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J Thorac Cardiovasc Surg 2002;124:43-49
© 2002 The American Association for Thoracic Surgery
Cardiopulmonary Support and Physiology (CSP) |
From the Department of Cardiovascular and Thoracic Surgery,a Division of Cardiovascular Medicine,b Stanford University School of Medicine, Stanford, Calif, and the Laboratory of Cardiovascular Physiology and Biophysics,c Research Institute of the Palo Alto Medical Foundation, Palo Alto, Calif.
Supported by grants HL-29589 and HL-67025 from the National Heart, Lung, and Blood Institute. Drs Tibayan, Lai, Timek, and Dagum are Carl and Leah McConnell Cardiovascular Surgical Research Fellows. Dr Timek is a recipient of the Thoracic Surgery Foundation Research Fellowship. Drs. Timek, Dagum, and Tibayan were supported by NHLBI Individual Research Service Awards HL-10452, HL-09569, and HL-67563, respectively. Dr Lai was supported by a fellowship from the American Heart Association, Western States Affiliate.
Received for publication Aug 8, 2001. Revisions requested Sept 17, 2001; revisions received Oct 12, 2001. Accepted for publication Oct 24, 2001. Address for reprints: D. Craig Miller, MD, Department of Cardiovascular Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247 (E-mail: dcm{at}leland.stanford.edu).
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Abstract |
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Introduction |
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1,2 results in torsion, a wringing motion as the apex rotates with respect to the base about the left ventricular (LV) long axis. 3,4 Torsion is thought to play an important role in decreasing gradients of LV transmural fiber strain and oxygen demand during systole, 5,6 and torsion recoil during diastole has been hypothesized to aid ventricular filling. 7 Dilated cardiomyopathy is associated with LV remodeling (dilatation, wall thinning, and, possibly, reduction in fiber angles) that may alter torsion and its beneficial effects. Surgical approaches for patients with dilated cardiomyopathy, ischemic cardiomyopathy, or both, such as the surgical anterior ventricular endocardial restoration procedure, may improve LV systolic function by restoring normal ventricular shape, fiber angle, and torsional mechanics 8,9; however, the effects of cardiomyopathy on LV torsion dynamics have not been characterized.
Tachycardia-induced cardiomyopathy (TIC), a model of dilated cardiomyopathy, is accompanied by ventricular remodeling, systolic and diastolic dysfunction, 10 and neurohumoral changes 11 similar to the clinical entity. We hypothesized that such changes would result in alterations of systolic and diastolic LV torsion dynamics and tested this hypothesis by measuring the 3-dimensional (3-D) dynamics of implanted radiopaque LV markers in sheep before and after the development of TIC.
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Methods |
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12 and will only be summarized briefly. Eight tantalum helices were inserted in the LV epicardial layer at 2 LV levels along 4 equally spaced longitudinal meridians (nos. 2, 3, 5, 6, 9, 10, 12, and 13; Figure 1), with one marker placed at the LV apex (no. 1) and subendocardial markers 26, 28, and 30 paired opposite subepicardial markers 3, 10, and 13, respectively. On cardiopulmonary bypass, 8 markers (nos. 15-22) were sutured around the circumference of the mitral anulus. A micromanometer pressure transducer was placed in the LV chamber through the apex. A monopolar pacing lead was sewn onto the anterior LV wall.
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Rapid-pacing protocol
After baseline data acquisition, a rapid-pacing pulse generator (Prodigy S 8164; Medtronic Inc, Minneapolis, Minn) was inserted subcutaneously and connected to the monopolar LV electrode. Rapid pacing was initiated 24 hours later. During the pacing period, transthoracic echocardiography was performed every 2 to 3 days to assess LV dimensions and systolic LV performance (with the pacer temporarily off). Pacing was continued until development of TIC, as evidenced by development of peripheral edema, ascites, and/or increase in end-systolic LV dimension. The first 2 animals were paced at a rate of 180 min-1, and subsequent animals were paced at 230 min-1, which resulted in faster development of heart failure. The average pacing period was 15 ± 6 days. Then the animals were returned to the catheterization laboratory, with the pacer turned off immediately before data acquisition. Hemodynamic, marker, and echocardiographic data were again acquired, as described above.
