Suppr超能文献

多普勒证据表明肥厚型心肌病中存在真正的左心室至主动脉压力梯度。

Doppler evidence that true left ventricular-to-aortic pressure gradients exist in hypertrophic cardiomyopathy.

作者信息

Come P C, Riley M F, Carl L V, Lorell B

机构信息

Charles A. Dana Research Institute, Beth Israel Hospital, Boston, MA 02215.

出版信息

Am Heart J. 1988 Nov;116(5 Pt 1):1253-61. doi: 10.1016/0002-8703(88)90448-6.

Abstract

The etiology of systolic left ventricular-to-aortic pressure gradients in hypertrophic cardiomyopathy is still controversial. While cavity obliteration has been proposed by some investigators as the cause for recording of a high left ventricular systolic pressure, the concept of left ventricular outflow tract obstruction has received more experimental support. To investigate further whether left ventricular pressure truly exceeds aortic pressure and implies obstruction, we studied, with imaging and Doppler echocardiographic techniques, five patients with asymmetric septal hypertrophy and systolic anterior movement of the mitral valve occasionally causing it to abut upon the septum. All had outflow tract pressure gradients (peak 85 +/- 10 mm Hg) and trace to mild mitral regurgitation. Continuous wave Doppler study recorded peak flow velocities in the outflow tract (4.6 +/- 0.3 m/sec), and mitral regurgitant (mean 6.6 +/- 0.3 m/sec) jets. Aortic systolic and diastolic blood pressures were measured by cuff sphygmomanometry, and simultaneous carotid pulse tracings were recorded. The magnitude of systolic aortic pressure was determined at the time of peak velocity in the mitral regurgitant jet. Since the peak systolic pressure gradient across the mitral valve (left ventricular minus left atrial pressure) should equal 4 times the square of the peak velocity (V) in the mitral regurgitant jet, peak left ventricular systolic pressure should equal 4 x V2 plus the height of left atrial pressure at the time of peak mitral regurgitant velocity. In each case, calculations were made assuming an upper normal left atrial pressure of 10 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

肥厚型心肌病中左心室与主动脉之间收缩期压力梯度的病因仍存在争议。一些研究者提出心室腔闭塞是记录到高左心室收缩压的原因,而左心室流出道梗阻的概念得到了更多实验支持。为了进一步研究左心室压力是否真的超过主动脉压力并意味着梗阻,我们使用成像和多普勒超声心动图技术研究了5例不对称性室间隔肥厚且二尖瓣收缩期前向运动偶尔导致其与室间隔接触的患者。所有患者均有流出道压力梯度(峰值85±10mmHg)及微量至轻度二尖瓣反流。连续波多普勒研究记录了流出道的峰值流速(4.6±0.3m/秒)和二尖瓣反流(平均6.6±0.3m/秒)射流。通过袖带血压计测量主动脉收缩压和舒张压,并同时记录颈动脉搏动曲线。在二尖瓣反流射流峰值速度时测定收缩期主动脉压力大小。由于二尖瓣跨瓣峰值收缩期压力梯度(左心室减去左心房压力)应等于二尖瓣反流射流峰值速度(V)平方的4倍,左心室峰值收缩压应等于4×V²加上二尖瓣反流峰值速度时左心房压力值。在每种情况下,计算时假设左心房压力上限为正常的10mmHg。(摘要截短于250字)

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验