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D. Emslie-Smith 《Heart (British Cardiac Society)》1955,17(2):219-224
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本院自1984年3月至1992年12月,应用侧倾碟瓣、牛心包生物瓣和St.Jude瓣施行心脏瓣膜替换122例。除1例外,病因均为风湿性病变。二尖瓣替换96例,双瓣膜替换17例,主动脉瓣替换9例。心功能(NYHA)Ⅲ级者78例,Ⅳ级者21例。术后1个月内死亡15例(12.3%)。死亡原因主要为心室颤动,细菌性、霉菌性心内膜炎,低心输出量综合征等。83例随访6~96个月,晚期死亡5例。余均症状改善,多数已恢复工作。本文还就换瓣手术指征,心室颤动的原因,重症患者机械呼吸的应用,术后心内膜炎等问题进行讨论。 相似文献
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CARDIAC MANIFESTATIONS IN A CASE OF TUBEROUS SCLEROSIS 总被引:1,自引:0,他引:1
Duras FP 《British heart journal》1945,7(1):37-40
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J. LINDHOLM B. GIWERCMAN A. GIWERCMAN J. ASTRUP P. BJERRE and N. E. SKAKKEBÆK 《Clinical endocrinology》1987,27(5):553-562
The outcome of treatment in acromegaly is usually assessed by measuring plasma concentrations of growth hormone (GH)--either basal spontaneous levels or during hyperglycaemia. There is no consensus on how cure should be defined. Many studies have considered basal plasma growth hormone concentrations below 20 mU/l (10 ng/ml) as proof of cure, although some recent studies have applied lower values. At present a limit of 10 mU/l (5 ng/ml) seems to be accepted as evidence of cure. We have studied 28 acromegalic patients after transsphenoidal adenomectomy. Plasma GH concentrations (basal and during hyperglycaemia) as well as plasma somatomedin C (SMC) concentrations were measured and compared to the clinical symptoms. There was a close correlation between plasma GH and SMC concentrations (except when plasma GH levels were low) and between the clinical assessment and SMC concentrations. Very low plasma GH levels (less than 1 mU/l or 0.5 ng/ml) were associated with normal SMC values and clinical cure, high GH levels (greater than 10 mU/l or 5 ng/ml) with elevated SMC levels and persisting acromegaly. Moderately elevated plasma GH concentrations (1.9-9.6 mU/l) did not allow any conclusions on the outcome of treatment as assessed from SMC determinations and clinical evaluation. It is concluded that the usual criteria for cure in acromegaly may not be sufficiently strict. 相似文献
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《Clinical and experimental hypertension (New York, N.Y. : 1993)》2013,35(1-2):35-43
The role of the sympathetic nervous system in the settings of cardiac hypertrophy is postulated on the basis of experimental and clinical evidence. Only recently, the intimate mechanisms underlying hypertrophic responses of cardiac cell have been explored. Recent evidence spots the role of adrenergic receptors in the activation of several intracellular pathways of signaling that lead to nuclear responses of myocardiocyte.The molecular structures involved in these pathways may represent novel targets of future therapeutic interventions for cardiac hypertrophy and vascular remodeling in hypertension. 相似文献
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