All animals received humane care in compliance with the "Principles of Laboratory Animal Care" formulated by the National Society for Medical Research and the "Guide for Care and Use of Laboratory Animals" prepared by the National Academy of Sciences and published by the National Institutes of Health (DHEW NIHG publication no. 85-23, revised 1985). This study was approved by the Stanford Medical Center Laboratory Research Animal Review Committee and conducted according to Stanford University policy.
Data analysis and computation of LV torsion
Values computed from 3 consecutive steady-state beats during normal sinus rhythm before and after TIC were averaged and labeled as "control" and "TIC" data for each animal. Instantaneous LV volume (LLV) was calculated from the epicardial LV markers by using a space-filling multiple tetrahedral volume method every 16.7 ms. 13 End-diastole (ED) was defined as the time of the peak of the electrocardiographic R-wave, end-ejection as the time of minimum LVV, and end-systole (ES) as the time of peak negative rate of LV pressure decrease (-dP/dt). Stroke volume (SV) was calculated as the difference between end-diastolic volume (EDV) and minimum LVV (LVVmin; SV = EDV - LVVmin).
At each sample time, all marker Cartesian 3-D coordinates (x, y, and z) were transformed into a moving internal cylindrical coordinate system (r, 
, and z) with the origin at the centroid of the annular markers (markers 15-22, Figure 1
), the z-axis passing through the centroid of the markers defining the apical transverse LV plane (markers 2, 5, 9, 12), the 0° reference passing through the anterior commissure (marker 16), and positive angles defined as counterclockwise when looking from apex to base.
For each apical-level epicardial marker (nos. 2, 5, 9, and 12; Figure 1), the circumferential rotational angle () change relative to ED was computed throughout the cardiac cycle. In each frame torsion was defined as the average angular displacement of the apical markers on the free walls of the ventricle, and data from 3 consecutive steady-state beats were averaged. As viewed from the LV apex, with positive angles counterclockwise, during beat b (from EDb to EDb+1), the torsional deformation 
at each sample time t (=0@EDb, 1, 2, ..., t@EDb+1) of marker m subtending angle m(t) was computed as follows:
(1) m(t) = m(t) - m(EDb)
Mean free-wall LV torsional deformation (
b[t]) for beat b was then computed as follows:
(2) b(t) = [2(t) + 9(t) + 12(t)]/3
and mean free-wall LV torsional deformation for the 3-beat sequences comprising each run in each heart as follows:
(3) (t) = [1(t) + 2(t) + 3(t)]/3
Fractional ejection at each sample time (t) for each beat (b) was defined as follows:
(4)
FRACb(t) = [LVVEDVb - LVVb(t)]/(LVVEDVb - LVVEEb)
where LVVb(t) is LVV at time t, LVVEDVb is LVV at EDV, and LVVEEb is LVV at end-ejection for beat b. Mean fractional ejection at each sample time (t) for the 3-beat sequences comprising each run in each heart was as follows:
(5)
FRAC(t) = [FRAC1(t) + FRAC2(t) + FRAC3(t)]/3
Figure 2 illustrates mean free-wall torsional deformation (t) plotted against FRAC(t) for both control and TIC conditions in a representative animal. (t) was characterized by minimum free-wall LV torsional deformation during early systole (min), maximum free-wall LV torsional deformation, typically occurring near ES (max), and absolute value of change in free-wall torsional deformation from end ejection to the first 5% of LV filling (5%) to assess early diastolic torsional recoil. 7 Time of max relative to end ejection (TmaxEE), was also calculated.
