ABSTRACT
Paradoxical embolism is the result of systemic arterial embolism and pulmonary embolism. It indicates the presence of an intracardial defect in the area of the atrial or ventricular septum. The most frequent cause of an intracardiac defect associated with paradoxical embolism is a patent foramen ovale (PFO). In the case presented here, the symptoms, diagnostics and surgical therapy are discussed.
Subject(s)
Brachiocephalic Trunk , Embolism, Paradoxical/etiology , Foramen Ovale, Patent/complications , Pulmonary Artery , Brachiocephalic Trunk/diagnostic imaging , Brachiocephalic Trunk/surgery , Cardiac Surgical Procedures , Echocardiography, Transesophageal , Embolectomy , Embolism, Paradoxical/diagnosis , Embolism, Paradoxical/therapy , Female , Foramen Ovale, Patent/diagnosis , Foramen Ovale, Patent/therapy , Humans , Middle Aged , Pulmonary Artery/diagnostic imaging , Pulmonary Artery/surgery , Thrombolytic Therapy , Tomography, X-Ray Computed , Treatment OutcomeABSTRACT
BACKGROUND: Bypass graft stenosis after venous revascularisation procedures is characterised by massive neointimal and vascular smooth muscle cell proliferation triggered via endothelin-1 synthesis in the vessel wall. Decoy oligodesoxynucleotides (ODN) against the transcription factor activator protein-1 (AP-1) inhibits pre-pro-endothelin-1 expression. METHODS: In 20 rabbits, an end-to-side jugular vein bypass to the carotid artery was performed: (group A) 8 grafts were treated with consensus AP-1 decoy ODN, (group B) 8 with mutated control ODN and (group C) 4 received no treatment. Explantation, histomorphometric and immunohistochemical evaluation was performed after 28 days. RESULTS: Median intimal thickness of groups: (A) 28.3 microm, (B) 48.4 microm, (C) 71.1 microm. The decoy ODN-treated group showed a significant reduction of neointima formation ( P = 0.029) and a downregulation of the endothelin receptor. CONCLUSIONS: In this model, neointima formation was reduced by local transfection with consensus decoy ODN against AP-1. Endothelin A and B receptor expression is downregulated. Molecular target nucleic acid-based therapies seem to be a future means of overcoming neointima proliferation in pressure-induced venous graft failure. Intraoperative local application makes it easy to use in routine revascularisation procedures.
Subject(s)
Coronary Artery Bypass , Graft Occlusion, Vascular/prevention & control , Oligonucleotides/therapeutic use , Transcription Factor AP-1/antagonists & inhibitors , Transfection , Animals , Carotid Arteries , Disease Models, Animal , Down-Regulation , Endothelin-1/metabolism , Genetic Therapy/methods , Male , Rabbits , Receptor, Endothelin A/metabolism , Receptor, Endothelin B/metabolism , Tunica Intima/pathologyABSTRACT
Mimicking the physiological characteristics of the circulatory system, pulsatile bloodflow has also been introduced into extracorporeal perfusion to avoid known postoperative complications. In a mathematical consideration of the situation bloodflow is seen as a function of time F(t) for approximately constant vessel diameter over a given time. The kinetic energy of a column of blood produced by the heart-lung machine is transmitted directly to the arterial circulation via the aorta. The nature of the energy release can give rise to both positive (organ perfusion) and negative (damage to endothelium) effects. This study investigates how this energy release can be optimised, using the following experimental approach. A Doppler flow-measuring probe is placed on the ascending aorta to monitor the extracorporeal circulation. At the same time, the blood pressure is measured and converted to a pressure-flow curve via an A/D converter. On the basis of the parameters thus obtained, the energy released by the heart-lung machine is calculated. By regulating the functional parameters of a new generation of heart-lung machines, the bloodflow can then be adapted to the physiological requirements. Within the pulse period (cycle) a 20% rise phase ending in a slightly increasing plateau is established. The energy increase within a cycle should not exceed 150 joules. To optimize the mode of functioning of the heart-lung machine, we introduced the "energy-equivalent pressure" (EEP). Adaptation of the EEP to the physiological conditions required a basic flow of 60% at a pulse rate of 60/min and a pulse duration of 35% within the pulsatile flow interval.
