WALL STRESS IN NORMAL AND HYPERTROPHIED HUMAN LEFT VENTRICLE
WALL STRESS IN NORMAL AND HYPERTROPHIED HUMAN LEFT VENTRICLE
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DOI：
10.1016/0002-9149(68)90161-6
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发表时间：
1968-01-01
影响因子：
2.8
通讯作者：
ROLETT, EL
中科院分区：
文献类型：
--
作者：
HOOD, WP;RACKLEY, CE;ROLETT, EL
应用心血管造影术，对6例无左室疾病的受试者，确定了舒张期末期和收缩期壁峰值应力的正常范围。在另外41名患有不同形式心脏病的患者中，根据室壁应力评估了左心室的解剖和功能适应性。作为反应适当性的指标，收缩峰值应力似乎比舒张期末期应力更好。这些数据表明，代表心肌外部刺激的慢性瓣膜疾病最佳地导致一定程度的肥厚，以使峰值收缩应力正常化。相反，内源性肌肉疾病可能会导致某种程度的肥大，就峰值应力而言，这种肥大程度不合适(过度或不足)。与二尖瓣狭窄不同，正常的峰值应力并不排除心脏功能受损，但峰值应力升高是失代偿状态的特征。
By the use of angiocardiographic technics, normal ranges for end-diastolic and peak systolic wall stresses have been defined in 6 subjects without left ventricular disease. In 41 other patients with various forms of heart disease the anatomic and functional adaptations of the left ventricle have been evaluated in terms of wall stress. Peak systolic stress appears to be better than end-diastolic stress as an index of the appropriateness of the responses. The data suggest that chronic valvular disease, representing a stimulus extrinsic to the myocardium, optimally results in a degree of hypertrophy appropriate to normalize peak systolic stress. In contrast, intrinsic muscle disease may result in a degree of hypertrophy inappropriate (either excessive or inadequate) in terms of peak stress. Normal peak stress does not preclude impaired cardiac performance, as in mitral stenosis, but elevated peak stress is characteristic of decompensated states.