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Results |
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, under control conditions, systole began with a small negative (ie, clockwise, as viewed from apex) torsional deformation. After this cocking twist, a relatively linear direct relationship between torsion and ejected volume was observed during the majority of systole until peaked just before end-ejection. Isovolumic relaxation (IVR) and early diastole (defined as the interval from end-ejection through the first 5% of ventricular filling) were characterized by abrupt torsional recoil (ie, a decrease in ), followed by more gradual untwisting during mid and late diastole. With dilated cardiomyopathy, the initial early systolic negative cocking torsion was larger and more sustained, and max was reduced, as well as delayed until after the time of end-ejection, such that was still increasing during IVR and early diastole.
Table 2 summarizes torsion dynamics before and after the development of cardiomyopathy. In the cardiomyopathic state, as compared with control conditions, early systolic clockwise (negative) torsion (min) increased significantly, max decreased significantly, and early diastolic recoil was abolished, as indicated by the change in sign of 5% from negative (clockwise) in control to positive (continued counterclockwise torsion) in TIC conditions. In control conditions max occurred 42 ± 30 ms before end-ejection; however, max was reached considerably after end-ejection (71 ± 72 ms) in the cardiomyopathic conditions.
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Discussion |
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min) was greater in amplitude in the cardiomyopathic state, maximal torsional deformation (max) was significantly reduced. It is thought that systolic torsion is a mechanism by which the ventricle equilibrates transmural gradients of fiber strain and oxygen demand. 5,6,14-16 Using computer models, others have demonstrated that LV systolic torsion may lower subendocardial oxygen demand 17 and increase subendocardial blood flow. 18 Thus when systolic LV torsion is reduced, as in cardiomyopathic hearts, the fiber-strain gradients and metabolic gradients across the LV wall would be expected to be larger, with greater subendocardial oxygen requirement. Indeed, animal models suggest that an imbalance of oxygen supply and demand plays a role in the pathophysiology of TIC, with the perfusion deficit being greatest in the subendocardial layers. 19,20 Decreased torsion may cause the ventricle to lose its ability to modulate these transmural metabolic gradients, thereby contributing to or exacerbating the imbalance of oxygen supply and demand. 21
In the present study max was not only reduced, but it was also delayed in the cardiomyopathic conditions compared with in the control state. Before pacing, max occurred slightly before or at the time of end-ejection, but with cardiomyopathy, max was delayed until after end-ejection. This suggests that not only is the ventricle less capable of equalizing transmural work and metabolic gradients but also that such equalization was not fully effective until after systolic force generation had peaked. Kroeker et al 22 reported that maximal torsional deformation was delayed into IVR in a canine model of acute LV ischemia and postulated that this might affect the release of restoring forces and thereby impair early filling of the ventricle.
The cardiomyopathic dilated hearts also had marked alterations in diastolic LV torsional dynamics. Studies of normal dogs 7,23 and human patients 24 indicate that the bulk of LV torsional recoil occurs during IVR. In the present study, during IVR and the first 5% of diastolic LV filling, a rapid untwisting or torsional recoil was seen during control conditions. With cardiomyopathy, this early diastolic recoil was lost, and torsion actually continued to increase slightly during this period. Early diastolic recoil represents rapid release of LV-restoring forces (potential energy) stored in the extracellular matrix and contractile elements during systole. 25,26 In turn, early diastolic recoil might play a role in the genesis of LV suction and enhance LV early diastolic filling. 7,22 Stuber and coworkers 24,27 suggested that delayed untwisting in patients with aortic stenosis and coronary artery disease could contribute to diastolic LV dysfunction. In a canine model of pacing-induced tachycardia, Bell and colleagues 23 recently reported a decrease in the rate of torsional recoil, which corresponded to a loss of the determinants of LV diastolic suction. Therefore the loss of early diastolic recoil with cardiomyopathy, as observed in the present study, could theoretically adversely affect LV filling and diastolic suction.
