(Circulation. 2006;113:2477-2479.)
© 2006 American Heart Association, Inc.
Editorial |
From the Departments of Medicine and Cardiology (E.F., K.E.L.), University of California, San Francisco.
Correspondence to Elyse Foster, MD, University of California, San Francisco, Moffitt 314A, Box 0214, 505 Parnassus Ave, San Francisco, CA 941943-0214. E-mail foster{at}medicine.ucsf.edu
Key Words: Editorials cardiomyopathy diastole echocardiography exercise
| Introduction |
|---|
|
|
|---|
Article p 2524
Recent work has elucidated both intracellular and extracellular mechanisms that contribute to diastolic dysfunction, and some progress has been made in finding new treatments for diastolic heart failure. Additional research has evaluated the contribution of LV architecture and its role in maintaining the normal contraction sequence that optimizes mechanical efficiency. The importance of systolic twist and the subsequent recoil that leads to diastolic untwisting was examined in the article by Notomi et al4 using tissue Doppler techniques in both normal subjects and patients with hypertrophic cardiomyopathy, at rest and during exercise.
| The Left Ventricle Viewed as a Double Helix That Twists and Untwists |
|---|
|
|
|---|
Using blunt dissection, Torrent-Guasp et al8 demonstrated that the ventricles consist of a single myofiber band starting at the right ventricle just below the pulmonary valve and forming a double helix extending to the left ventricle, where it attaches to the aorta (www.helicalheart.com). This architecture promotes systolic torsion. When viewed from the LV apex, the systolic rotation of the base is clockwise, and the rotation of the apex is counterclockwise. Torsion is defined as the difference between the basal and apical rotation. In diastole, the ventricle "untwists," rapidly recoiling and creating diastolic suction. This "suction" increases the diastolic intraventricular gradient and the left atrial to LV gradient to promote early filling.9,10
If the normal LV architecture has a major role in normal diastolic function, it stands to reason that the ventricle, remodeled in response to an injury such as myocardial infarction, would display diastolic dysfunction, in addition to systolic dysfunction.
| Diastolic Function During Exercise |
|---|
|
|
|---|
Using a method based on 2D imaging, Tischler and Niggel12 previously demonstrated that systolic twist is enhanced by 86% during exercise from
10° to 18°. However, there are no data on the effect of disease processes that impair systolic twist during exercise and how they affect the early diastolic untwisting or on those that primarily affect diastolic function. The importance of the untwisting of the ventricle in early diastole and its enhanced rate in exercise is demonstrated by the findings of the study by Notomi et al4.
| Measuring Twist and Untwist |
|---|
|
|
|---|
40% of the accumulated systolic torsion is released.13 In animals, the velocity of LV untwisting (recoil rate) has been correlated with invasive measurements of
, the time constant of relaxation, under a variety of loading and inotropic conditions. Dong et al13 showed that the recoil rate is a measure of LV relaxation that is independent of preload as reflected in left atrial pressure. Interestingly, this same group of investigators showed that the diastolic dysfunction associated with normal aging was not explained by diminished recoil rate.14 The precise timing of rapid recoil associated with ventricular untwisting and the response to exercise have not been elucidated by MRI studies, in part because of the slow frame rate of acquisition. | Tissue Doppler Applications for Measuring Twist and Torsion |
|---|
|
|
|---|
The results of the study by Notomi et al4 support previous work showing that systolic torsion results from clockwise basal rotation with more vigorous counterclockwise apical rotation and provide new information on the timing and magnitude of the diastolic untwisting. The rapid transition to untwisting begins just slightly before the end of systole as marked by aortic valve closure, followed in time by the peak IVPG and then peak early diastolic filling. The relative timing of long-axis lengthening and short-axis expansion also were examined; these events occur simultaneously with or slightly after the peak E velocity, suggesting that they are a consequence rather than a cause of diastolic filling. These data suggest that the initiation of ventricular untwisting is an early and key mechanism that promotes early diastolic relaxation and early diastolic filling, possibly more important than the recoil of systolic basal descent.
