Doppler-based renal resistance index for the detection of acute kidney injury and the non-invasive evaluation of paravalvular aortic regurgitation after transcatheter aortic valve implantation.

AIMS: Acute kidney injury (AKI) is a strong but rather late predictor of mortality after transcatheter aortic valve implantation (TAVI). Early clinically useful markers for the detection of AKI and prediction of outcome are needed in order to control and improve management of periprocedural complications after TAVI. The aim of our study was to assess the predictive value of the Doppler-based renal resistance index (RRI), which correlates inversely with effective renal blood flow and creatinine clearance, for AKI in patients undergoing TAVI and to evaluate its association with paravalvular aortic regurgitation (PAR). METHODS AND RESULTS: TAVI was performed with the Medtronic CoreValve prosthesis in 132 consecutive high-risk patients (mean logistic EuroSCORE: 30.3±18.2%). RRI, serum creatinine and cystatin C level were determined before, and 4 hrs, 24 hrs, 48 hrs, 72 hrs, and 7 days after TAVI. AKI occurred in 32/132 patients (24.2%). While serum creatinine and cystatin C levels decreased at first after TAVI (also in most patients developing AKI), the RRI increased significantly immediately after the procedure from 0.79±0.09 to 0.87±0.12 in patients developing AKI (p=0.003). A RRI >0.85 predicted post-interventional AKI with a sensitivity of 58% and specificity of 86%, and was superior to the serum creatinine level (p<0.001). In addition, an elevated RRI was significantly related to haemodynamic changes after TAVI and was associated with the occurrence of moderate/severe PAR (p<0.001). CONCLUSIONS: Measurement of the Doppler-based RRI predicts risk for AKI and increased mortality rates at an early post-procedural time point and is related to the occurrence of more-than-mild paravalvular aortic regurgitation after TAVI.

Aortic regurgitation index defines severity of peri-prosthetic regurgitation and predicts outcome in patients after transcatheter aortic valve implantation.

OBJECTIVES: The aim of this study was to provide a simple, reproducible, and point-of-care assessment of peri-prosthetic aortic regurgitation (periAR) during transcatheter aortic valve implantation (TAVI) and to decipher the impact of this peri-procedural parameter on outcome. BACKGROUND: Because periAR after TAVI might be associated with adverse outcome, precise quantification of periAR is of paramount importance but remains technically challenging. METHODS: The severity of periAR was prospectively evaluated in 146 patients treated with the Medtronic CoreValve (Minneapolis, Minnesota) prosthesis by echocardiography, angiography, and measurement of the aortic regurgitation (AR) index, which is calculated as ratio of the gradient between diastolic blood pressure (DBP) and left ventricular end-diastolic pressure (LVEDP) to systolic blood pressure (SBP): [(DBP - LVEDP)/SBP] × 100. RESULTS: After TAVI, 53 patients (36.3%) showed no signs of periAR and 71 patients (48.6%) showed only mild periAR, whereas 18 patients (12.3%) and 4 patients (2.7%) suffered from moderate and severe periAR, respectively. The AR index decreased stepwise from 31.7 ± 10.4 in patients without periAR, to 28.0 ± 8.5 with mild periAR, 19.6 ± 7.6 with moderate periAR, and 7.6 ± 2.6 with severe periAR (p < 0.001), respectively. Patients with AR index <25 had a significantly increased 1-year mortality risk compared with patients with AR index ≥25 (46.0% vs. 16.7%; p < 0.001). The AR index provided additional prognostic information beyond the echocardiographically assessed severity of periAR and independently predicted 1-year mortality (hazard ratio: 2.9, 95% confidence interval: 1.3 to 6.4; p = 0.009). CONCLUSIONS: The assessment of the AR index allows a precise judgment of periAR, independently predicts 1-year mortality after TAVI, and provides additional prognostic information that is complementary to the echocardiographically assessed severity of periAR.

Systemic inflammatory response syndrome predicts increased mortality in patients after transcatheter aortic valve implantation.

