Effect of cold storage on the haemostatic cascade systems

This study dealt with the effect of citrate phosphate dextrose adenine (CPDA) whole blood stored at 4 degrees C for 5 weeks and fresh frozen plasma at -30 degrees C for 12 months on coagulation, fibrinolytic and kallikrein system activation. Stored whole blood showed a significant decrease in ATIII activity by the second week with a significant decrease in thrombin-antithrombin complex by the fourth week. alpha 2-antiplasmin and plasminogen decreased significantly by the first and second week, respectively, accompanied by a significant increase in D-dimer level by the fourth week. A significant decrease in C1-inhibitor activity occurred by the first week associated with a significant increase in kallikrein activity by the third week. However, all measured parameters were minimally affected in fresh frozen plasma. Therefore, fresh frozen plasma supplemented with packed RBCs are preferred to whole blood stored over 3 weeks especially in patients with proteolytic enzyme system activation.     

Paravalvular Leak

Despite improvements and advancements in surgical technique, paravalvular leaks (PVL) continue to present a challenge when caring for patients with prosthetic valve disease.¹ Paravalvular leaks result from dehiscence of the surgical ring from the mitral annulus. Some theories suggest that uneven distribution of collagen fibers in the mitral annulus leaves the posterior mitral annulus without a well-formed fibrous structure, which may predispose it to recurrent mechanical injury that leads to PVL. The reported incidence of PVL is 2.2%.² Risk factors associated with PVL include the presence of mitral annular calcification, infective endocarditis, active steroid use, and continuous surgical suturing, which poses a greater risk than an interrupted surgical approach.³ Risk of PVL varies by prosthesis type, with mechanical prostheses carrying a higher risk of PVL than bioprosthetic valves.Below are images of a 70-year-old male with severe mitral stenosis and pulmonary hypertension who had previously undergone mitral valve commissurotomy and subsequent mitral valve replacement with a bioprosthetic mitral valve. He presented to the hospital with pulmonary edema. Initial transthoracic echocardiogram showed depressed biventricular function with a dehiscence of the bioprosthetic mitral valve and a large eccentric posterior PVL, severe tricuspid regurgitation, and severe pulmonary hypertension. Transesophageal images in Figure 1 illustrate a significant posterior PVL with dehiscence of the prosthetic valve from the mitral annulus. The patient underwent closure of the paravalvular leak with two 18-mm Amplatzer ventricular septal defect occluders (Abbott) with excellent results and trace residual mitral regurgitation post closure (Figure 2A, 2B).Open in a separate windowFigure 1(A) 3-dimensional (3D) enface view of the mitral valve (MV) with the aortic valve (AV) seen in the 12 o’clock position. The mitral bioprosthesis is visualized with a paravalvular defect located posteromedially (red arrow). (B) 3D Trueview image of the mitral valve showing eccentric systolic flow through the paravalvular defect.Open in a separate windowFigure 2(A, B) A 3-dimensional enface view of the mitral valve with two Amplatzer ventricular septal defect (Abbott) devices (yellow arrow) well seated within the paravalvular defect. Panel B shows a small amount of residual paravalvular leak. AV: aortic valve; MV: mitral valve     

A giant early second‐trimester placental chorioangioma associated with isolated proteinuria and histopathologically confirmed placental insufficiency,a novel association: A case report

We present a case of giant chorioangioma at 18 weeks of gestation leading to fetal hypertrophic cardiomyopathy without other evidences of fetal volume overload and late‐onset isolated proteinuria. Oligohydramnios developed at term and placental insufficiency was confirmed on histopathological examination and a nonanemic nonthrombocytopenic normal weight healthy baby was delivered.