The dynamic geometry of the left ventricle was assessed with the use of chronically implanted pulse-transit ultrasonic dimension transducers. The orientation of the transducers allowed the measurement of left ventricular minor and major axis diameters and equatorial wall thickness in the conscious dog. The left ventricle was modeled as a three-dimensional, prolate ellipsoidal shell. Left ventricular and pleural pressures were measured with high fidelity micromanometers. Aortic blood flow was obtained with electromagnetic flow probes. To test the assumptions inherent in this technique, left ventricular mass, internal volume, stroke volume, and peak aortic flow were computed from the dimension data and compared to directly measured values. Correlation coefficients of 0.95 or greater were obtained for each of these comparisons. In addition, the calculated left ventricular mass was constant to within +/- 6% of the mean value throughout the cardiac cycle. We found that the dynamic contraction pattern of the left ventricle was dependent on the physiological state of the dog. Furthermore, in the conscious state, shortening of the minor axis diameter, lengthening of the major axis diameter, and slight thickening or thinning of the wall were noted during isovolumic contraction (isovolumic ellipticalization pattern). In the open-chested, anesthetized state, however, marked rearrangements in geometry were observed during isovolumic contraction manifested by lengthening of the minor axis diameter, and significant thickening of the wall (isovolumic sphericalization pattern). We also observed that left ventricular volume was significantly diminished in the open-chested state. The isovolumic contraction pattern in open-chested dogs could be changed from sphericalization to ellipticalization by increasing end-diastolic volume with the infusion of saline. During a vena caval occlusion in the conscious state, the contraction pattern changed from isovolumic ellipticalization to isovolumic sphericalization as the end-diastolic volume decreased. Thus, the exact pattern of left ventricular contraction was found to be a function of left ventricular volume.

The three-dimensional dynamic geometry of the left ventricle in the conscious dog.

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.

Dynamic changes in left ventricular wall thickness and their use in analyzing cardiac function in the conscious dog.

In 15 open-chest, anesthetized dogs, regional systolic wall thickening (% delta WT) was measured with sonomicrometry and regional blood flow was determined with tracer microspheres (7-10 micron) before and after various degrees of coronary artery narrowing were created with a hydraulic occluder. The stenoses were categorized into four groups by the effect on % delta WT, and the corresponding myocardial blood flow (MBF) was determined in four layers across the ventricular wall (layer 1: subendocardium; layer 4: subepicardium). In group 1, % delta WT decreased 44 +/- 10% and only layer 1 MBF was significantly reduced (-28%); in group 2, % delta WT decreased 77 +/- 8% and MBF was reduced in both layers 1 and 2 (-52% and -36%, respectively); in group 3, % delta WT decreased 104 +/- 3% and MBF was reduced in the three inner layers (layer 1: -65%; layer 2: -58%; layer 3: -34%); in group 4, % delta WT decreased 145 +/- 9% (systolic wall thinning) and transmural reduction of MBF was found (layer 1: -74%; layer 2:...

Significance of regional wall thickening abnormalities relative to transmural myocardial perfusion in anesthetized dogs.

The ventricular myocardium consists of a syncytium of myocytes organized into branching, transmurally oriented laminar sheets approximately four cells thick. When systolic deformation is expressed ...

https://www.physiology.org/doi/pdf/10.1152/ajpheart.00261.2001

Contribution of laminar myofiber architecture to load-dependent changes in mechanics of LV myocardium.

The relation between transverse left ventricular cavity dimension and posterior wall thickness has been studied using digitised echocardiograms from 10 normal subjects and 63 patients with heart disease. In normal subjects, the peak systolic rate of wall thickening (4.6 ± 1-2 cm/s) is less than the peak diastolic rate of wall thinning (10.7 + 1-7 cm/s). Maximum wall thickness, minimum dimension, and mitral valve opening are synchronous, and there follows a distinct early period of rapid thinning of the wall (100 + 20 ms) which corresponds to the rapid filling period. In ischaemic heart disease the rate and duration of rapid thinning are normal, but the onset precedes mitral valve opening (by 50 + 30 ms). In hypertrophic cardiomyopathy the rate (7 4 + 4-6 cm/s) and pattern of wall thinning are more variable than normal, and closely predict the pattern of change in cavity dimension. Inflow obstruction, associated with slow and protracted increase in cavity dimension, causes the thinning period to be prolonged, but the peak rate of thinning is often not reduced to the same extent as the rate of increase in dimension. This entails reversal of septal movement. We conclude that rapid wall thinning is an intrinsic property of the left ventricular myocardium, normally associated with rapid filling, which may, however, be dissociated from filling by asynchronous relaxation or inflow obstruction, or modified by myocardial disease.

https://heart.bmj.com/content/heartjnl/40/2/162.full.pdf

W G Guntheroth

Papers

Changes in left ventricular wall thickness during the cardiac cycle.