AIMS: The outcome of patients undergoing surgical or interventional therapy is unfavourably influenced by severe systemic inflammation. We assessed the impact of a systemic inflammatory response syndrome (SIRS) on the outcome after transcatheter aortic valve implantation (TAVI). METHODS AND RESULTS: One hundred and fifty-two high-risk patients (mean age: 80.5 ± 6.5 years, mean logistic EuroSCORE: 30.4 ± 8.1%) with symptomatic severe aortic stenosis underwent TAVI. Proinflammatory cytokines [interleukin-6 (IL-6) and interleukin-8 (IL-8)], and acute phase reactants [C-reactive protein (CRP) and procalcitonin (PCT)] were measured at baseline and 1, 4, 24, 48, 72 h, and 7 days after TAVI. Sixty-one of 152 patients developed SIRS during the first 48 h after TAVI. Systemic inflammatory response syndrome patients were characterized by leucocytosis ≥12 × 10(9)/L (83.6 vs. 12.1%; P < 0.001), hyperventilation (80.3 vs. 35.2%; P < 0.001), tachycardia (37.7 vs. 9.9%; P < 0.001), and fever (31.1 vs. 3.3%; P < 0.001) compared with patients without SIRS. Furthermore, the occurrence of SIRS was characterized by a significantly elevated release of IL-6 and IL-8 with subsequent increase in the leucocyte count, CRP, and PCT. Major vascular complications [odds ratio (OR) 5.1, 95% confidence interval (CI): 1.3-19.6; P = 0.018] and the number of ventricular pacing runs (OR 1.7, 95% CI: 1.1-2.8; P = 0.025) were independent predictors of SIRS. The occurrence of SIRS was related to 30-day and 1-year mortality (18.0 vs. 1.1% and 52.5 vs. 9.9%, respectively; P < 0.001) and independently predicted 1-year mortality risk (hazard ratio: 4.3, 95% CI: 1.9-9.9; P < 0.001). CONCLUSIONS: SIRS may occur after TAVI and is a strong predictor of mortality. The development of SIRS could be easily identified by a significant increase in the leucocyte count shortly after TAVI.

Renal function as predictor of mortality in patients after percutaneous transcatheter aortic valve implantation.

OBJECTIVES: The aim of this study was to determine the influence of baseline renal function and periprocedural acute kidney injury (AKI) on prognosis after transcatheter aortic valve implantation (TAVI). BACKGROUND: Evidence is growing that renal function is a major predictor of mortality in patients after TAVI. METHODS: TAVI was performed with the 18-F CoreValve prosthesis via transfemoral access. All-cause mortality was determined 30 days and 1 year after TAVI in 77 patients with a mean Society of Thoracic Surgeons mortality score of 9.3 ± 6.1% and a mean logistic European System for Cardiac Operative Risk Evaluation of 31.2 ± 17.6%. RESULTS: Overall procedural success rate was 98% with 1 periprocedural death. The 30-day mortality was 10%, and 1-year mortality was 26%. The mortality risk increased stepwise across quartiles of baseline serum creatinine. An AKI occurred in 20 of 77 patients: 12 patients (60%) with AKI died during follow-up. The incidence of AKI was related to peripheral arterial disease (65% vs. 39%; p = 0.04), the occurrence of a systemic inflammatory response syndrome (60% vs. 21%, p = 0.002), and post-procedural peri-prosthetic regurgitation ≥2+ (35% vs. 9%, p = 0.02). Impaired renal function at baseline reflected by serum creatinine ≥1.58 mg/dl (hazard ratio: 3.9, 95% confidence interval: 1.6 to 9.5; p = 0.002) and the occurrence of AKI (hazard ratio: 5.9, 95% confidence interval: 2.4 to 14.5, p < 0.001) that was not related to the amount of contrast dye were strong predictors of 1-year mortality after TAVI. CONCLUSIONS: Impaired renal function at baseline and the occurrence of periprocedural AKI, independent whether renal function returns to baseline or not, are strong predictors of 30-day and 1-year mortality after TAVI.