperative creatinine was 1.23 mg/dL (standard error of the mean [SEM] ⫾ 0.14); the median preoperative serum creatinine in the group of patients with a preoperative serum creatinine less than 1.1 mg/dL was 0.85 (SEM ⫾ 0.03). The median preoperative creatinine in patients with preoperatively increased creatinine levels (⬎1.1 mg/dL) was 1.35 (SEM ⫾ 0.07). The individual levels did not differ significantly from the creatinine levels each patient presented prior to left heart catheterization. Due to the fact that left heart catheterization had been performed at least 25 days prior to TAP-AVI, we did not take the application of contrast during catheterization into consideration. Median overall postoperative peak creatinine was 2.1 mg/dL (SEM ⫾ 0.27). Overall postoperative peak creatinine occurred on day 4 (Fig 1). The median serum creatinine at 48 hours postoperatively was 1.63 mg/dL (SEM ⫾ 0.19) with a median increase of 0.42 mg/dL (SEM ⫾ 0.1) in comparison with preoperative levels. Patients who showed preoperatively increased creatinine levels (⬎1.1 mg/dL) showed a median creatinine level of 2.01 mg/dL (SEM ⫾ 0.14) 48 hours postoperatively and a median increase in serum creatinine levels of 0.60 mg/dL (SEM ⫾ 0.17). Patients with a preoperative serum creatinine less than 1.1 mg/dL showed a median creatinine level of 1.1 mg/dL (SEM ⫾ 0.14) and an increase of 0.27 mg/dL (SEM ⫾ 0.12) (Fig 1). Acute kidney injury occurred in 16 patients (57%). Six
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ADULT CARDIAC Fig 3. Upper curve (): changes in serum creatinine levels of patients with a serum creatinine greater than 1.1 mg/dL (n ⫽ 10). Lower curve (⽧): changes in serum creatinine levels of patients with a serum creatinine less than 1.1 mg/dL (n ⫽ 18).
patients (21%) needed temporary postoperative dialysis (37.5% of the AKI group). Ten of the patients (36%) presented preoperative renal dysfunction with a serum creatinine level greater than 1.1 mg/dL. Nine patients with a preoperatively elevated serum creatinine level developed AKI; only one did not suffer from postoperative AKI. Three patients (10%) who presented serum creatinine levels less than 1.1 mg/dL preoperatively developed AKI. Therefore a preoperative serum creatinine greater than 1.1 mg/dL was a strong predictor for developing AKI (p ⬍ 0.01) (Figs 2; 3). Looking at the long-term follow-up, creatinine levels did reach preoperative levels within six weeks after TAP-AVI was performed. Median serum creatinine in the group of patients with a preoperative serum creatinine less than 1.1 mg/dL was 0.85 (SEM ⫾ 0.05) after six weeks and 0.9 (SEM ⫾ 0.1) after 12
Fig 5. Mortality in patients with postsurgical acute kidney injury (AKI) is considerably higher in comparison with patients without postsurgical impairment of renal function, although univariate analysis revealed no statistical significance (p ⫽ 0.13).
weeks. The median creatinine in patients with preoperatively increased creatinine levels (⬎1.1 mg/dL) was 1.43 (SEM ⫾ 0.09) on postoperative day 42 and 1.37 (SEM ⫾ 0.07) on postoperative day 72. None of the patients suffered from an impairment of renal function in comparison with the preoperative status. The median dose of contrast agent used overall was 115 mL (SEM ⫾ 1 2.9), equal to 1.6 mL/kg (SEM ⫾ 0.19) in relation to body weight. The amount of contrast did not differ significantly in the two groups (1.5 mL/kg body weight in patients without impairment in renal function versus 1.7 mL/kg body weight in the patients who developed AKI), and statistical analysis revealed no significant influence on the risk of developing AKI caused by the dose of the applicated contrast medium; neither the absolute dose (p ⫽ 0.09) nor the dose in relation to bodyweight (p ⫽ 0.72). Similar results with regard to the development of AKI showed the univariate analysis concerning the patient’s age (p ⫽ 0.5) and the existence of diabetes (p ⫽ 0.16). Further analysis concerning the relationship between a preexisting coronary heart disease and AKI showed a tendency to be associated with a higher risk of the development of AKI (70% preexisting CHD in the AKI group versus 50%), although the analysis did not reach a statistical significance (p ⫽ 0.28) (Fig 4).
Morbidity and Mortality
Fig 4. Development of acute kidney injury (AKI) in patients with preexisting congenital heart disease (CHD) and patients without CHD. The left bar shows the prevalence of AKI in patients without CHD (50%), the right bar shows the prevalence in patients with preexisting CHD (70%). The analysis showed no statistical significance (p ⫽ 0.28).
Analysis of the postoperative morbidity in terms of ICU-LOS and the complete length of hospital stay revealed no difference between the patients with and the patients without AKI. Patients with AKI had a medium ICU-LOS of 4.4 days (SEM ⫾ 0.7). Patients without AKI had a medium ICU-LOS of 4.1 days (SEM ⫾ 0.6). With regard to the complete hospital stay analysis as well showed no difference between the two groups (AKI: 11.5 days ⫾ 0.8; no AKI: 12.1 days ⫾ 0.8). None of the patients died during the intervention, 4 patients died in the first seven days after the procedure. The cause of death was a postoperative low cardiac output syndrome with multiple organic failure in the following in all cases; 30 day mortality was 13% in all patients and 50% in patients with postoperative need for dialysis. Statistical analysis
showed a trend to a higher mortality in the AKI group but univariate analysis did not reach statistical significance (p ⫽ 0.13) (Fig 5).
