BACKGROUND: Cardiopulmonary bypass (CPB) and cardiac surgery cause an inflammatory response, as measurable by an increase in the concentration of C-reactive protein (CRP), a nonspecific inflammation marker. Previous publications have demonstrated typical perioperative CRP concentration profiles in cases of uncomplicated aortic valve replacement (AVR) with CPB. A regression analysis for modifying factors showed that chronic disease (heart failure, diabetes, and pulmonary disease), along with obesity and sex, all tend to influence the CRP response. We analyzed the inflammatory response to aortic valve implantation (AVI) with interventional techniques, mainly transapical but also transfemoral and transaxillary approaches, in a retrospective case-control study design. METHODS: Sixty-eight patients who underwent AVI by the transapical (59 patients), transfemoral (7 patients), or transaxillary (2 patients) approach were matched by age, sex, body mass index (BMI), and chronic-disease state (absence or presence of diabetes, pulmonary disease, and renal impairment) with 68 patients who underwent conventional AVR with CPB. We compared the 2 groups with respect to perioperative CRP concentration, EuroSCORE, and outcome data (time to extubation and 30-day mortality). All data were collected prospectively and analyzed retrospectively. RESULTS: The 2 groups-the study population (interventional) and the control population (conventional)-were similar in age, sex distribution, BMI, and chronic-disease status. As expected, the study population had a significantly higher median EuroSCORE. The 2 groups had similar postoperative CRP profiles over time, but the interventional group had significantly higher peak concentrations on days 2, 3, and 4. The short-term outcomes, as assessed by ventilation time and 30-day mortality, were similar for the 2 groups. CONCLUSIONS: Using an interventional transcatheter approach to AVI (thereby eliminating CPB from the procedure and reducing surgical trauma) does not attenuate the patient's innate inflammatory response.
BACKGROUND: Cardiopulmonary bypass (CPB) and cardiac surgery cause an inflammatory response, as measurable by an increase in the concentration of C-reactive protein (CRP), a nonspecific inflammation marker. Previous publications have demonstrated typical perioperative CRP concentration profiles in cases of uncomplicated aortic valve replacement (AVR) with CPB. A regression analysis for modifying factors showed that chronic disease (heart failure, diabetes, and pulmonary disease), along with obesity and sex, all tend to influence the CRP response. We analyzed the inflammatory response to aortic valve implantation (AVI) with interventional techniques, mainly transapical but also transfemoral and transaxillary approaches, in a retrospective case-control study design. METHODS: Sixty-eight patients who underwent AVI by the transapical (59 patients), transfemoral (7 patients), or transaxillary (2 patients) approach were matched by age, sex, body mass index (BMI), and chronic-disease state (absence or presence of diabetes, pulmonary disease, and renal impairment) with 68 patients who underwent conventional AVR with CPB. We compared the 2 groups with respect to perioperative CRP concentration, EuroSCORE, and outcome data (time to extubation and 30-day mortality). All data were collected prospectively and analyzed retrospectively. RESULTS: The 2 groups-the study population (interventional) and the control population (conventional)-were similar in age, sex distribution, BMI, and chronic-disease status. As expected, the study population had a significantly higher median EuroSCORE. The 2 groups had similar postoperative CRP profiles over time, but the interventional group had significantly higher peak concentrations on days 2, 3, and 4. The short-term outcomes, as assessed by ventilation time and 30-day mortality, were similar for the 2 groups. CONCLUSIONS: Using an interventional transcatheter approach to AVI (thereby eliminating CPB from the procedure and reducing surgical trauma) does not attenuate the patient's innate inflammatory response.