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SUMMARYLeft ventricular (LV) pressure and myocardial segment length, determined by an epicardial mercury-in-silastic length gauge, were plotted simultaneously to obtain a pressure-length loop before and after left anterior descending artery (LAD) occlusion in 11 dogs. Previous

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SUMMARY Regional differences in wall motion and wall thickening were quantitated in the normal left ventricle using two-dimensional echocardiography (2-D echo). Using a computer-aided system, the left ventricle was subdivided in a standardized manner into 40 segments of five 2-D echo short-axis cross sections from the mitral valve level to the low left ventricle or apex. Measurements of sectional and segmental cavity areas, muscle areas and endocardial as well as epicardial peritneters, allowed assessment of contractile function using such indexes as endocardial systolic fractional area change (FAC), wall thickening (WTh), and circumferential fiber shortening (shortening). In 50 normal anesthetized, closed-chest dogs (including 10 studies in the conscious state) and in 32 normal humans, left ventricular contractile function increased significantly from base to apex. Thus, in anesthetized dogs, sectional FAC, WTh and shortening increased from left ventricular base to apex as follows: 39.4 ± 5.1% to 61.6 ± 7.2%, 20.5 ± 6.6% to 46.7 11.5% and 22.7 ± 3.4% to 35.4 5.9%, respectively. Similar trends were noted in conscious dogs. In man, sectional FAC, WTh and shortening also increased from the mitral valve to the low left ventricular level: 38.8 3.3% to 60.7 4.5%, 23.9 ± 5.6% to 28.9 ± 7.6% and 21.4 ± 5.0% to 30.6 ± 5.6%, respectively. Detailed segmental analysis in individual cross sections also revealed regional differences in contraction. Generally, contraction was most vigorous in posterior regions of the left ventricle. The septal regions exhibited lowest contraction at the base, but also the greatest increase from base to apex, both in the canine and human. Lateral regions did not show significant changes along the length of the left ventricle. Diastolic wall thickness also varied. We conclude that contraction in the normal left ventricle cannot be assumed to be uniform or symmetrical. These normal regional differences in function should be taken into account when evaluating altered physiologic states and in studying effects of therapeutic interventions.FOR MANY YEARS cardiologists have assumed that the pattern of contraction in the normal left ventricle is concentric and uniform, classically defined as synergic motion. i Most of the earlier studies aimed at characterizing ventricular function were therefore based on models and assumed myocardial fiber structure consistent with uniform contraction.2 3 However, animal investigations have shown that the distribution of fiber angles is complex and changes during systolic contraction; endocardial and epicardial fibers tend to be oriented longitudinally and midwall fibers circumferentially.4 A study by Greenbaum et al.5 indicates that the human cardiac fiber architecture is even more complex than previously thought. Thus, models based on uniform wall motion may not adequately describe LV function in normal states, a prerequisite for studying altered physiologic conditions. Clinical studies using cineventriculography in man have indicated that myocardial performance ...

Cross-sectional echocardiography was used to quantify volume in 21 canine left ventricles that were fixed in formalin and immersed in mineral oil. Area, length and diameter measurements were obtained from short- and long-axis cross-sectional images of the left ventricle and volume was calculated by seven mathematic models. Calculated volume was then compared, by linear regression and percent error analyses, with fluid volume of the left ventricle, obtained by filling the chamber with a known amount of fluid. Volumes ranged from 13-146 ml. Mathematic models using short-axis area and long-axis length gave higher correlation coefficients (r = 0.982 and r = 0.969) and lower mean errors (10-20%) than standard formulas previously used for M-mode echo and angiography. Thus, short-axis area analysis with cross-sectional echocardiography is well-suited for quantifying left ventricular volumes in dogs.

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To investigate the effects of physical training on cardiac dimensions and function, eight dogs were exercised for 12 weeks by treadmill running 1 hour/ day, 5 days/week. Five dogs were confined in cages as controls for an 8-week period. Heart rates were monitored by telemetry during rest and exercise. Maximum QRS spatial magnitudes were calculated from records of McFee lead electrocardiograms. Left ventricular end-diastolic dimensions were determined radiographically by the bead and clip technique. No statistically significant changes occurred during the control period. Training produced statistically significant decreases in heart rate at rest (72 beats/min to 49 beats/min, P < 0.005) and at a standard work load of 6.1 mph on a level treadmill (205 beats/ min to 158 beats/min, P < 0.005) and statistically significant increases in work load (5.4 mph to 9.1 mph, P < 0.005) at a standard heart rate of 194 beats/min. Improvements were rapid during the first 4 weeks of training but gradual during the remaining 8 weeks. Training caused small but statistically significant increases in left ventricular end-diastolic wall thickness (8.7 mm to 9.3 mm, P < 0.0025), estimated left ventricular mass (83.6 g to 91.2 g, P < 0.01), and maximum (McFee) QRS spatial magnitude (4.0 mv to 4.8 mv, P < 0.05).