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CLINICAL RESEARCH: MRI AND RESYNCHRONIZATION

Propagation of Onset and PeakTime of Myocardial Shortening in Time of Myocardial Shortening in Ischemic Versus Nonischemic Cardiomyopathy

Assessment by Magnetic Resonance Imaging Myocardial Tagging

Jaco J.M. Zwanenburg, MSc^_*,_*, Marco J.W. Götte, MD, PhD^,, J. Tim Marcus, PhD^_*, Joost P.A. Kuijer, PhD^_*, Paul Knaapen, MD, Robert M. Heethaar, PhD^_* and Albert C. van Rossum, MD, PhD

^_* Department of Physics and Medical Technology, VU University Medical Center, Amsterdam, the Netherlands
Department of Cardiology, VU University Medical Center, Amsterdam, the Netherlands
Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands

Manuscript received February 28, 2005; revised manuscript received August 16, 2005, accepted August 22, 2005.

^_* Reprint requests and correspondence: Jaco J. M. Zwanenburg, Department of Physics and Medical Technology, VU University Medical Center, PO Box 7057, 1007 MB Amsterdam, the Netherlands (Email: jjm.zwanenburg{at}vumc.nl).

	Abstract

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OBJECTIVES: We aimed to study the relation between onset and peak time of circumferential shortening and the direction of propagation of these parameters in both ischemic and nonischemic patients.

BACKGROUND: Peak time is often used to select patients for cardiac resynchronization therapy, whereas pacing influences only the onset times directly. Furthermore, it is unclear whether there is a consistent direction of propagation delay and whether this depends on the etiology.

METHODS: Magnetic resonance imaging myocardial tagging with high temporal resolution (14 ms) was applied to 29 patients (18 nonischemic, 11 ischemic) and 17 healthy control subjects. Time to onset (T_onset), to first peak (T_peak,first), and to maximum peak (T_peak,max) of circumferential shortening were determined. Three-dimensional vectors were calculated to denote the main direction of asynchrony.

RESULTS: In both patient groups, T_onset showed a significant positive relation with both T_peak,first and T_peak,max; however, T_peak,first correlated considerably better with T_onset than did T_peak,max (p < 0.0001 for nonischemic, and p < 0.01 for ischemic patients). Moreover, the relations between T_peak and T_onset were stronger in the nonischemic patients than in the ischemic patients (p < 0.001). In nonischemic patients, the propagation of T_onset was consistently from septum to lateral wall. In the ischemic patients, however, no consistent direction of propagation was found. For both groups, the longitudinal propagation delays (between apex and base) were negligible compared with the short-axis delays.

CONCLUSIONS: The relation between peak time and onset time of shortening is strongest in nonischemic patients and is most consistent when time to first peak is used (instead of time to maximum peak).

Abbreviations and Acronyms   CRT = cardiac resynchronization therapy   ECG = electrocardiogram   EF = ejection fraction   LV = left ventricle/ventricular   MRI = magnetic resonance imaging   OS = onset of shortening   PS = peak shortening   SV = stroke volume   Tonset = time to onset   Tpeak,first = time to first peak   Tpeak,max = time to maximum peak

Furthermore, the direction of the asynchrony is often neglected by using the standard deviation over all available segments (9), the maximum asynchrony between any two measured locations (10), or by studying one fixed direction, normally the septum-to-lateral wall direction (5). Recently, however, Bader et al. (3) and Ghio et al. (4) reported interesting data from regional onset times of systolic velocity in patients with heart failure. Both studies reported that the lateral wall is the latest region in only one-third of the patients, suggesting a large spread in the direction of the asynchrony in these patients. From these data, the question arises as to the extent to which asynchrony is present between septum and lateral wall or whether other locations, including apex versus base, should be considered.

Intramural myocardial circumferential shortening, which can be measured by means of magnetic resonance imaging (MRI) tagging, is a strong parameter to study regional mechanical function (11). The MRI tagging has already been applied successfully in dogs to study the regional timing of circumferential shortening in the left ventricle (LV) (12). Owing to recent developments, the temporal resolution of MRI tagging has become sufficient (14 ms) to study the regional timing of circumferential shortening also in human subjects (13).

