Dynamics of Left Ventricular Apex Rotation During Angioplasty
A Sensitive Index of Ischemic Dysfunction
Background Apex rotation has been shown to provide a reliable index of the dynamics of left ventricular (LV) twist. In this study, we aimed to characterize twist at baseline and during acute ischemia in 20 patients undergoing percutaneous transluminal coronary angioplasty to the left anterior descending (LAD) artery and to test whether an old myocardial infarction or collateral flow affected twist dynamics.
Methods and Results Among patients with no previous infarction, five had no collaterals (group A) and six had angiographically visible collaterals (group B). Previous anterior infarction was present in nine patients (group C). Data were acquired with the LAD angioplasty wire passed beyond the apex using a view aligned with the LV long axis. Frame-by-frame dynamics of apex rotation were measured from the angular movement of the portion of the wire that traversed the apex. Aortic pressure recordings allowed precise temporal definition of the cardiac cycle. Dynamics of apex rotation were measured at fixed intervals until 60 seconds of occlusion and up to 60 seconds of reperfusion. In group A, counterclockwise apex rotation (twist) during ejection of −22.0±1.7° (mean±SEE) was followed by rapid clockwise rotation (untwist) during isovolumic relaxation. During 60 seconds of ischemia, maximum apex rotation decreased to −8.2±2.0° (P<.001 versus baseline). In group B, baseline apex rotation was similar (−26.2±6.9°) to that in group A, but ischemia had less effect, with apex rotation values of −17.7±3.4° (P<.05 versus group A values). Group C was characterized by reduced baseline apex rotation values (−9.7±3.1°, P<.05 versus group A values), with little change observed during ischemia (−8.1±2.6°).
Conclusions Apex rotation, an index of ventricular twist, is sensitive to acute ischemia in patients without previous myocardial infarction. Visible collaterals to the ischemic region attenuate the acute ischemic response at 60 seconds. Previous myocardial infarction causes abnormalities in the baseline twist pattern with no further deterioration at 60 seconds of ischemia.
Muscle fibers in the LV have a predominantly oblique orientation that varies across the wall.1 Contraction of these spiral fibers results in torsional deformation.2 3 4 5 6 7 8 The net result of the systolic contraction of differently oriented spiral fibers, as viewed from the apex, is a counterclockwise rotation of the apex, because the moments of the epicardial fibers, which follow a counterclockwise spiral, dominate.6 LV twist during systole has been classically defined as the counterclockwise rotation of the LV apex with respect to the base, as viewed from the apex.3 4 5
Studies have been performed to examine and quantify LV twist in both dogs and humans. Lower9 was the first to observe that the muscle fibers of the LV inner wall ran opposite to those of the outer wall and that contraction could be compared “…with the wringing of a linen cloth to squeeze out the water.” More than 300 years later, other studies confirmed this early observation. Using multiple implanted markers and biplane cine angiography in transplanted hearts, Ingels et al2 10 and Hansen et al7 11 calculated torsional deformation from the three-dimensional motion of the markers throughout systole. Using similar techniques, Waldman et al12 measured regional transmural deformation in the LV wall of instrumented dogs. Arts et al4 studied torsional deformation in the canine LV using two-dimensional echocardiography. By using echo-derived short-axis images of the LV at the levels of the mitral valve and the papillary muscles, twist was calculated as the difference between the angles of rotation at these two levels. Later, MRI and end-diastolic tagging were used to measure ventricular twist in patients.8
Beyar et al5 used radiopaque markers and biplane cine angiography to follow the dynamic twist-radial shortening relationship through the entire cardiac cycle and demonstrated rapid untwisting during the isovolumic relaxation phase. The fact that most of the untwisting occurs before the end of isovolumic relaxation has been confirmed by MRI tagging.13 The method described by Beyar et al5 was recently extended to hearts with multiple radiographic markers in patients undergoing heart transplantation, which showed that changes in the pattern of rapid untwisting can be used as a highly sensitive indicator of impending rejection14 and that twist is a reliable measurement of LV function.
