Abstract

OBJECTIVES Use of the Freedom SOLO (SOLO) stentless aortic bioprosthesis is associated with a unique, and as yet unexplained, observation of postoperative low platelet count. Potential causes include the valve design, tissue and chemicals used for anticalcification treatment. This study compares the platelet response associated with the SOLO to mechanical, stented, sutureless and stentless valve prostheses. METHODS In total, 1587 patients receiving mechanical ATS (n = 199), stented Perimount Magna (Perimount, n = 911), sutureless 3f Enable (n = 34) and Perceval S (n = 48), stentless Pericarbon Freedom (n = 29) or SOLO (n = 366) valves were analysed. The primary end-point was defined as maximum decrease in platelet count expressed as % reduction from baseline within 5 days of aortic valve replacement. RESULTS The smallest decrease in platelets was observed for mechanical valves (44 ± 12%), followed by stented Perimount (50 ± 11%) and sutureless 3f Enable (53 ± 12%) bioprostheses. Compared with these valves, significantly greater reductions in platelets of 61 ± 14%, 60 ± 10% and 64 ± 12% were observed for the Pericarbon Freedom, Perceval S and SOLO, respectively. Multivariable linear regression analysis identified combined procedures, female gender, body surface area, date of operation and longer extracorporeal circulation time, but neither age nor valve size, as significant independent predictors for postoperative low platelet count. After adjustment, Sorin valves caused 13% (95% confidence interval 11-14) greater decrease in platelet counts compared with non-Sorin valves, but were associated with lower need for red blood cell [OR 0.56 (CI 0.41-0.75), P < 0.001] and platelet [OR 0.49 (CI 0.33-0.74), P = 0.001] transfusions. CONCLUSION The Pericarbon Freedom, Perceval S and SOLO bioprostheses are associated with a significantly greater decrease in postoperative platelet count compared with non-Sorin valves. Use of these valves is, however, not associated with excess bleeding complications, suggesting a quantitative, rather than qualitative, transient side-effect on platelets. Our results argue for a cause associated with the anticalcification treatment using homocysteic acid.

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