In this study, MRI tagging was applied in both ischemic and nonischemic patients who were screened for CRT. The timing of circumferential shortening was analyzed for the following two research purposes: 1) to gain more knowledge of the relation between peak time and onset time of circumferential shortening, and 2) to study the three-dimensional propagation of the peak time and onset time over the LV. The propagation was characterized by a three-dimensional vector. This allowed a straightforward comparison between the longitudinal component of the propagation (apex vs. base) and the short-axis component. In the analysis, ischemic patients were distinguished from nonischemic patients to investigate whether differences were observed that could help to understand the lower response of ischemic patients to CRT compared with nonischemic patients (14,15).

	Methods

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Subjects.   Twenty-nine patients were selected from patients referred to our hospital to be screened for biventricular pacing. Inclusion criteria were: depressed LV function (ejection fraction [EF] 45% with MRI), wide QRS (120 ms), and New York Heart Association functional class II to IV. Eleven patients (age 66 ± 9 years, 4 women) were classified as ischemic (based on a history of myocardial infarction and/or significant coronary artery disease assessed by coronary angiography), and 18 (age 57 ± 14 years, 6 women) were nonischemic. All patients were in sinus rhythm, clinically stable, and received standard heart failure therapy, including diuretics, beta-blockers, angiotensin-converting enzyme inhibitors, and/or angiotensin II receptor blockers. Written informed consent was obtained according to our institutional guidelines. A group of 17 healthy subjects of whom the timing of shortening has been reported previously (13) served as control group.

Imaging.   Complementary tagged (CSPAMM) myocardial images were acquired with a high temporal resolution of 14 ms, using steady state free precession imaging and a multiple brief expiration breath-hold scheme (13). Imaging parameters are given in Table 1, and example images in Figure 1. Images for two-dimensional strain analysis were acquired in five short-axis planes, evenly distributed over the LV. Steady state free precession cine imaging (without tagging) was performed with full coverage of the LV to assess LV volumes and EF.

View larger version (197K): [in this window] [in a new window]   Figure 1 Example tagging images for a patient (top) and a healthy subject (bottom). Early shortening occurs in the septum of the patient (left), whereas this shortening is not preserved at aortic valve closure (end-systole, right).

Time to onset of shortening
Time to onset of shortening (T_onset; in ms from the electrocardiogram [ECG] R-wave) was defined as the beginning of the down-slope of the circumferential strain curve and was semi-automatically determined as described in the Appendix of reference (13). To optimize the algorithm for patient data, the earliest allowed onset time (T₁) was set to 15 ms after the ECG R-wave. Furthermore, the onset time of shortening was regarded as missing when the goodness of fit was <0.85 or when regions were akinetic, which were defined as regions with a peak shortening of <3%. In case the algorithm could not determine T_onset, two observers (T. M. and J. J. M. Z.) reviewed the strain curve and determined in mutual agreement the T_onset for that curve. The observers regarded T_onset as missing if artifacts or akinesia made a determination of T_onset not possible.

The propagation of the onset of shortening was characterized by a three-dimensional vector, called the onset of shortening delay vector (OS-delay vector) (16). The first component of the OS-delay vector yields the delay between the septum and the lateral wall (positive: lateral wall later than septum); the second component is the delay between inferior (IN) and anterior (AN) (positive: AN later than IN); and the third component is the delay between apex and base (positive: base later than apex). Thus, this vector points from the earliest activated region to the latest, and its magnitude is a measure for the delay between these two regions. The vector was not calculated when T_onset data were missing in 50% or more of the myocardial segments.