Previous studies using MRI tagging8 have shown that slice rotation increases gradually from base to apex and that the base of the heart rotates only minimally. Based on that observation and on direct measurement of base rotation, we have recently shown that apex rotation alone, studied by an optical method in dogs, can provide a reliable index of LV twist,15 which is markedly sensitive to acute ischemia in an experimental model.16
The effects of acute ischemia on LV twist have not been studied in human patients. It is hypothesized that ischemic dysfunction will result in marked alteration of twist amplitude and dynamics, similar to our observation in dogs.16 Measurement of apex rotation is feasible during coronary angiography through observation of the apical segment of the LAD by use of an apical long-axis view.17 Similarly, during angioplasty to the LAD, it is possible to measure the dynamics of apex rotation from this view by observing the motion of an angioplasty wire positioned in the apical segment of the LAD artery (Fig 1⇓). Using this approach, we measured the dynamics of apex rotation in patients undergoing angioplasty to the LAD as a human model of acute ischemia. The aims of the study were (1) to describe the dynamic pattern of apex rotation in patients, (2) to show the time course of the development and resolution of ischemic dysfunction as reflected by the measurement of apex rotation, (3) to show the relation between abnormalities in the dynamic pattern of twist and the presence of collateral flow, and (4) to study whether previous anterior MI affects the baseline twist and its response to acute ischemia.
Definition of Patient Groups
Twenty patients who underwent nonemergency balloon angioplasty to the LAD were studied. The patient and lesion characteristics are described in Table 1⇓. The patients were divided into three groups. Group A patients (n=5) had no previous infarction and no collaterals demonstrable by angiographic criteria (TIMI collateral flow 0 or 1). Group B patients (n=6) had angiographically visible collaterals (TIMI collateral flow 2 or 3). Group C patients (n=9) had a previous anterior infarction (duration, 3 to 120 days). All patients had a significant lesion in the proximal- or mid-LAD location. Percent-stenosis measurements (Digimatic calipers) before and after balloon angioplasty are shown in Table 1⇓.
The protocol was approved by the Conjoint Research Ethics Board of The University of Calgary and The Foothills Hospital, and all patients gave written informed consent. The ECG and aortic pressure were measured and recorded (VR16, Electronics for Medicine; Honeywell). An 8F sheath was introduced via a femoral arterial puncture, and the routine over-the-wire angioplasty procedure was followed. With the use of a diagnostic catheter, images of the LAD lesion were obtained in the most appropriate radiographic views. In addition, the apical view aligned along the long axis of the LV was selected and recorded. This view was selected so that the apical segment of the LAD appeared in the middle of the LV base, as defined by the course of the coronary sinus (visualized during the venous phase of the injection) and the position of the septum (visualized by the arterial blushing) (Fig 1⇑). An 8F angioplasty catheter was advanced and engaged in the left main coronary artery, and the angioplasty wire was advanced until it traversed the apex. A lateral view (Figs 1⇑ and 2⇓) was used to verify that the wire extended beyond the apex. Subsequently, a baseline measurement of apex rotation was obtained, and the angioplasty procedure proceeded. After a satisfactory result had been obtained (as determined by the PTCA operator), timed angiographic (30 frames/s) and hemodynamic measurements of cardiac cycles were obtained for baseline and at 20 and 60 seconds of ischemia (induced by balloon inflation to a maximum of 14 atm). After 60 seconds of occlusion, the balloon was deflated, and measurements were taken at 20 and 60 seconds of reperfusion.
Measurements of Apex Rotation
Images were digitized frame by frame into a computer by use of a frame grabber (Bioscan Snapshot Plus; INFRASCAN, Inc) and stored for further analysis. The phases of the cardiac cycle were defined from the ECG, and central aortic pressure was corrected for transmission delay.
ED was defined as the peak of the QRS deflection in lead II, and the beginning of ejection was defined by the rapid increase in aortic pressure. The maximum value of systolic twist was measured, and the time at which it occurred was recorded (the number of milliseconds before the end of ejection). ES was defined by the dicrotic notch. The end of isovolumic relaxation was approximated as the third frame after the dicrotic notch. This approximation was based on the calculation of the time from ES (frame with the smallest volume) to mitral valve opening, which was obtained using the LV angiogram taken before the PTCA.
