Thrombocytopenia following implantation of the stentless biological sorin freedom SOLO valve.

BACKGROUND AND AIM OF THE STUDY: Stentless biological valves have proven advantages in hemodynamic performance and left ventricular function compared to stented biological valves. Following a marked postoperative fall in the platelet count of patients after implantation of the Freedom SOLO valve, the study aim was to confirm clinical observations that this effect was more severe in patients receiving Freedom SOLO valves than in those receiving St. Jude Medical (SJM) mechanical aortic valves. METHODS: Preoperative and postoperative platelet counts were compared in two groups of patients who underwent aortic valve replacement (AVR) without any concomitant procedures between January and December 2007. Patients received either a Freedom SOLO valve (n = 28) or a SJM mechanical valve (n = 41). Mean values of platelet counts were compared using three multiple linear regression models. RESULTS: Platelet counts were significantly lower in the Freedom SOLO group than in the SJM group from the first postoperative day (POD 1) up to POD 6 (p <0.001). In three patients of the Freedom SOLO group the platelet count fell below 30x10(9)/l, while the lowest level in the SJM group was 75x10(9)/l. Based on multiple linear regression models, the type of valve implanted had a statistically significant influence on postoperative platelet counts on POD 1, POD 3, and POD 5 (p <0.001). CONCLUSION: Whilst the reason for this phenomenon is unknown, the use of consistent monitoring should prevent severe falls in platelet count from becoming dangerous for the patient. Further studies are required to investigate the phenomenon since, despite a shorter cardiopulmonary bypass time, the fall in platelet count was more profound in the Freedom SOLO group.

Expression of cyclooxygenase-1 and cyclooxygenase-2 in the normal human heart and in myocardial infarction.

INTRODUCTION: Cyclooxygenase is a key enzyme in prostanoid synthesis. It exists in two isoforms: cyclooxygenase-1 (COX-1), which is constitutively expressed in cells and tissues maintaining normal homeostasis, and cyclooxygenase-2 (COX-2), which is normally not present in most cells, but can be induced by various stimuli. Little is known about the significance of COX isoforms in the normal human heart and in myocardial infarction (MI). Thus, we aimed to investigate the immunohistochemical expression of COX-1 and COX-2 in the normal human heart and in MI. METHODS: Our study included autopsy samples of heart tissue from 15 healthy individuals who died in accidents, and from 40 patients with MI who died few hours to a month after the onset of symptoms. Immunohistochemistry was performed by a sensitive peroxidase-streptavidin method on formalin fixed, paraffin-embedded tissue, using monoclonal antibodies against COX-1 and COX-2. RESULTS: In normal hearts, COX-1 was found in endothelial and smooth muscle cells of blood vessels and in endothelial cells of the endocardium. In MI, it was expressed in inflammatory cells, as well as in myofibroblasts and capillaries of granulation and fibrous tissue. COX-2 was either not present or it was present in occasional myocytes in the normal hearts. In MI, its expression was induced in cardiomyocytes as well as in interstitial inflammatory cells, and in capillaries and myofibroblasts in granulation tissue. CONCLUSIONS: Our results suggest that COX-1 is associated with normal homeostasis in the heart, whereas COX-2 probably mediates inflammatory reaction in MI. It appears that both COX-1 and COX-2 are associated with the healing processes and scar formation after MI.