Late complications of an atrial septal occluder provoked by anticoagulant therapy.

Late complications of an atrial septal occluder device (ASO) are rare but may be serious. We report a case with extensive hemopericardium five years after ASO implantation most likely triggered by anticoagulant therapy. Although not surgically confirmed, indirect clues for erosion of the atrial wall by the device were the exclusion of other etiologies, lack of recurrence after pericardial drainage and withdrawal of anticoagulants. In addition, multimodality imaging using echocardiography, computed tomography, and cardiac magnetic resonance imaging were helpful to elucidate this unusual cause. Initiation of anticoagulant treatment in patients with an ASO should be carefully balanced and may warrant more frequent echocardiographic follow-up. .

Preoperative planning with three-dimensional reconstruction of patient's anatomy, rapid prototyping and simulation for endoscopic mitral valve repair.

Objectives: Mitral valve repair performed by an experienced surgeon is superior to mitral valve replacement for degenerative mitral valve disease; however, many surgeons are still deterred from adapting this procedure because of a steep learning curve. Simulation-based training and planning could improve the surgical performance and reduce the learning curve. The aim of this study was to develop a patient-specific simulation for mitral valve repair and provide a proof of concept of personalized medicine in a patient prospectively planned for mitral valve surgery. Methods: A 65-year old male with severe symptomatic mitral valve regurgitation was referred to our mitral valve heart team. On the basis of three-dimensional (3D) transoesophageal echocardiography and computed tomography, 3D reconstructions of the patient's anatomy were constructed. By navigating through these reconstructions, the repair options and surgical access were chosen (minimally invasive repair). Using rapid prototyping and negative mould fabrication, we developed a process to cast a patient-specific mitral valve silicone replica for preoperative repair in a high-fidelity simulator. Results: Mitral valve and negative mould were printed in systole to capture the pathology when the valve closes. A patient-specific mitral valve silicone replica was casted and mounted in the simulator. All repair techniques could be performed in the simulator to choose the best repair strategy. As the valve was printed in systole, no special testing other than adjusting the coaptation area was required. Subsequently, the patient was operated, mitral valve pathology was validated and repair was successfully done as in the simulation. Conclusions: The patient-specific simulation and planning could be applied for surgical training, starting the (minimally invasive) mitral valve repair programme, planning of complex cases and the evaluation of new interventional techniques. The personalized medicine could be a possible pathway towards enhancing reproducibility, patient's safety and effectiveness of a complex surgical procedure.

Cardiac Troponin T and I Release After a 30-km Run.

Prolonged endurance-type exercise is associated with elevated cardiac troponin (cTn) levels in asymptomatic recreational athletes. It is unclear whether exercise-induced cTn release mirrors a physiological or pathological underlying process. The aim of this study was to provide a direct comparison of the release kinetics of high-sensitivity cTnI (hs-cTnI) and T (hs-cTnT) after endurance-type exercise. In addition, the effect of remote ischemic preconditioning (RIPC), a cardioprotective strategy that limits ischemia-reperfusion injury, was investigated in a randomized controlled crossover manner. Twenty-five healthy volunteers completed an outdoor 30-km running trial preceded by RIPC (4 × 5 min 220 mm Hg unilateral occlusion) or control intervention. hs-cTnT, hs-cTnI, and sensitive cTnI (s-cTnI) concentrations were examined before, immediately after, 2 and 5 hours after the trial. The completion of a 30-km run resulted in a significant increase in circulating cTn (time: all p <0.001), with maximum hs-cTnT, hs-cTnI, and s-cTnI levels of 47 ± 27, 69 ± 62, and 82 ± 64 ng/L (mean ± SD), respectively. Maximum hs-cTnT concentrations were measured in 60% of the participants at 2 hours after exercise, compared with maximum hs-cTnI and s-cTnI concentrations at 5 hours in 84% and 80% of the participants. Application of an RIPC stimulus did not reduce exercise-induced cTn release (time × trial: all p >0.5). In conclusion, in contrast to acute myocardial infarction, maximum hs-cTnT levels after exercise precede maximum hs-cTnI levels. Distinct release kinetics of hs-cTnT and hs-cTnI and the absence of an effect of RIPC favors the concept that exercise-induced cTn release may be mechanistically distinct from cTn release in acute myocardial infarction.

Mechanical stress activates platelets at a subhemolysis level: an in vitro study.

A feasibility study is performed to quantify sheep platelets (PLTs) and to identify the relationship between PLT count and hemolysis as a consequence of mechanical stress. Six adult, healthy Dorset sheep have been used for in vitro blood sampling test procedures in a hemoresistometer device (HRM). In each experiment, blood of the same animal was exposed to six different shear rates. Free hemoglobin levels and PLT count for each shear rate were detected. In all animals (A-F), hemolysis increased significantly between the shear rates of 2325 and 3100/s (P < 0.05) and the mean PLT count dropped immediately (contact, low shear) 40% in the beginning, between the shear rates of 0 and 775/s (P < 0.05). PLT count increased slightly as soon as hemolysis started. At higher shear rates, hemolysis increased and PLTs reduced further. Precise counting of PLTs indicates that PLTs are consumed dramatically at very low shear (by contact) and further by applied mechanical stress when hemolysis is obvious. A repetition of these tests with human blood could indicate species differences.