As shown schematically in Fig 1⇑, this view was selected so that the apical segment of the LAD appeared in the middle of the LV base, as defined by the course of the coronary sinus (visualized during the venous phase of the injection) and the position of the septum (visualized by the arterial blushing). An angioplasty catheter was advanced and engaged in the left main coronary artery, and the angioplasty wire was advanced until it traversed the apex. A right anterior oblique view (Figs 1A⇑ and 2A⇑) was used to confirm that the wire position was over the LV apex. The apical view that is used for the analysis is shown in Fig 2B⇑. The segment of the apical wire to be measured when positioned at the LV apex was determined by use of both the lateral and apical views. A portion of the wire that traversed the apex but was not bent by the tortuosity of the LAD was selected.
From the apical view described above, the angle of the wire was measured for each frame throughout the cardiac cycle. In each frame, two points at the apical location of the wire were marked, and the angle of the wire was calculated. The procedure was repeated frame by frame until at least two complete cycles were digitized. After obtaining absolute angular measurements, the value of the apex rotation at ED was arbitrarily defined as 0°, and analysis of rotation throughout the cycle in relation to the end-diastolic angular position was obtained. Intraobserver variability was ascertained by having the same operator trace the same sequence of images days apart. The variability was very small, with very few variations between different digitization sessions. Similarly, interobserver variability was determined by having a research nurse blindly repeat the digitization process. Interobserver variability was also of minor value.
Averages, SDs, and SEEs were calculated for each group. Comparisons between groups were performed using the Student t test, and P<.05 was taken to be significant. Multivariate ANOVA was applied to take into account correlations in the data arising from repeated measurements of individuals. To improve power, attention was focused on the examination of particular linear combinations, in particular the average twist value, which is simply the average of values: maximum systolic twist, ES, and the end of the isovolumic relaxation period. Although this is somewhat simplistic, detailed examination of the more complex patterns over the cycle would require more subjects to provide adequate power. Within- and between-group comparisons were tested against the relevant components of the pooled error variance/covariance matrix. For multiple comparisons, the Tukey procedure was used where feasible; otherwise, Bonferroni corrections were applied. When available, “exact” probability values are reported; otherwise, statistical significance (P<.05) was noted. Statistical analysis was performed with the use of the SAS system, version 6.09 (SAS Institute Inc), on a Sun Sparc2 workstation.
Group A (No Visible Collateral Vessels, No Previous MI)
In Fig 3⇓, the angular rotation throughout the cardiac cycle (from the ED 0° position) for two patients with no visible collaterals is shown for baseline, occlusion, and reperfusion conditions. The patient shown in Fig 3A⇓ had normal regional wall motion at ventriculography, normal systolic twist during systole, and rapid untwisting during early diastole at baseline. The patient shown in Fig 3B⇓, with mild anterior wall hypokinesis at ventriculography, had slightly lower systolic twist and a slower untwisting during early diastole. A pattern of marked systolic twist attenuation is seen at 20 and 60 seconds of occlusion in Fig 3A⇓. Fig 3B⇓ shows a biphasic pattern accompanying twist attenuation, in which there was untwisting near the end of ejection followed during diastole by a second pair of twisting-untwisting transients, as demonstrated in Fig 3A⇓. After 60 seconds of ischemia, almost no twisting was observed during ejection, and most of the twisting motion was seen early during diastole. In both examples, reperfusion effected almost complete immediate restoration of the twist waveform to baseline levels. The results for group A are summarized in Fig 4⇓ and Table 2⇓. Under baseline conditions, ejection and twisting reached a maximum value of −22.0±1.7°, which occurred at 40.3±4.9% of the cycle before ES. At ES, the value of apex rotation was −18.4±0.9°. Rapid untwisting began immediately after twisting reached its maximum value; by the end of the isovolumic relaxation period, untwisting was 37.4±14.9% complete. The remainder of untwisting occurred during the diastolic filling period.
