109 research outputs found
Mini-Reoperative Mitral Valve Surgery
Background: Reoperative surgery involving the atrioventricular valves places the patient at risk for cardiac or bypass graft injury upon reoperative sternotomy. Standard right thoracotomy can avoid these problems but is associated with a large incision and possibly more pulmonary complications. Methods and Results : An alternative, minimally invasive approach for reoperative atrioventricular valve surgery was studied in 22 patients. Patient age was 66 ± 10 years. Postoperative mitral regurgitation was 3.4 ± 0.3 and New York Heart Association (NYHA) Class was III/IV, despite a mean ejection fraction of 44 ± 14%. These patients had 1–4 prior procedures a mean of 5 years previously. An anterior 5th interspace incision of 5- to 10-cm was performed. A 1-cm segment of 5th rib was removed to facilitate exposure. Cardiopulmonary bypass was performed via ascending aorta or femoral artery cannula and bicaval venous cannulae. Systemic cooling (25°) and fibrillatory arrest was used. Operations performed included mitral valve repair (12). mitral valve replacement (5), prosthetic mitral valve rereplacement (4). repair of perivalvular leak (3), tricuspid valve repair (5), and atrial septal defect closures (7). Mean bypass time was 109 ± 21 minutes with a mean fibrillatory time of 62 ± 12 minutes. There was no intraoperative or 30-day mortality. Patients were weaned from ventilation at a mean of 5 hours postoperatively and received 1.3 ± 1 unit of blood. There were no wound complications or re-explorations for bleeding. At a mean follow-up of 15 ± 8 months, survivors are NYHA Class I-II. When interviewed, all patients felt their recovery was more rapid and less painful than their original sternotomy. Conclusion : This minimally invasive approach to reoperative atrioventricular valve surgery is safe and technically feasible. It has become our preferred approach to the atrioventricular valves in patients with a previous sternotomy.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73273/1/j.1540-8191.1998.tb01084.x.pd
Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases
The production of peroxide and superoxide is an inevitable consequence of
aerobic metabolism, and while these particular "reactive oxygen species" (ROSs)
can exhibit a number of biological effects, they are not of themselves
excessively reactive and thus they are not especially damaging at physiological
concentrations. However, their reactions with poorly liganded iron species can
lead to the catalytic production of the very reactive and dangerous hydroxyl
radical, which is exceptionally damaging, and a major cause of chronic
inflammation. We review the considerable and wide-ranging evidence for the
involvement of this combination of (su)peroxide and poorly liganded iron in a
large number of physiological and indeed pathological processes and
inflammatory disorders, especially those involving the progressive degradation
of cellular and organismal performance. These diseases share a great many
similarities and thus might be considered to have a common cause (i.e.
iron-catalysed free radical and especially hydroxyl radical generation). The
studies reviewed include those focused on a series of cardiovascular, metabolic
and neurological diseases, where iron can be found at the sites of plaques and
lesions, as well as studies showing the significance of iron to aging and
longevity. The effective chelation of iron by natural or synthetic ligands is
thus of major physiological (and potentially therapeutic) importance. As
systems properties, we need to recognise that physiological observables have
multiple molecular causes, and studying them in isolation leads to inconsistent
patterns of apparent causality when it is the simultaneous combination of
multiple factors that is responsible. This explains, for instance, the
decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference
All rights of reproduction in any form reserved. Selenite-induced NAD(P)H Oxidation and Calcium Release in Isolated Mitochondria: Relationship to In Vivo Toxicity
Postinfarction Inferior Ventricular Septal Rupture: Surgical Repair Through the Right Atrium
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