Time to peak shortening
In healthy subjects, time to peak shortening (T_peak) was defined as the time of maximum shortening (13). Multiple shortening waves might exist in patients (Fig. 2). Therefore, two peak time parameters were determined: the time to the first peak of shortening (T_peak,first) and the time to the maximum peak of shortening (T_peak,max). The first peak was detected automatically with the first zero-crossing in the strain-rate from a negative strain rate (circumferential shortening) to a positive strain rate (circumferential lengthening). The peak shortening delay vector (PS-delay vector) was defined in complete analogy to OS-delay vector. The peak times were also reviewed and adjusted or rejected by two observers (T. M. and J. J. M. Z.) in mutual agreement.

View larger version (18K): [in this window] [in a new window]   Figure 2 Example circumferential strain curves over time for one septal segment and one lateral segment of a mid ventricular slice, showing the definitions of the several timing parameters. (A) Healthy subject, showing synchronous shortening. (B) Nonischemic patient with multiple shortening waves in the septum, leading to a first peak and a maximum peak of shortening. AL = anterolateral; AS = anteroseptal; ECG = electrocardiogram; IL = inferolateral; IS = inferoseptal; Tonset = onset time of shortening; Tpeak,first = time to first peak of shortening; Tpeak,max = time to maximum peak of shortening.

Because the multilevel analysis revealed that the dependency was only relevant on the subject level (i.e., the relation between T_onset and T_peak differs significantly between subjects, but not between slices), individual Pearson correlation coefficients between T_onset and T_peak are also presented. The individual correlation coefficients were calculated with the data from the available segments of each heart: five slices x six segments minus possible missing values (pair-wise).

To explore the direction of propagation of T_onset and T_peak, the components of the OS-delay vectors and the PS-delay vectors were compared between patients and control subjects with unpaired t tests assuming unequal variances. Values are presented as means ± SD, and p values <0.05 were regarded as significant.

	Results

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Example strain curves for two segments of the heart are shown in Figure 2. Note the difference in T_peak,first and T_peak,max in the septal segment of the patient. Figure 3 illustrates the timing of shortening for the two patient groups and the healthy volunteers. The uncoordinated onset of shortening in the patients is clearly visible from both earlier and later onsets times compared with the healthy subjects. No significant difference in global function was observed between the ischemic and the nonischemic group (Table 2).

View larger version (57K): [in this window] [in a new window]   Figure 3 Mean maps of the timing of shortening, illustrating the different timing patterns in nonischemic patients, ischemic patients, and healthy subjects. Note the similarity in the patterns between onset time and peak times for the nonischemic patients. These patterns are less similar and less distinct for the ischemic patients. The segments are defined in the bulls-eye top left. Tonset, Tpeak,first, and Tpeak,max all in ms from the ECG R-wave. AN = anterior; IN = inferior; other abbreviations as in Figure 2.

View larger version (20K): [in this window] [in a new window]   Figure 4 Individual correlation coefficients between onset time and peak time, plotted versus the individual asynchrony in Tonset. The asynchrony in Tonset is defined as the intra-subject variance in Tonset and is a measure for the range of values that is available for the correlation. Each data point represents one subject. (Top row) Correlation coefficients from nonischemic patients (n = 18), using (A) Tpeak,first and (B) Tpeak,max. For some nonischemic patients, no association between Tpeak,max and Tonset exists, even when there is a large asynchrony in Tonset, indicating an important discrepancy between Tpeak,max and Tonset, which is not observed between Tpeak,first and Tonset. (Bottom row) Correlation coefficients from ischemic patients (n = 11) for (C) Tpeak,first and (D) Tpeak,max. A considerable number of ischemic patients show a poor correlation between peak time and onset time, regardless of whether Tpeak,first or Tpeak,max is used. Abbreviations as in Figure 2.

The spatial distribution in T_onset, T_peak,first, and T_peak,max is shown for two nonischemic patients in Figure 5. The first patient (Fig. 5, upper row) had a good correlation for both T_onset versus T_peak,first and for T_onset versus T_peak,max, whereas the second patient had only a good correlation between T_onset versus T_peak,first but not between T_onset versus T_peak,max.