After 20 seconds of occlusion, twisting during ejection was markedly attenuated (the maximum value was −9.1±2.7°), and no significant untwisting occurred during the isovolumic relaxation period. Initial twisting during ejection was followed by untwisting at mid ejection and then further twisting during the isovolumic relaxation period, in contrast to the simpler “sawtooth” pattern observed during the control state.
After 60 seconds of occlusion, twisting during ejection was further attenuated (−8.2±2.0°) and, in some individuals (see Fig 3B⇑), was followed by a short twisting motion during the isovolumic relaxation period. This fully dysfunctional pattern did not change as ischemia continued (not shown). On release of balloon occlusion, as little as 20 seconds was required for almost complete recovery of the systolic twist pattern, with some abnormalities in the isovolumic relaxation pattern. Overall, these differences between conditions were statistically significant (P<.005). A significant difference was present between occlusion and baseline (P<.001) and occlusion and reperfusion (P<.05).
Group B (Visible Collateral Vessels, No Previous MI)
The baseline twist, ischemia, and reperfusion results are presented for a typical case subject in Fig 5⇓. Note that the baseline twist pattern is similar to the baseline pattern presented in Fig 3A⇑. However, 20 seconds of ischemia diminished systolic twisting only minimally. The average results for group B are shown in Fig 6⇓ and given in Table 2⇑. Note again that the magnitude and pattern of twist at baseline are similar to those of group A; however, twist at 60 seconds of occlusion showed a smaller decrease and was greater than at the corresponding time in group A. There was a trend toward a decrease in twist with occlusion for this group (P=.08). Therefore, the protective effect of the collateral circulation on myocardial function is clearly manifested by the altered twist response during acute ischemia.
Group C (Previous MI)
This group is heterogeneous in terms of the extent of the MI and the interval that elapsed before angioplasty (Table 1⇑), as well as in terms of the presence or absence of collaterals. Examples of two cases from this group are shown in Fig 7⇓. Note that baseline abnormalities in the twist pattern characterize both patients. In one patient (Fig 7A⇓), occlusion had a small effect on the twist amplitude and waveform. In the other example (Fig 7B⇓), 20 seconds of ischemia produced a dyskinetic pattern that disappeared after 60 seconds of ischemia with development of complete anterior wall dysfunction. The average results for group C are presented in Fig 8⇓ and Table 2⇑. Note that the baseline twist pattern is abnormal. Reduced twist as well as no untwisting before the end of isovolumic relaxation is apparent. Overall, there were no significant effects of occlusion or reperfusion on the twist magnitude (P=.24).
Comparison of Systolic Twist for the Three Groups
The end-systolic twist values for the three groups are summarized in Table 2⇑. There were significant differences among the three groups (P=.038 by Wilks’ lambda) under the three conditions (baseline, 60-second occlusion, and 60-second reperfusion). Individual examination of the three conditions revealed significant differences between groups at baseline (P=.034, F test for 1-way ANOVA), with a significant difference between the group with previous MI (group C) and the group with collaterals (group B) (Tukey multiple comparisons test). Similar results were obtained under occlusion (P=.04 for the F test and group C versus group B, different by the Tukey test). Examination of the groups after reperfusion revealed no statistically significant difference (P=.13), although because the comparisons lacked power, it would be erroneous to conclude that the groups were the same under this condition. Therefore, the statistical analysis supports the concept that under conditions of no collateral protection, ischemia causes a marked change in twist whereas collaterals provide partial protection, reflected in twist. In addition, baseline abnormalities exist in patients with previous MI.
Measurements of torsion were previously based on elaborate techniques that allowed for calculation of apex rotation versus base rotation2 and involved complex geometric models based on multiple myocardial radiopaque markers4 5 6 7 17 or MRI tagging.8 13 Because the base rotates only minimally,8 we recently used apex rotation measurements in dogs to measure the dynamics and amplitude of LV twist.15 In the current study, we propose a method by which apex rotation can be measured during LAD angioplasty by observing the rotation of the LAD angioplasty wire passed over the apex from the apex-to-base long-axis view. Using this method, we were able to define typical patterns of twist dynamics in three groups of patients and to relate twist events to acute ischemia and reperfusion in the LAD territory and to the presence of collateral circulation or to previous MI.
