SPECTRUM OF PURE MITRAL STENOSIS - HEMODYNAMIC STUDIES IN RELATION TO CLINICAL DISABILITY
SPECTRUM OF PURE MITRAL STENOSIS - HEMODYNAMIC STUDIES IN RELATION TO CLINICAL DISABILITY
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DOI：
10.1016/0002-9149(62)90171-6
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发表时间：
1962-01-01
影响因子：
2.8
通讯作者：
STEIN, SW
中科院分区：
文献类型：
--
作者：
HUGENHOLTZ, PG;RYAN, TJ;STEIN, SW
重新评估二尖瓣狭窄的病理生理学，特别强调生理变量与症状严重程度和残疾程度的关系。44例单纯二尖瓣狭窄患者的数据。均行左心导管插入术，25例行右心导管插入术，26例心功能Ⅰ、Ⅱ级（美国心脏协会功能分类）有轻度症状或根本没有症状，而18名患者属于III级，症状严重。不出所料，左房压力与二尖瓣面积呈负相关（r=-0.618）、肺动脉压和二尖瓣面积平均二尖瓣舒张压差与二尖瓣面积之间的相关系数为-0.575（r=-0.708）。心脏指数与二尖瓣面积呈正相关（r= + 0.407）。所有相关系数均达到1%的水平，I类和II类26例患者中有17例二尖瓣面积小于或等于1.5 cm 2，这表明重度二尖瓣狭窄可以在几乎无症状的状态下发现。所有18例III类患者的瓣膜面积均小于1.5 cm 2。比较两组患者瓣膜狭窄程度相似的情况。两类患者的心输出量均显著降低（p< 0.01）（2.81 L）。最小M2。I类和II类，以及2.82 L。最小M2。患者的等级）。两组的左心房压分别为18和19 mm Hg，平均舒张压差分别为11和13 mm Hg，均无显著差异。然而，肺动脉压（I类和II类为22 mmHg，II类为36 mmHg）以及肺小动脉阻力（105达因/秒）与425达因/秒相比，cm. -5，确实可以区分两个临床不同的组之间的血流动力学差异。这些数据表明，肺血管疾病的程度是二尖瓣狭窄症状的重要决定因素。对于I类和II类患者，病史、体格检查和放射学研究不能准确预测二尖瓣大小。这表明，二尖瓣阻滞的最早适应机制之一是心输出量减少，最初，肺血管阻力升高、心肌衰竭或心房纤颤。这是二尖瓣重度狭窄患者可能长时间保持无症状的方法之一。
The pathophysiology of mitral stenosis is reassessed, with special emphasis upon relation of physiologic variables to severity of symptoms and degree of disability. Data from 44 patients with pure mitral stenosis are presented. Cathetcrization of the left side of the heart was performed in all and catheterization of the right side of the heart in 25 patients.Twenty-six patients were in Class I or II (American Heart Association Functional Classification) with mild symptoms or none at all, while 18 patients were in Class III with severe symptoms.As expected, inverse relationships existed between left atrial pressure and mitral valve area (r= − 0.618), pulmonary arterial pressure and mitral valve area (r= − 0.575), and between mean mitral diastolic pressure gradient and mitral valve area (r= − 0.708). There was a positive relationship between cardiac index and mitral valve area (r= + 0.407). All correlation coefficients were significant to the 1 per cent level.Seventeen of the 26 patients in Classes I and II had mitral valve areas of 1.5 cm2, or less. This indicates that severe mitral stenosis can be found in a nearly asymptomatic state. All of the 18 Class III patients had valve areas of less than 1.5 cm2. These two groups of patients with similar degree of valve narrowing were compared. Cardiac output was significantly (p< 0.01) reduced in both categories (2.81 L. min. M2. for Classes I and II, and 2.82 L. min. M2. for Class in patients). Left atrial pressure in the two groups, 18 and 19 mm. Hg, respectively, and mean diastolic pressure gradient, 11 and 13 mm. Hg, respectively, did not show significant differences. However, pulmonary arterial pressure, 22 mm. Hg in Classes I and II and 36 mm. Hg in Class II, as well as pulmonary arteriolar resistance, 105 compared to 425 dynes sec. cm.−5, did allow a hemodynamic distinction between the two clinically different groups. These data suggest that the degree of pulmonary vascular disease is an important determinant of the symptoms of mitral stenosis.For Class I and II patients, history, physical examination and radiographic studies did not allow an accurate prediction of the mitral valve size.It is suggested that one of the earliest adaptive mechanisms to mitral blockade is a decrease in cardiac output and that this is not mediated, initially, through an elevated pulmonary vascular resistance, myocardial failure or atrial fibrillation. It is one of the means by which a patient with severe stenosis of the mitral valve may remain asymptomatic for prolonged periods of time.