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.
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.
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