Our findings of twist dynamics for the normally functioning LV are consistent with our earlier reports using apex rotation measurements15 18 as well as with our previous measurements by multiple markers,5 all of which demonstrated rapid untwisting during early diastole. Similar findings have been reported with the use of tagged MRI in patients13 and with the use of angiographic markers in the human transplanted heart.14 19 The magnitude of twist reported in the present study is also consistent with previous results (ie, 13°18 and 15°15 ).
The assumption behind the current method of twist measurement is that the rotation of the base is minimal and can be ignored. This assumption has been validated in our previous work in open-chest, open-pericardium dogs15 and is also substantiated by the results of a previous study that used MRI tagging techniques.8 Because the base rotates opposite to the apex to some extent,5 15 our measurements of apex rotation are a slight underestimation of the true rotation of the apex relative to the base. In contrast, the current method measures twist at its maximum point, ie, the apex, whereas previous methods did not usually measure true apical twist. Interestingly, our apex rotation measurements are similar to previously reported twist values measured by rotation of the apex relative to the base. Using multiple markers and biplane cineangiography, Hansen et al11 reported a value of 13.3±6.0°, and using MRI tagging, Buchalter et al8 reported a value of 11.2±1.3°. Therefore, we conclude that the error introduced by not accounting for base rotation is minimal.
The effects of acute ischemia on twist in patients have not been evaluated before. We show here that apex rotation is highly sensitive to ischemia and becomes abnormal within a few seconds after balloon occlusion.20 Early abnormalities include twist attenuation with a reversal of twist during mid systole, with untwisting during the second part of ejection and, subsequently, twisting during isovolumic relaxation (Figs 3B⇑ and 7B⇑). This pattern, which we have also observed during acute ischemia in the dog (using our optical device to measure apex rotation),15 16 21 is comparable to an early dyskinetic motion observed by Tyberg et al in hypoxic papillary muscles22 and in an experimental model of regional ischemia.23 This pattern probably results due to late contraction of the ischemic region as ventricular pressure is decreasing. When ischemia is fully developed, usually within 60 seconds of the occlusion, the dominant pattern is one of limited or absent twisting during ejection and paradoxical twisting during isovolumic relaxation (Fig 3B⇑). Obviously, our present observations are limited to acute occlusion of the LAD, which results in localized anterior ischemia. How ischemia of different territories would affect apical rotation has not been evaluated in patients. However, our observations in dogs suggest that circumflex occlusion produces significant, perhaps comparable effects on apical twist.16 21 They suggest that apex rotation is a parameter that integrates the performance of all regions of the LV. Nonetheless, it seems clear that during the procedure, the current method can provide the operator with important information related both to the amount of dysfunction caused by balloon occlusion and particularly to the recovery of function after deflation of the balloon.
Because LV twist has been proven as an index of ventricular systolic function as well as an index sensitive to diastolic dysfunction, it is important to compare the results of the current study with previous studies assessing systolic and diastolic function during angioplasty. Various studies have shown a reduction in global systolic function during angioplasty. Using various techniques, it has been shown that ejection fraction decreases reversibly.24 25 26 27 In most of these studies, LV function was measured at between 30 and 50 seconds of ischemia, and after such ischemic intervals, ischemic effects resolved completely within 5 to 15 minutes of reperfusion. Regional function has been measured by left ventriculography at 30 to 50 seconds of occlusion, and clear dyskinesis of the anterior and apical segments has been demonstrated.27 Transthoracic echocardiography has shown rapid changes in regional function at 16 to 20 seconds of ischemia and resolution within 10 to 20 seconds of reperfusion.28 Transesophageal echocardiography has shown that regional dysfunction develops with 10 seconds of coronary artery occlusion.29 These observations are consistent with the results of the present study showing that at 20 seconds of ischemia, severe dysfunction is present in most cases, and no further deterioration in function is seen at 60 seconds of ischemia. In the present study, recovery of systolic function was indeed immediate, with almost complete recovery being observed after 20 seconds of reperfusion. This time sequence of events is also supported by investigations that used Doppler indexes of aortic flow and showed decreased contractile function during occlusion and complete recovery after reperfusion.30
Diastolic dysfunction has also been reported after angioplasty. An increase in the time constant of relaxation was consistently observed during balloon occlusion.27 Diastolic abnormalities have also been documented by measuring a shift in the end-diastolic pressure-volume relationship, which, in contrast to systolic indexes, persisted 12 minutes after reperfusion.31 Additional evidence for delayed normalization of the diastolic abnormalities was provided by Doppler mitral-inflow measurements,32 which showed persistent diastolic dysfunction at 60 seconds of reperfusion. Other studies using radionuclide techniques have shown reduced LV filling that persisted at 5 minutes after reperfusion. Therefore, it seems that diastolic dysfunction is typical for acute ischemia and may persist longer than systolic dysfunction. Indeed, in the current study, we have shown that an abnormal relaxation pattern was still present at 20 seconds of reperfusion in some patients, although systolic function had recovered completely, consistent with previous observations.
