Geometry of Left Ventricular Contraction in the Systolic Click Syndrome

Liedtke, A. J.; Gault, James H.; Leaman, David M.; Blumenthal, Melvin S.

doi:10.1161/01.cir.47.1.27

Cited by 85 publications

(22 citation statements)

References 15 publications

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“…Regional variations in shortening were first detected in humans by Kong et al (12) using coronary bifurcations as surface markers during coronary angiography. These investigators, and Liedke et al (17), by using angiographic techniques, showed greater shortening at the apex compared with the base of the LV. With dimension gauges implanted at the midwall in the direction of the midwall myofibers, shortening was found to be greatest in the apex (ϳ20%) and less at the midwall and base of the ventricle (16).…”

Section: Regional End-systolic Strains and Effects Of Afterloadmentioning

confidence: 82%

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

Takayama

Costa

Covell

2002

American Journal of Physiology-Heart and Circulatory Physiology

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Takayama, Yasuo, Kevin D. Costa, and James W. Covell. Contribution of laminar myofiber architecture to load-dependent changes in mechanics of LV myocardium. Am J Physiol Heart Circ Physiol 282: H1510-H1520, 2002; 10.1152/ajpheart.00261.2001.-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 in an axis system determined by the anatomy of the laminar architecture, laminar sheets of myocytes shear and laterally extend in an approximately radial direction. These deformations account for ϳ90% of normal systolic wall thickening in the left ventricular free wall. In the present study, we investigated whether the changes in systolic and diastolic function of the sheets were sensitive to alterations in systolic and diastolic load. Our results indicate that there is substantial reorientation of the laminar architecture during systole and diastole. Moreover, this reorientation is both site and load dependent. Thus as end-diastolic pressure is increased and the left ventricular wall thins, sheets shorten and rotate away from the radial direction due to transverse shearing, opposite of what occurs in systole. Both mechanisms of thickening contribute substantially to normal left ventricular wall function. Whereas the relative contributions of shear and extension are comparable at the base, sheet shear is the predominant factor at the apex. The magnitude of shortening/extension and shear increases with preload and decreases with afterload. These findings underscore the essential contribution of the laminar myocardial architecture for normal ventricular function throughout the cardiac cycle. myocardium; wall thickening; systole; diastole THE VENTRICULAR MYOCARDIUM consists of a syncytium of myocytes organized into branching transmurally oriented laminar sheets approximately four cells thick (14). Recent evidence indicates that this laminar structure contributes importantly to systolic function. When systolic deformation is expressed in an axis system determined by the anatomy of the laminar architecture, laminar sheets of myocytes shear and laterally extend in an approximately radial direction. These deformations account for ϳ90% of normal systolic wall thickening in the left ventricular (LV) free wall. In a recent study (5) from this laboratory, we found regional variations in the relative contribution of sheet extension and shear to wall thickening. In the free wall of the ventricle, sheet extension accounted for the majority of wall thickening, whereas in the septum, sheet shear was the predominant factor. Systolic wall thickening is a commonly employed index of regional myocardial performance (8) in both clinical and experimental studies. However, wall thickening varies both transmurally and regionally (7). These variations were reported in clinical studies (3) using magnetic resonance imaging (MRI). Moreover, Villarreal et al. (36) have shown regional variations in the sensit...

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Section: Regional End-systolic Strains and Effects Of Afterloadmentioning

confidence: 82%

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

Takayama

Costa

Covell

2002

American Journal of Physiology-Heart and Circulatory Physiology

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“…Techniques such as contrast left ventriculography (Liedtke et al, 1973;Sniderman et al, 1973;Bove et al, 1978;Gelberg et al, 1979;Klausner et al, 1982;Sheehan et al, 1983) and echocardiography (Shapiro et al, 1981;Haendchen et al, 1983) demonstrate considerable nonuniformity of the contraction process. However, these techniques a priori impose a certain level of uniformity on the contraction process by presuming that different endocardial sites will all move along a perpendicular pathway to a common long axis, or along a prescribed radial pathway to a common center of mass.…”

Section: Discussionmentioning

confidence: 99%

“…We were particularly interested in the minor axis level because several indices of systolic function estimate the amount of circumferential shortening at this level by measuring the resultant shortening of an internal diameter, radius, or minor axis chord. Although considerable nonuniformity of contraction has been demonstrated by techniques such as left ventriculography (Liedtke et al, 1973;Sniderman et al, 1973;Bove et al, 1978;Gelberg et al, 1979;Klausner et al, 1982;Sheehan et al, 1983), echocardiography (Shapiro et al, 1981;Haendchen et al, 1983) and fluoroscopic tracking of midwall markers (Ingels et al, 1980(Ingels et al, , 1981, these methods do not directly measure regional circumferential shortening, but rather infer this from the resultant motion which occurs perpendicular to the assumed major direction of shortening.…”

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confidence: 99%

Regional comparison of midwall segment and area shortening in the canine left ventricle.

Lew¹,

LeWinter²

1986

Circulation Research

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SUMMARY. We used ultrasonic segment length gauges to examine the regional behavior of midwall fibers at different sites around the left ventricular minor axis in 12 anesthetized dogs. In six dogs (group I) with circumferentially oriented midwall gauges, significantly greater shortening of anterior than lateral or posterior wall segments was demonstrated over a range of left ventricular end-diastolic pressures from 2 to 18 mm Hg. Normalized end-diastolic segment lengths increased more in the anterior wall as end-diastolic pressure increased, suggesting that regional differences in diastolic distensibility may in part account for the observed shortening differences. To examine the extent to which shortening of longitudinally oriented fibers of the subendocardium and subepicardium might influence the behavior of the midwall circumferential fibers, we implanted mutually perpendicular midwall gauges circumferentially and longitudinally in the anterior and posterior walls in six dogs (group II). Longitudinal shortening of midwall fibers was negligible at low end-diastolic pressures, but increased significantly at higher end-diastolic pressures. In the anterior wall, there was greater circumferential than longitudinal shortening, whereas, in the posterior wall, shortening was similar in the two directions. Finally, we calculated the midwall area subtended by the mutually perpendicular gauges and found the systolic change in midwall area to be similar for the anterior and posterior walls at all end-diastolic pressures. We conclude that midwall fibers demonstrate considerable nonuniformity of contraction at different sites around the minor axis. This finding may be related in part to regional differences in diastolic distensibility or in functional interactions between fiber layers. Despite these complex regional, directional, and volume dependent differences in midwall segment function, the systolic changes in midwall area did not vary regionally. Thus, different midwall sites around the minor axis circumference appear to have similar overall contributions to the ejection of blood. (Circ Res 58: 678-691, 1986)

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“…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.…”

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confidence: 88%

Quantitation of regional cardiac function by two-dimensional echocardiography. I. Patterns of contraction in the normal left ventricle.

Haendchen¹,

Wyatt²,

Maurer³

et al. 1983

Circulation

185

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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 ...

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Geometry of Left Ventricular Contraction in the Systolic Click Syndrome

Cited by 85 publications

References 15 publications

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

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

Regional comparison of midwall segment and area shortening in the canine left ventricle.

Quantitation of regional cardiac function by two-dimensional echocardiography. I. Patterns of contraction in the normal left ventricle.

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