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1. Management of Arrhythmias in the Coronary Care Unit.- 2. Thrombolysis in the Management of Acute Myocardial Infarction.- 3. The Role of Free Radicals in the Pathogenesis of Postischemic Reperfusion Injury.- 4. Percutaneous Transluminal Coronary Angioplasty in Acute Myocardial Infarction.- 5. The Role of Emergency Bypass Surgery in Acute Myocardial Infarction.- 6. The Role of Nitroglycerin in Acute Myocardial Infarction.- 7. The Role of Calcium Antagonists in Acute Myocardial Infarction.- 8. Postinfarction Angina.- 9. The Management of Pump Failure.- 10. The Role of Nuclear Cardiology in the Assessment of Myocardial Infarction and the Evaluation of Early Interventions.- 11. Risk Stratification After Acute Myocardial Infarction: Theory and Practice.
In the last decade, the surgical therapy for acute type A aortic dissections (AAAD) has been modified by new techniques that have improved the outcome. Continuous efforts have led to safer, more rapid, and more durable operations using new technology and new knowledge concerning the pathophysiology of the disease and the surgical long-term results. Some of these procedures (like the use of glue or other adjuncts to reinforce the aortic stumps) are already established techniques. Others "in progress" (like different modes of cerebral protection, sites of arterial cannulation, aortic valve management, and the extended aortic arch replacement) are still debated. Finally, procedures like the combined treatment of ascending aortic replacement associated with a stent graft positioned in the aortic arch and other endovascular techniques (hybrid procedures) seem to be the vascular surgical options for the future. These procedures appear as adjuncts to conventional surgical interventions but need to be evaluated for indications, feasibility, and long-term results.
Aortic dissection is characterized by separation of the layers within the aortic wall and the subsequent inflow of blood into the intima-media space with further propagation of the dissection. The clinical onset of aortic dissection may mimic a wide array of conditions, such as myocardial ischemia, heart failure, neurologic event, visceral ischemia, or peripheral vascular insufficiency. Clinical signs of aortic dissection include among others chest pain with a ripping nature and immediate onset, widening of the mediastinum and the aortic knob, pulse and blood pressure differentials, limb ischemia, presence of a diastolic aortic murmur due to aortic regurgitation, or physical findings may be totally absent1,4.
Aortic dissection and related syndromes / , Aortic dissection and related syndromes / , کتابخانه دیجیتال جندی شاپور اهواز
Disorders of impulse formation account for approximately 10% of the tachycardias in infants and children. These include automatic atrial tachycardia (AAT), also known as ectopic atrial tachycardia (AET), originating from a single focus in the atrium, multifocal atrial tachycardia (MAT, or chaotic atrial tachycardia) thought to arise from multiple foci within the atria (Chapter 11), congenital junctional ectopic tachycardia (JET), and accelerated junctional rhythm, both originating from tissue in the region of the atrioventricular (AV) node. They are characterized electrophysiologically by a point origin, in contrast to tachycardias supported by macrorentrant circuits where larger segments of tissue with abnormal conduction perpetuate the arrhythmia. The precise cellular mechanism of disorders of impulse formation can only be inferred in patients with abnormal automaticity. Both abnormal transmembrane potassium (pacemaker) and calcium (triggered activity) currents have been proposed, based on both cellular laboratory observations and indirect clinical evidence. AUTOMATIC ATRIAL TACHYCARDIA/ATRIAL ECTOPIC TACHYCARDIA
Restenosis remains the principal limitation of percutaneous coronary intervention (PCI). We have learned from animal studies that constrictive remodeling is the principal mechanism of restenosis after balloon angioplasty^^'^l In contrast, in-stent restenosis is related to neointimal hyperplasia^^l These data were confirmed in humans by intravascular ultrasound (IVUS)^ ' After balloon arterial injury, oxidative stress is increased and contributes to endothelial dysfunction, macrophage activation, and release of cytokines and growth factors^^ In the past decade, several antioxidants have been evaluated in various animal models after balloon angioplasty. Probucol and vitamins (E with or without C) effectively reduced restenosis by promoting favorable remodeling (i.e., enlargement remodeling). Moreover, these treatments decreased neointimal hyperplasia which is the target for in-stent restenosis. In an era of nearly 100% stent implantation, it is now time to evaluate their efficacy in animal models of instent restenosis after either systemic administration or local delivery.
Nurse-patient-family interactions afford key opportunities for education, support, and interventions aimed at facilitating positive child and family adjustments for children with arrhythmias. While some situations are relatively minor requiring minimal nursing intervention, others are very demanding requiring an intensive, long-term level of care. As the complexity of care advances, the need for collaboration amongst all care providers involved increases.
