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Ann Thorac Surg 2001;72:1454-1456
© 2001 The Society of Thoracic Surgeons

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Editorial

What’s in a name? Would that which we call death by any other name be less tragic?

^a MCP-Hahnemann University Medical School, Philadelphia, Pennsylvania, USA
^b University of Michigan Health Systems, Ann Arbor, Michigan, USA

* Address reprint requests to Dr Narula, Hahnemann University Hospital, Broad & Vine, MS115-NT742, Philadelphia, PA 19102-1192, USA
e-mail: jagat.narula@drexel.edu

Open-heart surgery, particularly coronary artery bypass grafting (CABG) for coronary artery disease, is one of the great success stories in modern cardiovascular therapeutics, with more than 500,000 bypass procedures performed in the United States each year [1]. It not only improves survival but also relieves angina and improves exercise tolerance. This success story, however, has its trade-offs, including injury to the myocardium and central nervous system during circulatory arrest or low-flow bypass [2, 3]. Surgeons and researchers have grappled with different techniques to minimize neurologic dysfunction after open-heart surgery. The incidence of adverse cerebral outcomes after CABG ranges from 0.4% to approximately 80%. Perioperative cerebral injury has been divided into major deficits, which include focal neurologic deficits, coma, delirium and stupor; or relatively minor deficits, which include deterioration in short-term and long-term cognitive functions such as intellectual function and memory [1]. These cognitive changes may be subtle and may include problems with following directions, mental arithmetic, and planning complex actions [4]. In addition, family members and colleagues may observe that the patient is more prone to be short-tempered, is less able to withstand frustration, and has wider mood swings. The deterioration in cognitive function may demonstrate a biphasic temporal pattern with an immediate postoperative decline and then a late decline on long-term follow-up [5]. The pathogenesis of neurologic deficits after CABG has been ascribed to hypoxia, recurrent emboli, hemorrhage and metabolic abnormalities. The cellular and molecular mechanisms that result in neurologic deficits, particularly the decline in late cognitive function, continue to be defined. In a very elegant article in . . . [Full Text of this Article]

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