During angioplasty, the effects of collaterals on ventricular function have been studied by use of Doppler-measured aortic-root acceleration.33 It was shown that in the presence of visible collaterals, no decrease in contractile function was measured compared with a group of patients without collaterals. This finding is consistent with our observations that the effect of balloon occlusion on ventricular twist is markedly attenuated in the presence of visible collaterals. An important observation is that the presence of collaterals markedly attenuates the ischemia-induced decrease in twisting during balloon angioplasty. The presence of a normal baseline twist pattern that is minimally attenuated during balloon occlusion indicates that the collateral circulation is sufficient to limit regional dysfunction during the short ischemic periods studied here.
Previous MI had a marked effect on the averaged baseline twist pattern, with only a small additional effect being observed during acute occlusion. Interestingly, some patients showed a pattern of no twist at all during ejection, with no effect of occlusion, whereas other patients with reduced baseline twist demonstrated additional ischemic effects on balloon inflation. In the entire group of patients with previous MI, a tendency toward increased postreperfusion twist may indicate that reflex mechanisms may play a role in increasing regional function after reperfusion.
The present study emphasizes the tool as a research modality allowing measurements of dynamic systolic parameters of ventricular function in patients during rapid ischemic maneuvers. This is the first study of its kind and can form the basis for studies of various interventions on twist dynamics. Validations for the use of apex rotation for twist measurements are based on our previous animal experiments.15 16 The method can also be used in the catheterization laboratory as a quick way to assess ventricular function during LAD angioplasty or even during left coronary injections of contrast material. However, assessing the value of such a method as a clinical tool requires further investigation and feasibility studies.
In summary, a method has been demonstrated whereby the systolic and diastolic dynamics of LV twist can be evaluated during angioplasty from the angular motion of the apical portion of the angioplasty wire. We have shown a typical baseline pattern of ejection twisting and rapid isovolumic-relaxation untwisting, consistent with earlier observations. This twist pattern is highly sensitive to ischemia, with characteristic changes appearing a few seconds after balloon occlusion and disappearing immediately after reperfusion. In addition, collateral protection has been shown to reduce twist abnormalities during ischemia. In the presence of previous MI, baseline twist abnormalities reflect the permanent insult to the myocardium, but an increase in twist after reperfusion may reflect a secondary postischemic inotropic response of viable myocardium in that territory. Therefore, measurements of apex rotation during angioplasty provide a new window for observations of pathophysiological twist dynamics in patients and help us to understand the effects of ischemia and regional dysfunction on twist.
Selected Abbreviations and Acronyms
|LAD||=||left anterior descending artery|
|LV||=||left ventricle, left ventricular|
|PTCA||=||percutaneous transluminal coronary angioplasty|
|TIMI||=||Thrombolysis In Myocardial Infarction|
We acknowledge the statistical support and expertise of Dr Rollin Brant of The Center for Advancement of Health at The Foothills Hospital and the University of Calgary.
- Received December 9, 1996.
- Revision received February 18, 1997.
- Accepted February 24, 1997.
- Copyright © 1997 by American Heart Association
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