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Heterogeneous Onset of Myocardial Relaxation in Subendocardial and Subepicardial Layers Assessed With Tissue Strain Imaging

Comparison of Normal and Hypertrophied Myocardium

Takuya Hasegawa, MD^_*, Satoshi Nakatani, MD^,_*, Hideaki Kanzaki, MD^_*, Haruhiko Abe, MD^_*, Masafumi Kitakaze, MD^_*

^_* Department of Cardiology, National Cardiovascular Center, Osaka, Japan
Division of Functional Diagnostics, Department of Health Sciences, Osaka University Graduate School of Medicine, Osaka, Japan

	Abstract

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Objectives: We sought to investigate the existence of a time difference in myocardial relaxation between the subendocardium and subepicardium in patients with and without myocardial hypertrophy.

Background: Regional differences in mechanical and electrical properties between the subendocardium and subepicardium have been described for the left ventricle in animals. However, this difference has not been well evaluated in clinical conditions.

Methods: Time-to-peak radial strain with reference to the QRS complex was measured at the subendocardium and subepicardium at the mid-posterior wall of the left ventricle in 12 normal subjects, 14 patients with hypertensive heart disease, and 27 patients with aortic stenosis (16 with and 11 without strain electrocardiogram [ECG] pattern) using tissue Doppler-based strain imaging.

Results: Time-to-peak radial strain in the subepicardium (381 ± 60 ms) was shorter than that in the subendocardium (463 ± 29 ms; p < 0.001) in normal subjects, suggesting that the subepicardial relaxation precedes subendocardial relaxation. No significant difference was found between normal subjects and patients with hypertensive heart disease (388 ± 67 ms for the subepicardium; 455 ± 36 ms for the subendocardium in hypertensive heart disease). In cases with hypertrophied myocardium due to aortic stenosis, time-to-peak radial strain in the subendocardium was shortened and that in the subepicardium was prolonged. In 10 (63%) of 16 patients with aortic stenosis and strain ECG pattern, the timing of peak strain in the subendocardium (417 ± 63 ms) preceded that in the subepicardium (452 ± 62 ms).

Conclusions: There is heterogeneous onset of myocardial relaxation in the subendocardial and subepicardial layers at the mid-posterior wall of the left ventricle. Subepicardial myocardial relaxation precedes subendocardial relaxation in normal subjects. In contrast, there is inversion of the transmural sequence of myocardial relaxation between the subendocardium and subepicardium in some patients with aortic stenosis and strain ECG pattern.

Key Words: echocardiography • hypertrophy • electrocardiography

Abbreviations and Acronyms   AS-NT = aortic stenosis without strain T on electrocardiogram   AS-ST = aortic stenosis with strain T on electrocardiogram   AVC = aortic valve closure   ECG = electrocardiogram   HT = hypertensive heart disease   LV = left ventricular   N = normal subjects   TP- = time-to-peak radial strain

Tissue Doppler imaging enables us to measure change in regional myocardial length noninvasively over the complete cardiac cycle. With the recent development of myocardial strain imaging obtained by tissue Doppler imaging, we can estimate regional myocardial thickening over an entire cardiac cycle without being affected by cardiac translation and assess transmural distribution of myocardial strain (5). In the present study, we used myocardial strain imaging to determine whether the time difference to peak myocardial thickening between the subendocardium and subepicardium was observed in normal and hypertrophied human hearts.

	Methods

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Study patients.   The study subjects consisted of 27 patients with left ventricular (LV) hypertrophy caused by severe aortic stenosis, 14 patients with LV hypertrophy and a history of hypertension (Group HT), and 12 normal subjects (Group N). The subjects in Groups HT and N had no symptoms or echocardiographic findings suggestive of any cardiovascular disease other than hypertension. The patients with severe aortic stenosis were divided into 2 groups: 11 patients without strain T on electrocardiogram (ECG) (Group AS-NT) and 16 patients with strain T (Group AS-ST). Strain T was defined as asymmetric ST depression in any lead except aVR, and V₁ to V₃ in the absence of bundle-branch block. No significant coronary artery lesions were demonstrated by coronary angiography in any of patients with aortic stenosis. This study was conducted in accordance with institutional ethical guidelines, and all patients gave written, informed consent.

Standard echocardiography.   Standard echocardiography and color tissue Doppler imaging were performed using a commercially available ultrasound scanner with a 2.5-MHz transducer (Aplio, Toshiba Medical Systems, Tokyo, Japan). The LV dimension, wall thickness, and transmitral inflow pattern were measured according to the guidelines of the American Society of Echocardiography (6). The LV ejection fraction was calculated using the Quinones formula (7). The LV mass was calculated using the Devereux formula (8). The severity of aortic stenosis was assessed by peak aortic valve pressure gradient and aortic valve area calculated using the continuity equation (9).

Tissue strain imaging.   The LV short-axis image at the mid-level was obtained by color tissue Doppler imaging with a frame rate of 60 to 80 Hz and was analyzed offline using commercially available software (TDI-Q, Toshiba Medical Systems, Tokyo, Japan).

TDI-Q software enables accurate evaluation of regional myocardial strain using 2 novel techniques: the tissue Doppler tracking technique (5,10–12) and the angle-correction technique (5,12). Briefly, with the tissue Doppler tracking technique, motion of an arbitrary point on the myocardium is tracked during a cardiac cycle, based on the myocardial velocity information as follows (10). By integrating the velocity of an indexed point on the ventricular wall known from tissue Doppler imaging, we can obtain myocardial displacement and predict where the point will move next. By repeating this procedure, the system automatically tracks the motion of the point. The influence of myocardial translation can be neglected using this technique.

