Sasayama S, Franklin D, Ross J, Kemper W S, McKown D
Am J Cardiol. 1976 Dec;38(7):870-9. doi: 10.1016/0002-9149(76)90800-6.
The thickness of the left ventricular free wall and internal chamber diameter were continuously measured by pairs of ultrasonic crystals together with left ventricular pressure in normal conscious dogs. During the resting state, wall thickness decreased abruptly with the onset of atrial contraction from 10.5 mm to an average end-diastolic valueof9.8 mm. In contrast to most previous studies, there was no change in wall thickness during isovolumic systole, and with ejection the wall thickened by 31.3 percent of end-diastolic wall thickness. Atrial pacing, phenylephrine, isoproterenol and propranolol produced significant changes in chamber size with reciprocal changes in wall thickness. In addition, changes in the extent and velocity of left ventricular chamber shortening in the minor equator were associated with comparable reciprocal changes in the extent and velocity of free wall thickening (correlation coefficients 0.97 to 0.99). During acute coronary occlusion, progressive reductions in the extent and velocity of regional wall shortening with partial ischemia were associated with comparable changes in systolic wall thickening characteristics (r = 0.96 and 0.95), and holosystolic elongation in fully ischemic areas was associated with holosystolic wall thinning. During chronic pressure overload, despite wall thickening, the relation between chamber shortening and wall thickening were retained and direct computation of dynamic wall stress variations was possible. These measurements allowed precise definition of the dynamics of the left ventricular wall during normal and abnormal cardiac states. The demonstration that in the absence of regional dysfunction analysis of wall thickness in a single region of ventricular free wall can be used to describe myocardial and overall left ventricular function, as well as regional function in the presence of ischemia, constitutes a new approach to the assessment of cardiac function that has potential for echocardiographic applications.
在正常清醒犬中，通过成对的超声晶体与左心室压力一起连续测量左心室游离壁厚度和心腔内径。在静息状态下，随着心房收缩开始，壁厚度从10.5毫米突然降至平均舒张末期值9.8毫米。与大多数先前的研究相反，等容收缩期壁厚度没有变化，而在射血期壁增厚至舒张末期壁厚度的31.3%。心房起搏、去氧肾上腺素、异丙肾上腺素和普萘洛尔使心腔大小发生显著变化，壁厚度也相应改变。此外，左心室短轴缩短的程度和速度变化与游离壁增厚的程度和速度的相应变化相关（相关系数为0.97至0.99）。在急性冠状动脉闭塞期间，局部缺血导致局部壁缩短的程度和速度逐渐降低，同时收缩期壁增厚特征也有类似变化（r = 0.96和0.95），完全缺血区域的全收缩期伸长与全收缩期壁变薄相关。在慢性压力超负荷期间，尽管壁增厚，但腔室缩短与壁增厚之间的关系仍然存在，并且可以直接计算动态壁应力变化。这些测量允许精确界定正常和异常心脏状态下左心室壁的动力学。证明在没有区域功能障碍的情况下，对心室游离壁单个区域的壁厚度分析可用于描述心肌和整体左心室功能，以及缺血时的区域功能，这构成了一种评估心脏功能的新方法，具有超声心动图应用的潜力。