During exercise, the degree of systolic LV torsion increased primarily as a consequence of increased apical counterclockwise rotation velocity. Untwisting began earlier, and velocities were markedly increased during exercise. The magnitude of increase in twisting and untwisting velocities during exercise was significantly greater than the corresponding changes in LV length and radius. This finding suggests that the enhanced diastolic suction during exercise results in large part from the more vigorous untwisting motion of the ventricle, especially at the apex. Not surprisingly, the measured IVPG, a marker for the suction phenomenon during diastole, was correspondingly increased with exercise in the normal subjects.
To explore the pathophysiological implications of their findings, Notomi et al then applied these methods of measuring LV rotation, torsion, and IVPGs in patients with hypertrophic cardiomyopathy (HCM) both at rest and during exercise. Interestingly, at rest, peak systolic torsion values in HCM patients were higher than in normal subjects. However, during exercise, the increased twisting and untwisting velocities so clearly demonstrated in normal subjects were blunted in HCM patients. The IVPG in HCM subjects increased with exercise but to a much smaller degree than in normal subjects. Moreover, the timing of untwisting was delayed within the cardiac cycle in these patients. These data suggest that a prominent mechanism for exercise intolerance in HCM is an inability to enhance diastolic untwisting, resulting in less diastolic suction, impaired LV filling, and increased left atrial pressure.
| Implications |
|---|
|
|
|---|
The measurements of twist, torsion, and IVPG obtained in the study by Notomi et al4 offer a more complex and detailed quantification of diastolic function. However, there is no new insight as to whether the mechanism is energy consuming or is the result of the release of elastic energy without energy consumption. It would be intriguing to study these measures in other conditions associated with diastolic dysfunction such as hypertensive heart disease and infiltrative disorders of the myocardium. The important role of apical torsional enhancement may explain the diastolic dysfunction observed in patients with apical aneurysms. Recent efforts to affect ventricular mechanics with surgical procedures that alter ventricular geometry such as the Dor procedure are likely to affect twist and torsion during both systole and diastole. MRI data have shown that systolic torsion is not restored after partial left ventriculectomy in patients with dilated cardiomyopathy despite clinical improvement.17 The effects of this restorative surgical procedure on diastolic untwisting should be studied with the tissue Doppler methodology used in this report. Additionally, measurements of twisting and untwisting velocities and diastolic suction could be followed clinically as a response to pharmacological therapy as our armamentarium expands to include agents that are targeted primarily at diastolic function.
| Bringing Twist and Untwist to the Clinical Echocardiography Laboratory |
|---|
|
|
|---|
With the "Twist," Chubby Checker changed dancing forever by separating the dancers, freeing them to express themselves.20 Looking beyond traditional measures of diastolic function, echocardiographers may now be able to express twist, untwist, and torsion.
| Acknowledgments |
|---|
None.
| Footnotes |
|---|
| References |
|---|
|
|
|---|
2. Angeja BG, Grossman W. Evaluation and management of diastolic heart failure. Circulation. 2003; 107: 659663.
3. Oh JK, Hatle L, Tajik AJ, Little WC. Diastolic heart failure can be diagnosed by comprehensive two-dimensional and Doppler echocardiography. J Am Coll Cardiol. 2006; 47: 500506.
4. Notomi Y, Martin-Miklovic MG, Oryszak SJ, Shiota T, Deserranno D, Popovic ZB, Garcia MJ, Greenberg NL, Thomas JD. Enhanced ventricular untwisting during exercise: a mechanistic manifestation of elastic recoil described by Doppler tissue imaging. Circulation. 2006; 113: 25242533.
5. DaVinci L. In: Evans L, ed. Starlings Principles of Human Physiology. London, UK: J.A. Churchill; 1936: 706.
6. Rushmore RF. Anatomy and physiology of ventricular function. Physiol Rev. 1956; 36: 400425.
7. McDonald IG. The shape and movements of the human left ventricle during systole: a study by cineangiography and by cineradiography of epicardial markers. Am J Cardiol. 1970; 26: 221230.[CrossRef][Medline] [Order article via Infotrieve]
8. Torrent-Guasp F, Ballester M, Buckberg GD, Carreras F, Flotats A, Carrio I, Ferreira A, Samuels LE, Narula J. Spatial orientation of the ventricular muscle band: physiologic contribution and surgical implications. J Thorac Cardiovasc Surg. 2001; 122: 389392.