View larger version (42K): [in this window] [in a new window]   Figure 5 Individual maps of the timing of shortening, illustrating the difference in performance between Tpeak,first and Tpeak,max. (Subject A) nonischemic patient for whom both Tpeak,first and the Tpeak,max correlated well with Tonset. (Subject B) nonischemic patient for whom only Tpeak,first correlated well with Tonset. *Missing values. Abbreviations as in Figures 2 and 3.

In the nonischemic patient group, the asynchrony of T_onset in the short-axis direction dominated the asynchrony in the long-axis direction, because the magnitude of the short-axis component of the OS-delay vector was a factor of 8 ± 9 (range: 0.3 to 38) larger than the long-axis component. Within the short-axis direction, the septum to lateral wall component was much larger than the AN-IN component (88 ± 30 ms vs. –6 ± 25 ms) (Table 4). The septum to lateral wall component was always positive (range: 5.1 to 115 ms), indicating that the septum was always earlier than the lateral wall in the nonischemic group. Compared with control subjects, the septum to lateral wall component pointed in the opposite direction and was much larger (88 ± 30 ms vs. –12 ± 10 ms, p < 0.0001) (Table 4). The longitudinal component pointed from the apex to the base, although propagation was slightly delayed in comparison with the control subjects (22 ± 18 ms vs. 9 ± 7 ms, p < 0.01) (Table 4).

In all patients, the PS-delay vector based on T_peak,first showed generally a similar pattern of propagation as the OS-delay vector (Table 4). On average, the direction of the PS-delay vector based on T_peak,max was also similar to that of the OS-delay vector, but in individual cases, important discrepancies were observed (Fig. 5).

An interesting observation was that the asynchrony, quantified as the magnitudes of the delay vectors, tended to be larger for the nonischemic patient group than for the ischemic patient group, although the global function characteristics (SV, EF, and heart rate) were similar (p > 0.11 for SV, and p > 0.5 for EF and heart rate). The observed differences were: 97 ± 22 ms versus 73 ± 27 ms for the magnitude of the OS-delay vector (nonischemic vs. ischemic, p = 0.05); 371 ± 92 ms versus 264 ± 149 for the magnitude for the PS-delay vector based on T_peak,first (p = 0.061); and 328 ± 111 ms versus 219 ± 78 ms for the magnitude of the PS-delay vector based on T_peak,max (p < 0.005).

	Discussion

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This study focused on two basal questions related to CRT. First, we studied whether peak time of regional myocardial shortening, which is normally used to assess LV asynchrony, is correlated to the onset time, which is most directly influenced by pacing. Second, we studied whether there is a consistent pattern in the propagation of onset and peak time. Both ischemic and nonischemic patients were studied with MRI myocardial tagging with high temporal resolution.

Onset time versus peak time.   T_peak,first yielded better correlations with T_onset than T_peak,max. This can be explained by the occurrence of multiple shortening waves in the early-activated regions (Fig. 2A). The actual peak value of each shortening wave is determined by regional wall stress and contractile force and might vary from region to region. As a consequence, whether maximum shortening occurs at the first, second, or third shortening wave is variable from region to region, leading to inconsistent T_peak,max values.

The origin of the multiple septal shortening waves might be related to interaction of the left and right ventricles in combination with the weak contraction of the early activated septum (18,19). The effect of the interaction depends on several factors, including the compliance of the wall (influenced by fibrosis), wall stress, and contractility and might, therefore, vary from patient to patient.

From the regression coefficients between T_onset and T_peak,first (Table 3) it can be observed that the asynchrony in T_peak,first is an amplified version of the asynchrony in T_onset: the range in T_onset is 0.23 times the range in T_peak,first (for the nonischemic patients), implying that the asynchrony in T_peak,first is about 4 times larger than that in T_onset. This amplification might make T_peak,first a more sensitive parameter to detect asynchrony than T_onset. The amplification in asynchrony might be related to the fact that early activated regions, which operate at a low load, have a short and weak contraction (18,20).

