fibrin and Heart-Septal-Defects--Ventricular

We sought to evaluate tissue reactions within and at the surface of devices for interventional therapy of septal defects and to identify antigen characteristics of neotissues.. Atrial or ventricular septal defect-occlusion devices (Amplatzer, n=7; Cardioseal/Starflex, n=3) were processed using a uniform protocol after surgical removal from humans (implantation time, 5 days to 4 years). Devices were fixed in formalin and embedded in methylmethacrylate. Serial sections were obtained by sectioning with a diamond cutter and grinding, thus saving the metal/tissue interface for histologic evaluation. Immunohistochemical staining was performed using conventional protocols. Superficial endothelial cells stained positive for von Willebrand factor. Within the newly formed tissues, fibroblast-like cells were identified with a time-dependent expression of smooth muscle cell maturation markers (smooth muscle actin, smooth muscle myosin, h-caldesmon, and desmin) beside extracellular matrix components. Neovascularization of the newly formed tissues was demonstrated with the typical immunohistochemical pattern of capillaries and small vessels. Inflammatory cells could be identified as macrophages (CD68+) and both T-type and B-type lymphocytes (CD3+, CD79+).. This is the first presentation of results from serial immunohistochemical staining of a collection of explanted human septal-occlusion devices. A time-dependent maturation pattern of the fibroblast-like cells in the neotissues around the implants could be described. Neoendothelialization was seen in all specimens with implantation times of 10 weeks or more. The time course of neoendothelialization, as seen in our study, further supports the clinical practice of anticoagulant or antiplatelet therapy for 6 months after implantation. This time interval should be sufficient to prevent thromboembolic events due to thrombus formation at the foreign surface of cardiovascular implants.

Topics: Biomarkers; Cardiac Catheterization; Cell Proliferation; Coronary Vessels; Device Removal; Endothelial Cells; Fibrin; Fibroblasts; Foreign-Body Reaction; Heart Septal Defects, Atrial; Heart Septal Defects, Ventricular; Humans; Immunohistochemistry; Inflammation; Prosthesis Design; Prosthesis Failure; Septal Occluder Device; Time Factors; Tunica Intima

Eighteen percent of heart specimens with isolated ventricular septal defect also had a floppy mitral valve. There was no statistical difference in the incidence of floppy mitral valve in the three age groups considered (less than 1 year, 1 to 16 years and 17 to 91 years). In no patient was a floppy mitral valve considered to be the cause of death. Complications of floppy mitral valve (ruptured chordae tendineae, bacterial endocarditis, mitral regurgitation and fibrin deposits at the mitral valve-left atrial angle) occurred at approximately the same frequency as that reported in autopsy studies of isolated floppy mitral valve. In the specimens with floppy mitral valve and ventricular septal defect, 63% also had floppiness of the tricuspid valve, 16% of the pulmonary valve and 5% of the aortic valve. The anatomic basis for floppy mitral valve was considered to be spongiosal invasion and disruption of the fibrosa of the valve leaflet. In this study, spongiosal invasion of the fibrosa was fully developed by 3 months of age and there was no evidence that the incidence or severity of spongiosal invasion increased between the ages of 3 months and 88 years. These data suggest that the floppy mitral valve is a congenital lesion that reaches full anatomic expression in infancy. No evidence was found that ventricular septal defect and floppy mitral valve share a common etiology.

Topics: Adolescent; Adult; Age Factors; Aged; Child; Child, Preschool; Chordae Tendineae; Endocarditis, Bacterial; Female; Fibrin; Heart Diseases; Heart Septal Defects, Ventricular; Humans; Infant; Male; Middle Aged; Mitral Valve; Mitral Valve Insufficiency; Mitral Valve Prolapse; Rupture, Spontaneous