Comment Minimally invasive transapical aortic valve implantation is an innovative approach in search of less invasive treatment modalities for high-risk patients with severe aortic valve disease and has been introduced into clinical practice at a few centers recently. The ultimate goal is to reduce the morbidity and mortality of conventional aortic valve replacement while achieving similar good patient outcome. First data suggest that this procedure is safe and reliable with minimal operative risk and good early outcome [5]. In the present study we analyzed the renal outcome of 30 patients undergoing TAP-AVI at a single center. Moreover, two patients on chronic hemodialysis were followed up. According to the available literature, a total of three patients underwent TAP-AVI before without information with regard to outcome or survival of these patients [18, 19]. The TAP-AVI may impair renal function at least transiently in some patients. The AKI occurred in 57% of the patients and 21% required postsurgical renal replacement therapy. Compared with the estimated risk of 4.5% for renal replacement therapy in patients undergoing AVR with CBP [24], 21% is considerably higher but on the other hand the patient population in these studies is not comparable with our high risk patients with a high incidence of severe comorbidities and more frequent chronic kidney disease. To analyze the definite outcome concerning long time restitution of renal function, studies with larger patient populations and longer time follow-up have to be done. Concerning the potential mechanisms of developing AKI after TAPAVI we cannot give valid information or explanation by analyzing our data. One noticeable fact in this context is the frequent occurrence (11 patients of 16 patients with AKI) of elevated serum creatinine levels during the first 48 hours after surgery. Following the current definition of contrast-induced nephropathy (CIN) with an increase in serum creatinine of 44 mol/L (0.5 mg/dL) or a 25% increase from the baseline value 48 hours after intravascular injection of contrast media, or by the requirement of some form of renal replacement therapy [14, 15], these findings might lead to the conclusion of CIN as a major postoperative risk factor after TAP-AVI. On the other hand, there is no significant difference in the amount of contrast concerning the patients with AKI in comparison with the other group. Nevertheless, to clearly attribute these impairments of renal function to the need of contrast more studies have to be done and other risk factors such as intravascular coagulation, systemic inflammatory response syndrome, or atheroembolism have to be excluded. The importance of focussing on renal function may also result from the shown data. Acute kidney injury is, as a recently published analysis of cardiothoracic surgery patients from 2008 shows [25], a significant independent predictor of increased mortality, length of stay, and ventilator days [25]. Although we
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could not show any difference concerning length of ICU or hospital stay, we could show a considerable higher mortality in patients with AKI after TAP-AVI, although analysis did not reach statistical significance. With regard to preoperative risk assessment we could show that impaired preoperative renal function defined as a serum creatinine greater than 1.1 mg/dLl, is a significant indicator for postsurgical AKI and should be taken into consideration while assessing the patients for this procedure. We could not show any correlation between other known risk factors for AKI such as older age or diabetes mellitus [18, 19]. Furthermore, there has been no statistically significant coherency concerning the dose of applicated contrast and postsurgical outcome. Although the question of dose-related nephrotoxicity by using contrast agent in different clinical procedures is still discussed [25], there is no evidence from our data to suggest any dose-related nephrotoxicity. The prevalence of congenital heart disease (CHD) in patients undergoing TAP-AVI emerged as another possible risk factor for AKI. Although we could only show a light trend towards an increased risk, the most likely explanation is the more prominent generalized atherosclerosis in these patients. In this context we have to name the limitations of this study. We are aware of the fact that the studied number of patients is small, especially with regard to the possibilities of statistical analysis. On the other hand the surgical procedure is relatively new and deals with a collective of high-risk patients not comparable with other published studies of renal function after cardiac surgery. In conclusion, TAP-AVI seems to be a feasible procedure for high-risk patients with an adjustable but clear risk of developing AKI. In spite of the promising results concerning the surgical outcome one should have in mind that, especially in the selected collective of high risk patients with a high incidence of comorbidities, the risk of AKI is not a negligible factor for the valuation of this procedure. Although it is not arguable that the detraction of the renal function is of minor importance in comparison with the risk of a conventional open heart surgery with CPB, or rather to the risk of a complete avoidance of surgical treatment, the risk of a postprocedural AKI should be incorporated as a not uncommonly appearing complication. To reduce the risk of AKI and to achieve an optimal treatment of a possibly occurring AKI, and therewith to aim the goal of establishing a procedure with a reduced perioperative risk especially in polymorbid patients, further studies with a larger patient population need to be done to identify risk factors for the development of AKI; patients at risk for AKI (eg, those with elevated preoperative creatinine levels and contingently those with accompanying CHD) should be identified and treated in collaboration with the attending nephrologists. Furthermore preventive strategies, especially for the patients with high risk for AKI, deserve consideration; for example, the prevention of contrast-induced tubular necrosis by using N-acetylcystein or sodium bicarbonate, the possibility of careful intravenous hydration with respect
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to and based on the individual cardiac performance of the patients, as well as the controversially discussed option of immediate dialysis after surgery [26, 27]. Considering the present data, further studies need to be done to scrutinize the incidence of AKI after TAP-AVI, its influence of perioperative morbidity and mortality, and the effectiveness of preoperative prophylaxis, particularly because of the high-risk profile of this patient population.
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