Propagation.   Regardless of the etiology, the propagation delays occurred dominantly in the short-axis direction. In patients, the propagation of T_onset in the long-axis direction was only slightly delayed in comparison with the control subjects and directed from apex to base, which is the favorable direction, because it propels the blood towards the outflow tract.

For the nonischemic patients, the short-axis component of the propagation was very consistently directed from the septum to the lateral wall. For the ischemic patients, however, no consistent direction of the short-axis component of the propagation was found. Therefore, regarding the nonischemic patients, it is justifiable to focus only on the septum to lateral wall delay; but in the ischemic patients, asynchrony can be expected in any (short-axis) direction. One might speculate that the dispersion in propagation directions for the ischemic patients is related to variable patterns of scar tissue, which influence the propagation.

van de Veire et al. (21), using the time to peak systolic motion, also found a more consistent pattern of asynchrony in nonischemic patients than in ischemic patients, with mainly the lateral wall as the most delayed region; however, they found two nonischemic patients (12%) in whom the septum was the most delayed region, whereas in our study, the lateral wall was always later than the septum. This might be attributed to the difference in the parameter that was studied (motion vs. circumferential strain). Ghio et al. (4), using regional onset time of velocity, found a heterogeneous pattern of most delayed regions. This might be partly explained by the fact that they didn’t separate the ischemic patients from the nonischemic patients in the analysis but might also be related to the use of velocity instead of strain (8). Besides, for studying the direction of propagation, the parameter "most delayed region" is probably more sensitive to noise and outliers in the data than the delay vector, which was used in the present study.

Ischemic versus nonischemic.   The fact that the ischemic patients showed less mechanical asynchrony than nonischemic patients, despite similar global function, suggests that mechanical asynchrony contributes less to the impaired ventricular function in ischemic patients than in nonischemic patients. Hence, resynchronization might be less effective in these patients compared with the nonischemic patients, as is also observed in some studies (14,15,22).

The observation that the ischemic patients have a significantly weaker correlation between T_onset and T_peak,first might help to explain why it is more difficult to predict the response to CRT for these patients when peak times are used (23). With CRT, one tries to synchronize T_onset, whereas the asynchrony measure used to predict the response is based on peak times, which are often not correlated to T_onset in individual ischemic patients (Fig. 4).

Study limitations.   A limitation of this study is that early shortening before the ECG R-wave is not detected, because the MRI acquisition triggers on the peak R-wave of the ECG. Consequently, T_onset times in the septum might be too late. The observed asynchrony in T_onset must, therefore, be regarded as a lower bound of the actual asynchrony.

We did not compare the timing of circumferential strain with that of regional velocity, wall motion, or longitudinal strain rates, as can be obtained with echocardiography. Therefore, although this study shows that onset time and (first) peak time of regional function are, in principle, correlated, no firm conclusion can be drawn from this work for the (clinical) use of peak times obtained with echocardiography. Which echocardiographic measure is most suitable for the prediction of the response to CRT, however, seems to be controversial and certainly needs further research (8,23).

Conclusions.   Time to first peak (T_peak,first) of circumferential shortening and time to maximum peak (T_peak,max) both correlated with the onset time of shortening (T_onset). T_peak,first performed considerably better than T_peak,max, however, and the relations between T_peak,first and T_onset in individual subjects were more consistent in the nonischemic patient group than in the ischemic patient group.

For all patients, the longitudinal components of the propagation delay in both T_onset and T_peak,first were negligible in comparison with the short-axis component. For the nonischemic patients, the main direction of the propagation of T_onset and T_peak,first was consistently from septum to lateral wall. In the ischemic patients, however, no consistent direction was found.

	Acknowledgments

 
The authors thank Mark B. M. Hofman for the helpful discussions, Jos Twisk for performing the multilevel regression analysis, and Vroni van der Land for assistance with drawing contours.

	Footnotes

 
Supported by the Netherlands Heart Foundation (The Hague, the Netherlands), grant 2000B220.

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