9. Buckberg GD, Weisfeldt ML, Ballester M, Beyar R, Burkhoff D, Coghlan HC, Doyle M, Epstein ND, Gharib M, Ideker RE, Ingels NB, LeWinter MM, McCulloch AD, Pohost GM, Reinlib LJ, Sahn DJ, Sopko G, Spinale FG, Spotnitz HM, Torrent-Guasp F, Shapiro EP. Left ventricular form and function: scientific priorities and strategic planning for development of new views of disease. Circulation. 2004; 110: e333e336.
10. Corno AF, Kocica MJ, Torrent-Guasp F. The helical ventricular myocardial band of Torrent-Guasp: potential implications in congenital heart defects. Eur J Cardiothorac Surg. 2006; 29 (suppl 1): S61S68.
11. Cheng CP, Igarashi Y, Little WC. Mechanism of augmented rate of left ventricular filling during exercise. Circ Res. 1992; 70: 919.
12. Tischler M, Niggel J. Left ventricular systolic torsion and exercise in normal hearts. J Am Soc Echocardiogr. 2003; 16: 670674.[CrossRef][Medline] [Order article via Infotrieve]
13. Dong SJ, Hees PS, Siu CO, Weiss JL, Shapiro EP. MRI assessment of LV relaxation by untwisting rate: a new isovolumic phase measure of tau. Am J Physiol Heart Circ Physiol. 2001; 281: H2002H2009.
14. Hees PS, Fleg JL, Dong SJ, Shapiro EP. MRI and echocardiographic assessment of the diastolic dysfunction of normal aging: altered LV pressure decline or load? Am J Physiol Heart Circ Physiol. 2004; 286: H782H788.
15. Notomi Y, Setser RM, Shiota T, Martin-Miklovic MG, Weaver JA, Popovic ZB, Yamada H, Greenberg NL, White RD, Thomas JD. Assessment of left ventricular torsional deformation by Doppler tissue imaging: validation study with tagged magnetic resonance imaging. Circulation. 2005; 111: 11411147.
16. Rovner A, Greenberg NL, Thomas JD, Garcia MJ. Relationship of diastolic intraventricular pressure gradients and aerobic capacity in patients with diastolic heart failure. Am J Physiol Heart Circ Physiol. 2005; 289: H2081H2088.
17. Setser RM, Kasper JM, Lieber ML, Starling RC, McCarthy PM, White RD. Persistent abnormal left ventricular systolic torsion in dilated cardiomyopathy after partial left ventriculectomy. J Thorac Cardiovasc Surg. 2003; 126: 4855.
18. Notomi Y, Lysyansky P, Setser RM, Shiota T, Popovic ZB, Martin-Miklovic MG, Weaver JA, Oryszak SJ, Greenberg NL, White RD, Thomas JD. Measurement of ventricular torsion by two-dimensional ultrasound speckle tracking imaging. J Am Coll Cardiol. 2005; 45: 20342041.
19. Helle-Valle T, Crosby J, Edvardsen T, Lyseggen E, Amundsen BH, Smith HJ, Rosen BD, Lima JA, Torp H, Ihlen H, Smiseth OA. New noninvasive method for assessment of left ventricular rotation: speckle tracking echocardiography. Circulation. 2005; 112: 31493156.
20. Richard De La Font Agency, Inc. Available at: http://www.delafont.com. Accessed May 16, 2006.
This article has been cited by other articles:
![]() |
C. Tousignant CON: Intraoperative Doppler Tissue Imaging Is a Valuable Addition to Cardiac Anesthesiologists' Armamentarium Anesth. Analg., January 1, 2009; 108(1): 41 - 47. [Full Text] [PDF] |
||||
![]() |
P. Ferrazzi, M. Senni, M. R. Iascone, M. Merlo, M. Triggiani, R. Lorusso, P. Herijgers, J. J. Schreuder, S. Pentiricci, A. Iacovoni, et al. Implantation of an Elastic Ring at Equator of the Left Ventricle Influences Cardiac Mechanics in Experimental Acute Ventricular Dysfunction J. Am. Coll. Cardiol., October 30, 2007; 50(18): 1791 - 1798. [Abstract] [Full Text] [PDF] |
||||
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2006 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |