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Left ventricular systolic torsion and exercise in normal hearts
Left Ventricular Systolic Torsion and Exercise in Normal Hearts Marc Tischler, MD, and Joelyn Niggel, RN, Burlington, Vermont
This study examines the use of a novel 2-dimensional echocardiographic technique to measure left ventricular (LV) systolic torsion or twist in normal human hearts during maximal exercise. The effects of dynamic exercise on LV twist have not previously been determined. LV twist was measured in 25 healthy human control patients before and after maximal treadmill exercise. LV end-systolic volume
First described in the 17th century by Sir William 1
Harvey, left ventricular (LV) torsion, or twist, refers to the counterclockwise rotation of the ventricular apex with respect to its base during systole, with untwisting occurring during isovolumic relaxation and filling. This phenomenon, ascribed to asymmetric shortening of the internal and external layers of spiral muscles in the ventricular wall, has been postulated to result in the storage of potential energy, for which conversion to kinetic energy may contribute to ventricular suction and early diastolic filling.2,3 Several techniques have been used to describe and quantify ventricular torsion in human beings including cineangiography of radio-opaque markers,4-10 magnetic resonance imaging,11,12 and 2-dimensional (2D) echocardiography.13 Cineangiography of radio-opaque markers requires implantation at the time of cardiac operation, limiting the population available for study of twist to patients with significant cardiac disease. Magnetic resonance imaging using myocardial tagging remains expensive and its use is limited to basal conditions. Recently, we described a novel, 2D echocardiographic technique to quantify LV twist that correlates well with indices of early ventricular filling.14 The technique uses spatial rotation of the base of the anterolateral papillary muscle as a surrogate for more direct measurements. Although the effects of pharmacologic volume loading, pressure loading, and inotropic stimulation on ventricular torsion have been examined in both From the Cardiology Unit, Fletcher Allen Health Care (M. T.) and University of Vermont College of Medicine. Reprint requests: Marc Tischler, MD, Cardiology Unit, McClure 1, Fletcher Allen Health Care, Burlington, VT 05401 (E-mail: [email protected]). Copyright 2003 by the American Society of Echocardiography. 0894-7317/2003/$30.00 ⫹ 0 doi:10.1016/S0894-7317(03)00225-6
670
decreased and LV ejection fraction increased in a predictable manner. Systolic twist increased by 8.4 ⴞ 2.8 degrees (86%). Twist is believed to store potential energy and to play an important role in generating diastolic suction. The increase in twist observed may play an important role in facilitating LV diastolic filling during maximal exercise. (J Am Soc Echocardiogr 2003;16:670-4.)
canines and human beings9,10,12,15 the effect of dynamic exercise on twist is unknown. During exercise in dogs and human beings, the early diastolic portion of the ventricular pressure-volume relation shifts downward, an observation consistent with increased suction as a mechanism of filling. Thus, suction may be important in preventing diastolic pressure from increasing during exercise despite an increased volume and rate of ventricular filling. Correspondingly, increased inotropic stimulation and reduced end-systolic volume, both of which occur during exercise, are known to increase twist. In this study, we used our echocardiographic method14 to test the hypothesis that twist increases during dynamic exercise in healthy human beings.
METHODS Patient Selection The study group included 25 participants (14 men and 11 women; mean age 35.6 years, range: 21 to 58) with normal resting LV systolic function and no detectable structural heart disease by echocardiography. Of these patients, 10 were referred for stress echocardiography to assess palpitations and 15 were healthy volunteers. Exclusion criteria included LV hypertrophy or dilation, valvular stenosis, valvular regurgitation beyond a trivial degree, a known history of heart disease, an abnormal baseline electrocardiogram, an inadequate stress test (defined as a maximal heart rate response ⬍85% of the maximally predicted heart rate), electrocardiographic or echocardiographic evidence of ischemia, and echocardiographic images that were technically inadequate for this analysis. Echocardiography Two-dimensional echocardiographic examinations were performed at rest with the patient supine in the left lateral decubitus position; a phased-array ultrasonoscope device
Journal of the American Society of Echocardiography Volume 16 Number 6
Tischler and Niggel 671
(Acuson Sequoia, Mountain View, Calif) with a 3.5-MHz transducer was used. Images were obtained in sequential fashion from the parasternal long- and short-axis, and apical 4- and 2-chamber views. Each patient then underwent a symptom-limited treadmill exercise stress test using a standard Bruce protocol. Immediately after exercise, the patient was returned to the left lateral decubitus position and 2D imaging was repeated. Image acquisition was completed within 60 seconds. Data Analysis Conventional 2D echocardiographic data and twist measurements were analyzed at separate times. All tapes were reviewed in nonconsecutive fashion to minimize potential recording bias. Using a workstation (Image-Vue, Nova Microsonics Inc, Mahwah, NJ), 3 cardiac cycles from each baseline and postexercise recording were digitized from end-diastole (R-wave peak) to end-systole (smallest cavity area). End-systolic volume, end-diastolic volume, stroke volume, and ejection fraction (EF) were calculated using the 5/6 area-length bullet method.16-17 Ventricular twist was measured at rest and after exercise as previously described.14 Briefly, at end-diastole, a line was drawn from the apex of the scanning sector through a point at the center of the ventricular cavity (the midpoint of the chord connecting the anterior and posterior endocardial surfaces). A second line was drawn from the midpoint of the base of the anterolateral papillary muscle, where it inserts into the myocardium through the center of the ventricular cavity. The angle inscribed by these 2 intersecting lines was considered angle diastole (Figure 1). These steps were repeated for end-systole, yielding systole (Figure 2). The absolute difference in degrees between angles systole and diastole is the twist angle. By convention, rotation in the counterclockwise direction as viewed from the apex is denoted as a positive sign and rotation in the clockwise direction as a negative sign. To assess measurement reproducibility in the assessment of ventricular volumes and twist, 10 studies were reanalyzed at a temporarily remote time at least 7 days after the initial measurement. All measurements were obtained with the reader blinded to the initial 2D data. Statistical Analysis Data management and statistical analysis tasks were performed using software (Minitab, Version 11, Minitab, Inc, State College, Pa) on a compatible personal computer (IBM). Data are presented as mean ⫾ SD. Within-group differences between variables at rest and at peak exercise were assessed using a 2-tailed, paired Student t test. Differences were considered significant if the null hypothesis could be rejected at P ⬍ .05.
RESULTS
Figure 1 Two-dimensional parasternal short-axis image at level of papillary muscle at end-diastole (A) and accompanying line diagram (B) demonstrating measurement of diastole (D).
diastolic volume of 97 ⫾ 28 mL, and a LV EF of 67 ⫾ 4%. End-systolic twist was 10 ⫾ 5 degrees. Stress Participants exercised for an average of 14 ⫾ 4 minutes, all stopping secondary to exhaustion. No patient had chest pain or electrocardiographic evidence of ischemia. All patients achieved a peak heart rate ⱖ 85% of maximally predicted for age with a mean peak heart rate of 178 ⫾ 11 bpm. End-systolic volume decreased and EF increased in predictable and uniform fashion (Figure 3). LV endsystolic twist increased 86%, from 10 ⫾ 5 to 18 ⫾ 6 degrees (P ⬍ .001) (Figure 4).
Baseline: Results are shown in Table 1.
Reproducibility
Under resting conditions, participants had an average end-systolic volume of 32 ⫾ 10 mL, an end-
For end-systolic and end-diastolic volume at rest the correlation coefficients were r ⫽ 0.99, and r ⫽ 0.98,
672 Tischler and Niggel
Journal of the American Society of Echocardiography June 2003
Figure 3 Plot of left ventricular ejection fraction at rest and immediately after peak exercise.
Figure 2 Two-dimensional parasternal short-axis image at level of papillary muscle at end-systole (A) and accompanying line diagram (B) demonstrating measurement of systole (S).
respectively. For end-systolic twist, the correlation coefficient was r ⫽ 0.96. DISCUSSION In this study, we apply a simple 2D echocardiographic method of measuring the rotational motion of the LV to examine dynamic changes in systolic LV twist during maximal exercise. Twist increased virtually uniformly by approximately 80% in these young, healthy individuals. Hansen et al9 have previously reported that LV torsion is influenced by changes in contractile state, independent of preload and afterload. They studied 7 human orthotopic cardiac allograft recipients with implanted intramyocardial markers. Inotropic stimulation with dobutamine resulted in an increase in the largest torsion angle from 15.8 ⫾ 7.7 degrees to 25.2 ⫾ 10.5 degrees (P ⬍ .001). The observed increase in the largest torsion angle was greater than that of such conventional load-dependent markers
Figure 4 Plot of left ventricular end-systolic twist at rest and immediately after peak exercise.
of LV systolic performance as stroke volume and EF. These results were confirmed and extended by Moon et al.10 Using similar methods, they confirmed that pressure and volume loading did not affect LV systolic twist. However, dobutamine augmented both systolic twist and early diastolic untwisting. Augmentation of early diastolic untwisting during inotropic stimulation had been previously reported in open-chest dogs.12 In this canine model, systolic twist was again found to increase at higher levels of inotropic stimulation. Although we did not specifically measure diastolic variables, it is attractive to hypothesize that the observed increase in twist may play an important role in facilitating LV diastolic filling during maximal exercise. In patients with systolic LV dysfunction, measurement of resting LV volumes and EF have yielded disappointing results with regard to predicting exercise capacity.18-19 In contrast, chamber geometry does correlate with exercise duration in these patients both at rest20 and during exercise.21 This is not entirely surprising in that conventional measurement of EF is determined from the degree of circumferential myofibril shortening independent of more longitudinal and obliquely oriented myofibrils. In an
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Tischler and Niggel 673
Table 1 Heart rate and echocardiographic responses to exercise Age (y)
38 36 27 25 35 38 28 39 30 25 30 45 34 58 49 51 21 24 34 41 30 30 36 38 47
Sex
Exercise time (min)
Peak HR
% of max HR
ESV1
ESV2
EDV1
EDV2
SV1
SV2
LVEF1
LVEF2
Twist1
Twist2
F F M F M F M M F F M F F F M F M M F M M M M M M
11:21 10:30 15:00 16:20 21:15 17:00 13:00 15:00 19:00 10:14 14:13 14:00 10:03 7:05 10:30 9:31 10:55 13:00 12:00 11:00 15:00 19:00 19:07 18:15 15:00
158 184 168 170 165 155 182 169 188 186 179 176 179 176 166 159 183 187 192 189 193 178 191 193 175
87 100 87 87 85 85 95 93 99 95 94 95 100 107 97 89 92 95 103 106 102 92 104 106 101
18.6 22.6 31.9 16.1 27.2 33.6 16.7 28.1 29.6 32.5 40.6 24.0 34.8 40.9 32.0 24.2 40.6 39.9 48.3 32.9 25.2 27.1 42.7 50.5 47.9
15.0 7.3 21.2 14.1 15.9 15.7 10.4 16.3 25.3 28.3 26.6 23.9 27.9 14.5 11.2 10.5 16.6 21.2 34.2 15.9 26.9 10.2 10.4 36.7 40.6
56.4 83.6 74.3 57.6 75.6 93.3 52.2 85.1 72.1 85.5 131.1 74.3 94.3 133.0 112.6 88.0 105.6 110.8 138.3 96.8 88.6 86.2 141.6 132.4 145.7
57.6 66.7 73.3 56.4 69.0 74.9 49.3 74.3 76.7 104.7 171.8 115.2 131.3 125.3 129.6 79.4 57.5 102.2 100.0 86.1 119.3 58.3 83.8 137.7 131.1
37.8 61.0 42.3 41.5 48.4 59.7 35.5 57.0 42.5 53.0 90.5 50.3 59.5 92.1 80.6 63.8 65.0 70.9 90.0 63.9 63.4 59.1 98.9 81.9 97.8
42.7 59.3 52.0 42.3 53.1 59.1 39.0 57.9 51.4 76.4 145.2 91.3 103.4 110.8 118.4 68.9 40.9 81.0 65.8 70.2 92.4 48.1 73.4 101.0 90.5
0.67 0.73 0.57 0.72 0.64 0.64 0.68 0.67 0.59 0.62 0.69 0.68 0.63 0.69 0.72 0.73 0.62 0.64 0.65 0.66 0.72 0.69 0.70 0.62 0.67
0.74 0.89 0.71 0.75 0.77 0.79 0.79 0.78 0.67 0.73 0.85 0.79 0.79 0.88 0.91 0.87 0.71 0.79 0.66 0.82 0.77 0.83 0.88 0.73 0.69
15 3 9 6 12 0 6 5 3 9 11 17 6 18 9 7 15 14 20 8 6 13 11 15 6
24 10 12 12 26 7 18 9 10 19 18 26 17 22 17 16 28 26 29 16 17 19 21 23 12
EDV, End-diastolic volume; ESV, end-systolic volume; F, female; HR, heart rate; LVEF, left ventricular ejection fraction; M, male; Max, maximum; SV, stroke volume.
open-chest dog model of pacing, pacing tachycardia results in reductions in both systolic twist and diastolic untwisting rates.15 Thus, in this animal model of heart failure, determinants of suction at the level of the LV were impaired. It is possible that analogous abnormalities are present in the failing human heart. However, it is necessary to characterize the normal response as a prelude to human investigation. The current study suggests that an approximate 80% increase in twist can be expected with maximal exercise in healthy patients. The incremental clinical use of measuring systolic twist remains to be defined. Hansen et al6 has demonstrated that systolic twist is attenuated during episodes of acute rejection in cardiac allograft recipients and that this occurs in the absence of significant changes in LV EF. Measurement of twist might also provide useful incremental information in assessing responses to pharmacologic interventions in patients with dilated cardiomyopathy and in identifying subclinical LV dysfunction in patients who are asymptomatic with chronic, severe mitral regurgitation. This method relies on estimation of the LV cavity center. This, it may not be as applicable in patients with asymmetric ventricular cavities. Although torsion may prove to be more accurately measured using magnetic resonance imaging or
implanted tags, the ability to assess it with conventional ultrasound equipment and yield highly reproducible results further enhances its potential clinical applications. These same features make it well suited for serial examinations.
REFERENCES 1. Harvey W. Exercitatis anatomica de Motu Cordis et Sanguinis in Animalibus. Chaper 5. Frankfurt: 1628. 2. Waldman LK, Nosan D, Villarrea F, Covell JW. Relationship between transmural deformation and local myofiber direction in canine left ventricle. Circ Res 1988;63:550-62. 3. Yun KL, Miller DC. Torsional deformation of the left ventricle. J Heart Valve Dis 1995;4:S214-22. 4. 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: 221-37. 5. Ingels NB, Daughters GT, Stinson EB, Alderman EL. Measurements of midwall dynamics in intact man by radiography of surgically implanted markers. Circulation 1975;52:859-67. 6. Hansen DE, Daughters GT II, Alderman EL, Stinson EB, Baldwin JC, Miller DC. Effect of human cardiac allograft rejection on left ventricular systolic torsion and diastolic recoil measured by intramyocardial markers. Circulation 1987;76: 998-1008.
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7. Hansen DE, Daughters GT, Alderman EL, Ingels NB, Miller DC. Torsional deformation of the left ventricular midwall in human hearts with intramyocardial markers: regional heterogeneity and sensitivity to the inotropic effects of abrupt rate changes. Circ Res 1988;62:941-52. 8. Ingels NB Jr, Hansen DE, Daughters GT II, Stinson EB, Alderman EL, Miller DC. Relation between longitudinal, circumferential and oblique shortening and torsion deformation in the left ventricle of the transplanted human heart. Circ Res 1989;64:915-27. 9. Hansen DE, Daughters GT II, Alderman EL, Ingels NB, Stinson EB, Miller DC. Effect of volume loading, pressure loading, and inotropic stimulation on left ventricular torsion in humans. Circulation 1991;83:1315-26. 10. Moon MR, Ingels NB Jr, Daughters GT II, Stinson EB, Hansen DE, Miller DC. Alterations in left ventricular twist mechanics with inotropic stimulation and volume loading in human subjects. Circulation 1994;89:142-50. 11. Buchalter MB, Weiss J-L, Rogers WJ, Zerhouni EA, Weisfeldt ML, Beyar R, et al. Noninvasive quantification of left ventricular rotational deformation in normal humans using magnetic resonance imaging myocardial tagging. Circulation 1990;81: 1236-44. 12. Rademakers FE, Buchalter MB, Rogers WJ, Zerhouni EA, Weisfeldt ML, Weiss IL, et al. Dissociation between left ventricular untwisting and filling: accentuation by catecholamines. Circulation 1992;85:1572-81. 13. Mirro MJ, Rogers EW, Weyman AE, Feigenbaum H. Angular displacement of the papillary muscles during the cardiac cycle. Circulation 1979;60:327-33.
Journal of the American Society of Echocardiography June 2003
14. Rothfeld JM, LeWinter MM, Tischler MD. Left ventricular systolic torsion and early diastolic filling by echocardiography in normal humans. Am J Cardiol 1998;81:1465-9. 15. Kroeker CA, Tyberg JV, Beyar R. Effects of load manipulations, heart rate, and contractility on left ventricular apical rotation: an experimental study in anesthetized dogs. Circulation 1995;92:130-41. 16. Helak J, Reichek N. Quantification of human left ventricular mass and volume by 2-dimensional echocardiography: in vivo anatomic validation. Circulation 1981;63:1398-407. 17. St John Sutton M, Plappert T, Spiegel A, Raichlen J, Douglas P, Reichek N, et al. Early postoperative changes in left ventricular chamber size, architecture, and function in aortic stenosis and aortic regurgitation and their relation to intraoperative changes in afterload: a prospective 2-dimensional echocardiographic study. Circulation 1987;76:77-89. 18. Franciosa JA, Park M, Levine TGB. Lack of correlation between exercise capacity and indexes of resting left ventricular performance in heart failure. Am J Cardiol 1981;48:33-9. 19. Meiler SE, Ashton JJ, Moeschberger ML, Unverferth DV, Leier CV. An analysis of the determinants of exercise capacity in congestive heart failure. Am Heart J 1987;113:120717. 20. Lamas GA, Vaughn DE, Parisi AF, Pfeifer MA. Effects of left ventricular shape and captopril therapy on exercise capacity after acute anterior myocardial infarction. Am J Cardiol 1989; 63:1167-73. 21. Tischler M, Niggel J, Borowski D, LeWinter M. Relation between left ventricular shape and exercise capacity in patients with left ventricular sysfunction. J Am Coll Cardiol 1993;22: 751-7.
This study examines the use of a novel 2-dimensional echocardiographic technique to measure left ventricular (LV) systolic torsion or twist in normal human hearts during maximal exercise. The effects of dynamic exercise on LV twist have not previously been determined. LV twist was measured in 25 healthy human control patients before and after maximal treadmill exercise. LV end-systolic volume
First described in the 17th century by Sir William 1
Harvey, left ventricular (LV) torsion, or twist, refers to the counterclockwise rotation of the ventricular apex with respect to its base during systole, with untwisting occurring during isovolumic relaxation and filling. This phenomenon, ascribed to asymmetric shortening of the internal and external layers of spiral muscles in the ventricular wall, has been postulated to result in the storage of potential energy, for which conversion to kinetic energy may contribute to ventricular suction and early diastolic filling.2,3 Several techniques have been used to describe and quantify ventricular torsion in human beings including cineangiography of radio-opaque markers,4-10 magnetic resonance imaging,11,12 and 2-dimensional (2D) echocardiography.13 Cineangiography of radio-opaque markers requires implantation at the time of cardiac operation, limiting the population available for study of twist to patients with significant cardiac disease. Magnetic resonance imaging using myocardial tagging remains expensive and its use is limited to basal conditions. Recently, we described a novel, 2D echocardiographic technique to quantify LV twist that correlates well with indices of early ventricular filling.14 The technique uses spatial rotation of the base of the anterolateral papillary muscle as a surrogate for more direct measurements. Although the effects of pharmacologic volume loading, pressure loading, and inotropic stimulation on ventricular torsion have been examined in both From the Cardiology Unit, Fletcher Allen Health Care (M. T.) and University of Vermont College of Medicine. Reprint requests: Marc Tischler, MD, Cardiology Unit, McClure 1, Fletcher Allen Health Care, Burlington, VT 05401 (E-mail: [email protected]). Copyright 2003 by the American Society of Echocardiography. 0894-7317/2003/$30.00 ⫹ 0 doi:10.1016/S0894-7317(03)00225-6
670
decreased and LV ejection fraction increased in a predictable manner. Systolic twist increased by 8.4 ⴞ 2.8 degrees (86%). Twist is believed to store potential energy and to play an important role in generating diastolic suction. The increase in twist observed may play an important role in facilitating LV diastolic filling during maximal exercise. (J Am Soc Echocardiogr 2003;16:670-4.)
canines and human beings9,10,12,15 the effect of dynamic exercise on twist is unknown. During exercise in dogs and human beings, the early diastolic portion of the ventricular pressure-volume relation shifts downward, an observation consistent with increased suction as a mechanism of filling. Thus, suction may be important in preventing diastolic pressure from increasing during exercise despite an increased volume and rate of ventricular filling. Correspondingly, increased inotropic stimulation and reduced end-systolic volume, both of which occur during exercise, are known to increase twist. In this study, we used our echocardiographic method14 to test the hypothesis that twist increases during dynamic exercise in healthy human beings.
METHODS Patient Selection The study group included 25 participants (14 men and 11 women; mean age 35.6 years, range: 21 to 58) with normal resting LV systolic function and no detectable structural heart disease by echocardiography. Of these patients, 10 were referred for stress echocardiography to assess palpitations and 15 were healthy volunteers. Exclusion criteria included LV hypertrophy or dilation, valvular stenosis, valvular regurgitation beyond a trivial degree, a known history of heart disease, an abnormal baseline electrocardiogram, an inadequate stress test (defined as a maximal heart rate response ⬍85% of the maximally predicted heart rate), electrocardiographic or echocardiographic evidence of ischemia, and echocardiographic images that were technically inadequate for this analysis. Echocardiography Two-dimensional echocardiographic examinations were performed at rest with the patient supine in the left lateral decubitus position; a phased-array ultrasonoscope device
Journal of the American Society of Echocardiography Volume 16 Number 6
Tischler and Niggel 671
(Acuson Sequoia, Mountain View, Calif) with a 3.5-MHz transducer was used. Images were obtained in sequential fashion from the parasternal long- and short-axis, and apical 4- and 2-chamber views. Each patient then underwent a symptom-limited treadmill exercise stress test using a standard Bruce protocol. Immediately after exercise, the patient was returned to the left lateral decubitus position and 2D imaging was repeated. Image acquisition was completed within 60 seconds. Data Analysis Conventional 2D echocardiographic data and twist measurements were analyzed at separate times. All tapes were reviewed in nonconsecutive fashion to minimize potential recording bias. Using a workstation (Image-Vue, Nova Microsonics Inc, Mahwah, NJ), 3 cardiac cycles from each baseline and postexercise recording were digitized from end-diastole (R-wave peak) to end-systole (smallest cavity area). End-systolic volume, end-diastolic volume, stroke volume, and ejection fraction (EF) were calculated using the 5/6 area-length bullet method.16-17 Ventricular twist was measured at rest and after exercise as previously described.14 Briefly, at end-diastole, a line was drawn from the apex of the scanning sector through a point at the center of the ventricular cavity (the midpoint of the chord connecting the anterior and posterior endocardial surfaces). A second line was drawn from the midpoint of the base of the anterolateral papillary muscle, where it inserts into the myocardium through the center of the ventricular cavity. The angle inscribed by these 2 intersecting lines was considered angle diastole (Figure 1). These steps were repeated for end-systole, yielding systole (Figure 2). The absolute difference in degrees between angles systole and diastole is the twist angle. By convention, rotation in the counterclockwise direction as viewed from the apex is denoted as a positive sign and rotation in the clockwise direction as a negative sign. To assess measurement reproducibility in the assessment of ventricular volumes and twist, 10 studies were reanalyzed at a temporarily remote time at least 7 days after the initial measurement. All measurements were obtained with the reader blinded to the initial 2D data. Statistical Analysis Data management and statistical analysis tasks were performed using software (Minitab, Version 11, Minitab, Inc, State College, Pa) on a compatible personal computer (IBM). Data are presented as mean ⫾ SD. Within-group differences between variables at rest and at peak exercise were assessed using a 2-tailed, paired Student t test. Differences were considered significant if the null hypothesis could be rejected at P ⬍ .05.
RESULTS
Figure 1 Two-dimensional parasternal short-axis image at level of papillary muscle at end-diastole (A) and accompanying line diagram (B) demonstrating measurement of diastole (D).
diastolic volume of 97 ⫾ 28 mL, and a LV EF of 67 ⫾ 4%. End-systolic twist was 10 ⫾ 5 degrees. Stress Participants exercised for an average of 14 ⫾ 4 minutes, all stopping secondary to exhaustion. No patient had chest pain or electrocardiographic evidence of ischemia. All patients achieved a peak heart rate ⱖ 85% of maximally predicted for age with a mean peak heart rate of 178 ⫾ 11 bpm. End-systolic volume decreased and EF increased in predictable and uniform fashion (Figure 3). LV endsystolic twist increased 86%, from 10 ⫾ 5 to 18 ⫾ 6 degrees (P ⬍ .001) (Figure 4).
Baseline: Results are shown in Table 1.
Reproducibility
Under resting conditions, participants had an average end-systolic volume of 32 ⫾ 10 mL, an end-
For end-systolic and end-diastolic volume at rest the correlation coefficients were r ⫽ 0.99, and r ⫽ 0.98,
672 Tischler and Niggel
Journal of the American Society of Echocardiography June 2003
Figure 3 Plot of left ventricular ejection fraction at rest and immediately after peak exercise.
Figure 2 Two-dimensional parasternal short-axis image at level of papillary muscle at end-systole (A) and accompanying line diagram (B) demonstrating measurement of systole (S).
respectively. For end-systolic twist, the correlation coefficient was r ⫽ 0.96. DISCUSSION In this study, we apply a simple 2D echocardiographic method of measuring the rotational motion of the LV to examine dynamic changes in systolic LV twist during maximal exercise. Twist increased virtually uniformly by approximately 80% in these young, healthy individuals. Hansen et al9 have previously reported that LV torsion is influenced by changes in contractile state, independent of preload and afterload. They studied 7 human orthotopic cardiac allograft recipients with implanted intramyocardial markers. Inotropic stimulation with dobutamine resulted in an increase in the largest torsion angle from 15.8 ⫾ 7.7 degrees to 25.2 ⫾ 10.5 degrees (P ⬍ .001). The observed increase in the largest torsion angle was greater than that of such conventional load-dependent markers
Figure 4 Plot of left ventricular end-systolic twist at rest and immediately after peak exercise.
of LV systolic performance as stroke volume and EF. These results were confirmed and extended by Moon et al.10 Using similar methods, they confirmed that pressure and volume loading did not affect LV systolic twist. However, dobutamine augmented both systolic twist and early diastolic untwisting. Augmentation of early diastolic untwisting during inotropic stimulation had been previously reported in open-chest dogs.12 In this canine model, systolic twist was again found to increase at higher levels of inotropic stimulation. Although we did not specifically measure diastolic variables, it is attractive to hypothesize that the observed increase in twist may play an important role in facilitating LV diastolic filling during maximal exercise. In patients with systolic LV dysfunction, measurement of resting LV volumes and EF have yielded disappointing results with regard to predicting exercise capacity.18-19 In contrast, chamber geometry does correlate with exercise duration in these patients both at rest20 and during exercise.21 This is not entirely surprising in that conventional measurement of EF is determined from the degree of circumferential myofibril shortening independent of more longitudinal and obliquely oriented myofibrils. In an
Journal of the American Society of Echocardiography Volume 16 Number 6
Tischler and Niggel 673
Table 1 Heart rate and echocardiographic responses to exercise Age (y)
38 36 27 25 35 38 28 39 30 25 30 45 34 58 49 51 21 24 34 41 30 30 36 38 47
Sex
Exercise time (min)
Peak HR
% of max HR
ESV1
ESV2
EDV1
EDV2
SV1
SV2
LVEF1
LVEF2
Twist1
Twist2
F F M F M F M M F F M F F F M F M M F M M M M M M
11:21 10:30 15:00 16:20 21:15 17:00 13:00 15:00 19:00 10:14 14:13 14:00 10:03 7:05 10:30 9:31 10:55 13:00 12:00 11:00 15:00 19:00 19:07 18:15 15:00
158 184 168 170 165 155 182 169 188 186 179 176 179 176 166 159 183 187 192 189 193 178 191 193 175
87 100 87 87 85 85 95 93 99 95 94 95 100 107 97 89 92 95 103 106 102 92 104 106 101
18.6 22.6 31.9 16.1 27.2 33.6 16.7 28.1 29.6 32.5 40.6 24.0 34.8 40.9 32.0 24.2 40.6 39.9 48.3 32.9 25.2 27.1 42.7 50.5 47.9
15.0 7.3 21.2 14.1 15.9 15.7 10.4 16.3 25.3 28.3 26.6 23.9 27.9 14.5 11.2 10.5 16.6 21.2 34.2 15.9 26.9 10.2 10.4 36.7 40.6
56.4 83.6 74.3 57.6 75.6 93.3 52.2 85.1 72.1 85.5 131.1 74.3 94.3 133.0 112.6 88.0 105.6 110.8 138.3 96.8 88.6 86.2 141.6 132.4 145.7
57.6 66.7 73.3 56.4 69.0 74.9 49.3 74.3 76.7 104.7 171.8 115.2 131.3 125.3 129.6 79.4 57.5 102.2 100.0 86.1 119.3 58.3 83.8 137.7 131.1
37.8 61.0 42.3 41.5 48.4 59.7 35.5 57.0 42.5 53.0 90.5 50.3 59.5 92.1 80.6 63.8 65.0 70.9 90.0 63.9 63.4 59.1 98.9 81.9 97.8
42.7 59.3 52.0 42.3 53.1 59.1 39.0 57.9 51.4 76.4 145.2 91.3 103.4 110.8 118.4 68.9 40.9 81.0 65.8 70.2 92.4 48.1 73.4 101.0 90.5
0.67 0.73 0.57 0.72 0.64 0.64 0.68 0.67 0.59 0.62 0.69 0.68 0.63 0.69 0.72 0.73 0.62 0.64 0.65 0.66 0.72 0.69 0.70 0.62 0.67
0.74 0.89 0.71 0.75 0.77 0.79 0.79 0.78 0.67 0.73 0.85 0.79 0.79 0.88 0.91 0.87 0.71 0.79 0.66 0.82 0.77 0.83 0.88 0.73 0.69
15 3 9 6 12 0 6 5 3 9 11 17 6 18 9 7 15 14 20 8 6 13 11 15 6
24 10 12 12 26 7 18 9 10 19 18 26 17 22 17 16 28 26 29 16 17 19 21 23 12
EDV, End-diastolic volume; ESV, end-systolic volume; F, female; HR, heart rate; LVEF, left ventricular ejection fraction; M, male; Max, maximum; SV, stroke volume.
open-chest dog model of pacing, pacing tachycardia results in reductions in both systolic twist and diastolic untwisting rates.15 Thus, in this animal model of heart failure, determinants of suction at the level of the LV were impaired. It is possible that analogous abnormalities are present in the failing human heart. However, it is necessary to characterize the normal response as a prelude to human investigation. The current study suggests that an approximate 80% increase in twist can be expected with maximal exercise in healthy patients. The incremental clinical use of measuring systolic twist remains to be defined. Hansen et al6 has demonstrated that systolic twist is attenuated during episodes of acute rejection in cardiac allograft recipients and that this occurs in the absence of significant changes in LV EF. Measurement of twist might also provide useful incremental information in assessing responses to pharmacologic interventions in patients with dilated cardiomyopathy and in identifying subclinical LV dysfunction in patients who are asymptomatic with chronic, severe mitral regurgitation. This method relies on estimation of the LV cavity center. This, it may not be as applicable in patients with asymmetric ventricular cavities. Although torsion may prove to be more accurately measured using magnetic resonance imaging or
implanted tags, the ability to assess it with conventional ultrasound equipment and yield highly reproducible results further enhances its potential clinical applications. These same features make it well suited for serial examinations.
REFERENCES 1. Harvey W. Exercitatis anatomica de Motu Cordis et Sanguinis in Animalibus. Chaper 5. Frankfurt: 1628. 2. Waldman LK, Nosan D, Villarrea F, Covell JW. Relationship between transmural deformation and local myofiber direction in canine left ventricle. Circ Res 1988;63:550-62. 3. Yun KL, Miller DC. Torsional deformation of the left ventricle. J Heart Valve Dis 1995;4:S214-22. 4. 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: 221-37. 5. Ingels NB, Daughters GT, Stinson EB, Alderman EL. Measurements of midwall dynamics in intact man by radiography of surgically implanted markers. Circulation 1975;52:859-67. 6. Hansen DE, Daughters GT II, Alderman EL, Stinson EB, Baldwin JC, Miller DC. Effect of human cardiac allograft rejection on left ventricular systolic torsion and diastolic recoil measured by intramyocardial markers. Circulation 1987;76: 998-1008.
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7. Hansen DE, Daughters GT, Alderman EL, Ingels NB, Miller DC. Torsional deformation of the left ventricular midwall in human hearts with intramyocardial markers: regional heterogeneity and sensitivity to the inotropic effects of abrupt rate changes. Circ Res 1988;62:941-52. 8. Ingels NB Jr, Hansen DE, Daughters GT II, Stinson EB, Alderman EL, Miller DC. Relation between longitudinal, circumferential and oblique shortening and torsion deformation in the left ventricle of the transplanted human heart. Circ Res 1989;64:915-27. 9. Hansen DE, Daughters GT II, Alderman EL, Ingels NB, Stinson EB, Miller DC. Effect of volume loading, pressure loading, and inotropic stimulation on left ventricular torsion in humans. Circulation 1991;83:1315-26. 10. Moon MR, Ingels NB Jr, Daughters GT II, Stinson EB, Hansen DE, Miller DC. Alterations in left ventricular twist mechanics with inotropic stimulation and volume loading in human subjects. Circulation 1994;89:142-50. 11. Buchalter MB, Weiss J-L, Rogers WJ, Zerhouni EA, Weisfeldt ML, Beyar R, et al. Noninvasive quantification of left ventricular rotational deformation in normal humans using magnetic resonance imaging myocardial tagging. Circulation 1990;81: 1236-44. 12. Rademakers FE, Buchalter MB, Rogers WJ, Zerhouni EA, Weisfeldt ML, Weiss IL, et al. Dissociation between left ventricular untwisting and filling: accentuation by catecholamines. Circulation 1992;85:1572-81. 13. Mirro MJ, Rogers EW, Weyman AE, Feigenbaum H. Angular displacement of the papillary muscles during the cardiac cycle. Circulation 1979;60:327-33.
Journal of the American Society of Echocardiography June 2003
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