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排序方式: 共有1029条查询结果,搜索用时 484 毫秒
91.
92.
Sanders GD Al-Khatib SM Berliner E Bigger JT Buxton AE Califf RM Carlson M Curtis AB Curtis JP Domanski M Fain E Gersh BJ Gold MR Goldberger J Haghighi-Mood A Hammill SC Harder J Healey J Hlatky MA Hohnloser SH Lee KL Mark DB Mitchell B Phurrough S Prystowsky E Smith JM Stockbridge N Temple R;Expert panel participating in a Duke Center for the Prevention of Sudden Cardiac Death-sponsored conference 《American heart journal》2007,153(6):951-959
Although current evidence supporting a more precise strategy for identifying patients at highest risk for sudden cardiac death (SCD) is sparse, strategies for translating existing and future evidence into clinical practice and policy are needed today. A great many unanswered questions exist. Examples include the following: At what level of risk for SCD should we pursue further testing or therapy? How should clinical strategies ethically and economically balance alternative outcomes? How can we best translate optimal strategies into clinical practice so as to prevent tomorrow's SCDs? On July 20 and 21, 2006, a group of individuals with expertise in clinical cardiovascular medicine, biostatistics, economics, and health policy was joined by government (Food and Drug Administration; Centers for Medicare and Medicaid Services; National Heart, Lung, and Blood Institute; Agency for Healthcare Research and Quality), professional societies (Heart Rhythm Society), and industry to discuss strategies for risk assessment and prevention of SCD. The meeting was organized by the Duke Center for the Prevention of Sudden Cardiac Death and the Duke Clinical Research Institute. This article, the second of 2 documents, summarizes the policy discussions of that meeting, discusses an analytic framework for evaluating the risks and benefits associated with SCD prevention and risk stratification, and addresses the translation of SCD risk assessment strategies into practice and policy. 相似文献
93.
94.
M D Hibbard D R Holmes K R Bailey G S Reeder J F Bresnahan B J Gersh 《Journal of the American College of Cardiology》1992,19(3):639-646
In cardiogenic shock complicating acute myocardial infarction, percutaneous transluminal coronary angioplasty has been reported to significantly improve the modest survival benefits afforded by emergency surgical revascularization and thrombolytic therapy. The records of all patients who underwent angioplasty for acute myocardial infarction complicated by cardiogenic shock were retrospectively reviewed to determine whether coronary angioplasty improves survival. Of the 45 patients, 28 (group 1, 62%) had successful dilation of the infarct-related artery and 17 (group 2, 38%) had unsuccessful angioplasty. The groups were similar in extent of coronary artery disease, infarct location, incidence of multivessel disease and hemodynamic variables. The overall hospital survival rate was 56% (71% in group 1 and 29% in group 2). Group 1 patients had more left main coronary artery disease, and group 2 patients were older and had a higher incidence of prior myocardial infarction. Multivariate analysis showed that the survival advantage in patients with successful angioplasty was statistically significant (p = 0.014) when these factors were taken into account. At a mean follow-up interval of 2.3 years (range 1 month to 5.6 years), there were five deaths (four cardiac and one noncardiac), for a 2.3-year survival rate of 80% in patients surviving to hospital discharge. During the follow-up period, 36% of hospital survivors had repeat hospitalization for cardiac evaluation, 8% had myocardial infarction, 8% had coronary artery bypass surgery and 24% had angina. 相似文献
95.
Histopathology is a major diagnostic tool in dermatology, particularly in psoriasiform diseases. Morphological studies showed that the initial event in psoriatic lesions is perivascular infiltrate, followed by dilatation of superficial papillary vessels. Proliferation of keratinocytes and neutrophil exocytosis are secondary events. Fully developed psoriasis has a very characteristic pattern, which includes elongation of rete ridges leading to regular acanthosis, oedema of the papillary dermis associated with tortuous dilated vessels, thinning of suprapapillar area, decreased thickness of granular layer, and exocytosis of neutrophils in the spinous layer (Kogoj's pustule) or in the cornified parakeratotic layer (Munro microabscesses). Pustular psoriasis is characterized by large or confluent intra‐epidermal multilocular pustules. Whatever the clinical variant of psoriasis, common morphological signs suggest that it is basically a unique pathological process, with many possible presentations according to various factors such as age, size and localization of lesions, or therapy. Similar microscopic elementary lesions indicate that Hallopeau's acrodermatitis continua, Reiter's disease and geographical tongue are variants of psoriasis. Because of the many faces of the disease, psoriasis can resemble many other squamous or pustular disorders. Differential diagnosis by microscopic analysis is based on pattern analysis, PAS (Periodic Acid Schiff) staining to rule out fungal infection, and immunohistochemistry to characterize lymphocytic infiltrate. Psoriasis is one of the most common inflammatory skin diseases. In its characteristic presentation, psoriasis comprises well‐circumscribed red scaly papules and plaques. In this form, the disease is generally easy to identify, especially when the elbows, knees and scalp are affected. Nevertheless, the term ‘psoriasis’ includes more clinical variants than any other inflammatory dermatosis: psoriasis vulgaris vs. pustular, localized vs. generalized, topographic variants, mucous membranes involvement, hair and nail lesions. Although some of these conditions might be extremely different from psoriasis vulgaris, common pathological findings can be identified in all of them. Microscopic analysis of psoriatic lesions may therefore help clinicians to make the diagnosis and to understand that, whatever the clinical presentation, signs and symptoms are mainly due to a unique pathological process. 相似文献
96.
目的:严重的黏膜损伤是诱发造血干细胞移植后出现并发症的一常见原因,已有证据显示谷氨酰胺能降低接受化疗患儿黏膜炎的发生率。观察谷氨酰胺对异基因外周造血干细胞移植患者并发症及恢复的影响。方法:选择于2002-03/2006-11在河南省血液病研究所接受同胞异基因外周造血干细胞移植的48例血液系统肿瘤患者。所有患者及其家属对治疗和实验均知情同意,并经医院伦理委员会批准。所有患者移植前均处于完全缓解状态,营养中等或良好,心、肝、肾功能正常,将48例患者随机分为标准化全胃肠外营养液组(标准组,n=13)和加用谷氨酰胺的全胃肠外营养液组(谷氨酰胺组,n=35)。待患者中性粒细胞升至1.0×109L-1,且无任何感染指征,进行异基因外周造血干细胞移植。造血干细胞输注后第1天开始给予全胃肠外营养与胃肠外营养联合谷氨酰胺双肽,至中性粒细胞≥1.0×109L-1,且无消化道症状时停用。观察两组患者中性粒细胞恢复时间、出层流室时间以及关于感染、急性移植物抗宿主病等情况有无差异。结果:48例患者均进入结果分析。两组患者营养物质的摄入基本相同,谷氨酰胺组有6例发生黏膜炎,标准组有11例,差异显著(P<0.05);谷氨酰胺组有1例发生严重腹泻,标准组有5例,差异显著(P<0.05);谷氨酰胺组有3例发生临床感染,标准组有7例,差异显著(P<0.05);标准组中性粒细胞≥0.5×109L-1的持续时间短于谷氨酰胺组(P>0.05);谷氨酰胺组抗生素治疗时间及无菌病房居住时间较标准组短(P<0.05);两组急性移植物抗宿主病发生率差异无统计学意义(P>0.05)。结论:添加谷氨酰胺的全胃肠外营养可改善异基因造血干细胞移植患者的营养状态,减少感染及肠损害,减少急性移植物抗宿主病的发生,有利于异基因移植患者恢复。 相似文献
97.
In human immune deficiency virus (HIV)-seropositive hemophilia patients, a low number of CD4 + lymphocytes is found, as well as a low CD4+/CD8+ ratio. In previous studies, it has been shown that antigen- specific T-helper cell (CD4+) function was present and no excessive antigen-specific T-suppressor cell (CD8+) function could be demonstrated. In this report, we studied another activity of CD4+ cells, namely the capacity to induce T-suppressor cell activity. The results clearly show a selective dysfunction of CD4+ suppressor-inducer (Tsi) cell function. Since these HIV-seropositive hemophilia patients showed the presence of activated B cells in the peripheral circulation refractory to antigen-specific T-helper cell signals and secreting specific antibodies spontaneously, we raised the hypothesis that the activated B cells in the patients activate the Tsi cells in vivo. This constant activation leads to a functional exhaustion of the Tsi cell pool. 相似文献
98.
Recovery of T cell subsets after autologous bone marrow transplantation is mainly due to proliferation of mature T cells in the graft 总被引:3,自引:3,他引:3
de Gast GC; Verdonck LF; Middeldorp JM; The TH; Hekker A; v.d. Linden JA; Kreeft HA; Bast BJ 《Blood》1985,66(2):428-431
In 22 patients with malignancies, treated with high-dose chemoradiotherapy and autologous bone marrow transplantation (BMT), peripheral blood T cell subsets and functions were studied. In ten cytomegalovirus (CMV)-negative patients, CD4+ and CD8+ T cells (representing T cells of the helper/inducer phenotype and T cells of the suppressor/cytotoxic phenotype, respectively), recovered slowly and simultaneously. In 12 CMV-positive patients, however, CD8+ T cells recovered more rapidly than CD4+ T cells and rose to increased counts. No T cells with an immature phenotype (CD1+, OKT6+) were observed. Lymphocyte stimulation by herpes simplex virus infected fibroblasts (and by CMV-infected fibroblasts in CMV-positive patients) in contrast remained high and even increased after BMT in both groups. These data indicate that T cell recovery after autologous BMT is mainly due to proliferation of mature T cells present in the BM graft and not to generation of new T cells from T cell precursors. 相似文献
99.
Heart failure after myocardial infarction: a review 总被引:1,自引:0,他引:1
Hellermann JP Jacobsen SJ Gersh BJ Rodeheffer RJ Reeder GS Roger VL 《The American journal of medicine》2002,113(4):324-330
PURPOSE: The effects of survival after myocardial infarction on the prevalence of chronic heart failure have not been well characterized. We reviewed studies of the incidence, mortality, and predictors of heart failure after myocardial infarction, and suggest directions for further research. METHODS AND RESULTS: We conducted a review of the literature from 1978 to 2000. Of 33 identified articles, 18 (55%) included heart failure as a primary endpoint. The mean in-hospital incidence of heart failure after myocardial infarction differed significantly by study design; it was highest in population-based studies and lowest in clinical trials (37% vs. 18%, P <0.01). Only 10 studies reported the incidence of subsequent heart failure. One-year mortality ranged from 16% to 39% and showed no improvement with time. Patients with in-hospital heart failure after myocardial infarction had a two- to sixfold greater in-hospital mortality and up to a fivefold increased 1-year mortality compared with patients without heart failure. The most consistent risk factors for the development of heart failure after myocardial infarction were advanced age, female sex, diabetes, and an increased heart rate at the time of admission. CONCLUSIONS: The reported incidence of, and mortality from, heart failure after myocardial infarction varies by study design. Additional research on the etiology and prognosis of late heart failure after myocardial infarction is needed. 相似文献
100.
Meena P. Rao Dragos Vinereanu Daniel M. Wojdyla John H. Alexander Dan Atar Elaine M. Hylek Michael Hanna Lars Wallentin Renato D. Lopes Bernard J. Gersh Christopher B. Granger 《The American journal of medicine》2018,131(3):269-275.e2