In addition to alterations in torsion dynamics, rapid pacing caused significant hemodynamic changes. Cardiomyopathy was evidenced by peripheral edema, ascites, lethargy, ventricular dilatation, increased LV end-diastolic pressure, and reduced preload recruitable stroke work, a load-independent measure of contractility. Contractility has a direct effect on torsion independent of loading conditions. 28,29 Therefore decreased contractility might contribute to a reduction of max in TIC because it is the shortening of the myofibers that drives the torsional deformation. Dilatation may play a part in the alterations in torsion by equalizing the lengths of the opposing lever arms that give rise to torsion (vide infra). Although other investigators of TIC have noted decreased maximum LV pressure and dP/dt, these load-dependent measures were unchanged in the present study. Because the degree of cardiomyopathy in TIC is related to the intensity and length of pacing, 30 such differences may be accounted for by a faster rate, 31,32 a longer period of pacing, 10,32 or species differences.
The mechanisms underlying the changes in torsion dynamics are unknown but probably encompass many factors, including remodeling of the cardiomyocytes and connective tissue matrix, slowed transmural fiber activation, and alterations in excitation-contraction coupling. First, LV dilatation accompanies TIC, as observed in this study and reported by others. 31,33 To see how this might affect torsion, consider that, at a given instant, the net moment giving rise to torsion can be thought of as a sum (resultant) of the opposing circumferential moments (vectors) of the LV subendocardium and the subepicardium. Ingels and coworkers 34 proposed several factors that influence the magnitude and direction of these vectors: fiber orientation, number of fibers, and lengths of the lever arms of the respective layers. Thus although the angles of inclination of the subendocardial and subepicardial fibers are roughly equal (but opposite in sign), physiologic torsion during systole is dominated by the subepicardial fibers caused by their larger radii. Both ventricular dilatation and wall thinning tend to equalize the radii of the subendocardial and subepicardial layers, thus allowing a relatively greater contribution from the subendocardium to the net torsion moment. In a model examining the effects of ventricular geometry on torsion, Taber et al 14 predicted such a result by reasoning that in eccentric hypertrophy the epicardial fibers would lose some of their mechanical advantage. This is consistent with the findings of larger initial clockwise torsion in very early systole, as well as the decrease in max observed with cardiomyopathy. In addition, fiber-angle remodeling, which was not measured in this study, could also contribute to the torsion changes we observed. An alternative hypothesis is suggested by the anatomic studies of Torrent-Guasp and colleagues, 35 who found that ventricular muscle can be unwrapped into basal and apical loops. If the sequence of activation of muscle proceeds linearly along this band, the delayed max and loss of recoil during IVR may be explained by slowed activation of the apical loop. Further studies of the electrical activation of this band, however, must be done to support this theory. The present interpretation is consistent with findings that demonstrate an endocardial to epicardial activation wave. 36-38
Second, transmural fiber activation is slowed during LV ischemia and TIC conditions, a finding attributed to fibrosis and remodeling of gap junctions in models of heart failure. 37,39,40 Slowed transmural conduction would leave the subendocardial fibers unopposed relative to subepicardial fibers for a longer period of time in early systole, allowing for a larger and longer initial clockwise twist, as seen in cardiomyopathic hearts in this study. The increase in min might contribute to a decrease in max because the positive torsional deformation attributed to the subepicardium must begin at a lower baseline after the delay. Delayed subepicardial activation caused by slowed transmural conduction, as reported by Delhass and coworkers, 37 might slightly prolong systolic contraction and contribute to the delay in the timing of max.
A third factor possibly contributing to the observed changes in torsion mechanics are the alterations in myocyte action potentials and intracellular calcium regulation associated with heart failure. TIC causes decreased amplitude and increased duration of the action potential. 41 TIC has also been linked to reduction in Ca2+ transients, 42 maximal Ca2+-activated tension, and peak force generation. 43 Such decreased tension generation might reduce all torsional moments and contribute to the decrease in max in cardiomyopathic hearts. Similarly, pacing-induced cardiomyopathy results in prolongation of both the Ca2+ transient and isometric contraction. 43,44 As in the case of delayed epicardial activation, these changes might prolong systolic contraction, leading to the delay in reaching max and loss of early diastolic recoil.
Extracellular changes associated with TIC may also help explain the derangements in torsional dynamics. Loss of the orderly collagen latticework 45 has been linked to reduced force generation in TIC. Spinale and coworkers 30 found that activation of matrix metalloproteinases and degradation of the fibrillar collagen matrix is an early event in TIC. Such matrix degradation could lead to ventricular dilatation and loss of coordinated myocyte contractile performance. In addition, because the extracellular matrix stores potential energy that is thought to be released during early diastole, 25 its degradation and disarray may contribute to the loss of diastolic torsional recoil.
The present findings indicate that dilated cardiomyopathy induced by rapid pacing significantly perturbs normal systolic and diastolic LV torsional mechanics. We speculate that decreased torsion may play a role in the pathophysiology of TIC as part of a positive feedback loop. The ventricle compensates for systolic dysfunction and decreased cardiac output by dilating as TIC evolves, thereby reducing the mechanical advantage of the subepicardial LV fibers relative to the subendocardial fibers and decreasing systolic torsion. The associated steeper transmural gradients of fiber strain and oxygen demand lead to further systolic dysfunction, thereby continuing the cycle.
Limitations
The present study used an ovine TIC model, and therefore caution must be exercised in extrapolating these results to human subjects. Other investigators, however, have demonstrated that TIC has a hemodynamic and neurohumoral profile similar to that of dilated cardiomyopathy seen clinically. 10,11
Previous studies have measured twist, or the longitudinal gradient of torsional displacement, along the long axis of the ventricle. 46 Measurement of twist, however, assumes homogeneous deformation of an isotropic cylindrical ventricle, resulting in a linear relationship of torsion and distance along the long axis. Instead, the present analysis measured rotation of the apex relative to the base, which is similar to that seen in other studies. 22,24,47 Stuber and colleagues 24 found that measurements of longitudinal gradient of rotation deformation (twist) correlated well with those of apical torsion. To ascertain whether the findings in this study, namely a decrease and delay in max and a decline in early LV diastolic torsional recoil, might have been phenomena specific to the apex, the analysis was repeated by using the markers located in the equatorial LV plane, midway between the base and apex (ie, nos. 3, 10, and 13; Figure 1). The torsion measurements at this level corroborate those at the apical level, both during ejection and during IVR and early diastole. Specifically, max was decreased and delayed, with a loss of early diastolic recoil.
Calculations of angular displacement are directly affected by ventricular dilatation (ie, arc length = radius · ). Normalization of max, min, and 5% for changes in ventricular size, however, did not significantly change the differences found between the control and TIC conditions. Similarly, normalization to correct for the faster heart rate after development of cardiomyopathy did not alter the delay of TmaxEE observed in the TIC group. In the presence of mitral regurgitation, which developed in the TIC animals, ES and end-ejection may become temporally dissociated 48; however, when the timing of max was measured relative to ES, the same trends were observed, as reported above.
This protocol was only approved by the Research Animal Use Committee for 2 data-acquisition studies, baseline and after development of cardiomyopathy. Thus we can only speculate about the time course of changes in ventricular geometry, hemodynamics, and torsion. Further experiments are underway to examine the temporal relationship between alterations in torsion, ventricular remodeling, and functional decline. Finally, the mitral regurgitation seen in the cardiomyopathic conditions could have been, at least in part, responsible for the altered hemodynamics and torsion mechanics seen in TIC.
Implications and inferences
The current wave of clinical surgical enthusiasm for the Surgical Anterior Ventricular Endocardial Restoration 8 procedure, as promulgated by the Reconstructive Endoventricular Surgery returning Torsion Original Radius Elliptical shape to the LV (RESTORE) group, purports to reapproximate normal LV shape, size, and fiber angles, thereby theoretically restoring normal LV torsion mechanics in patients with ischemic and nonischemic dilated cardiomyopathy. 9 The present study supports the hypothesis that dilated cardiomyopathy is associated with derangements of physiologic torsion dynamics, and we speculate that these alterations may contribute to a cycle of progressive ventricular functional decline. LV systolic torsion and diastolic recoil can be measured noninvasively with radiofrequencytagging magnetic resonance imaging. 24 Further clinical studies are needed to clarify the role of torsion in the pathophysiology of human cardiomyopathy.
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