The angle-correction technique has been used to partly overcome the Doppler angle dependency that has been described in previous reports (5,12). To correct the Doppler incident angle, a contraction center is manually set at the center of the LV cavity in the LV short-axis view at end-systole. The myocardial velocity toward the contraction center (V motion) is automatically calculated by dividing the velocity toward the transducer (V beam) by the cosine of the angle () between the Doppler beam and the direction to the contraction center:

V motion = V beam/cos

Using these 2 techniques, TDI-Q provides myocardial velocity, and displacement and strain as a result of velocity integration toward the contraction center without being affected by myocardial translation or the Doppler incident angle (5,10,11). In a previous experiment, the displacement data obtained by this method correlated well with true displacement (r = 0.99, p < 0.0001) (11).

Strain is defined as the change in distance between 2 myocardial points divided by the initial length (L₀). In clinical studies with echocardiography, myocardial strain is calculated using the following equation:

(L – L₀)/L₀

where L is the instantaneous length (13). In the present study, the distance of all 2-pixel pairs at end-diastole (equivalent to L₀) was set at 2 mm. Using the tissue tracking technique, we can obtain the displacement of the 2 points in the subendocardium or the subepicardium toward the contraction center. Therefore, we can obtain myocardial radial strain in the subendocardium and subepicardium separately in a cardiac cycle.

Measurement of time-to-peak strain.   Figure 1 shows the temporal changes in myocardial radial strain in the subendocardium and subepicardium at the mid-LV posterior wall using TDI-Q. In the present study, subendocardium was defined as the inner one-third of the LV myocardium, and subepicardium was defined as the outer one-third of the LV myocardium. The myocardium contracts until myocardial radial strain reaches a peak, after which it relaxes.

View larger version (32K): [in this window] [in a new window] [Download PPT slide]   Figure 1 Temporal Myocardial Radial Strain Profile of the Subendocardium and Subepicardium in a Normal Subject and a Subject With Aortic Stenosis and Strain ECG Pattern The upper left panel shows a left ventricular short-axis image from a parasternal approach at end-diastole in a normal subject. The red dot is on the subendocardium, and the orange dot is on the subepicardium. The lower left panel shows M-mode imaging of the mid–left ventricular posterior region in the normal subject. The upper right panel shows temporal radial strain profile at the mid–left ventricular posterior region in the normal subject. The red curve in the lower panel shows the myocardial strain profile in the subendocardium; the orange curve shows that in the subepicardium. The lower right panel shows temporal radial strain profile in a subject with aortic stenosis and strain ECG pattern. The arrows indicate the peak myocardial strain in each layer. AVC = aortic valve closure; ECG = electrocardiogram; MVO = mitral valve closure.

Statistical analysis.   Data were expressed as mean ± SD. Comparison of the parameters of clinical characteristics and echocardiography among the groups was performed using one-way analysis of variance followed by Fisher multiple comparison tests. Categorical data among the groups were compared using the Pearson chi-square test. Unpaired Student t testing was used to compare the severity of aortic stenosis between patients with and without strain T and to compare the difference in TP- between the subendocardium and subepicardium. A p value of <0.05 was considered statistically significant. All statistical analyses were performed using Stat View 5.0 for Windows (SAS Institute, Cary, North Carolina).

TP- was measured by 2 independent observers and by 1 observer twice, a week apart, in 10 randomly selected segments to determine inter- and intraobserver variability. Variability was expressed as the absolute difference between the 2 measurements as a percentage of their mean values. Interobserver and intraobserver variability for TP- were 5.6 ± 6.4% and 4.8 ± 6.9%, respectively.

	Results

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Clinical and echocardiographic characteristics.   The characteristics of the patients are shown in Table 1. There was no significant difference in age and gender among the patients and normal subjects.

Time-to-peak radial strain in the subendocardium and subepicardium.   Figure 2 shows the difference in TP- among the 4 groups. Although LV hypertrophy was observed in patients in Group HT, TP- in Group HT was similar to that of Group N in both the subendocardium and subepicardium. However, TP- in the subendocardium was shorter (p < 0.05) in patients with aortic stenosis than that in normal subjects, suggesting that subendocardial relaxation at the mid-LV posterior wall occurs earlier in patients with aortic stenosis than in normal subjects. TP- in the subepicardium was longer in Group AS-ST (452 ± 62 ms, p < 0.05) than in the other groups.

View larger version (25K): [in this window] [in a new window] [Download PPT slide]   Figure 2 TP- in the Subendocardium and Subepicardium Time-to-peak radial strain in the subendocardium (A) and subepicardium (B). *p < 0.05 versus Group N (normal subjects); p < 0.05 versus Group N and Group HT (patients with hypertensive heart disease); p < 0.05 versus the other groups. AS-NT = aortic stenosis without strain T on electrocardiogram; AS-ST = aortic stenosis with strain T on electrocardiogram; TP- = time-to-peak strain from the onset of QRS on electrocardiogram; other abbreviations as in Figure 1.

View larger version (24K): [in this window] [in a new window] [Download PPT slide]   Figure 3 Ratio of TP- to Time to AVC Time-to-peak radial strain /AVC in the subendocardium (A) and.subepicardium (B). If the TP-/AVC ratio is greater than 1.0, the timing of strain peak is located beyond that of AVC. *p < 0.05 versus Group N and Group HT; p < 0.05 versus other groups. TP-/AVC = ratio of TP- to time to AVC from the onset of QRS on ECG; other abbreviations as in Figures 1 and 2.

View larger version (13K): [in this window] [in a new window] [Download PPT slide]   Figure 4 Difference in TP- Between the Subendocardium and the Subepicardium The negative value for Group AS-ST indicates that the timing of strain peak in the subendocardium precedes that in the subepicardium at the mid-left ventricular posterior region. *p < 0.01 versus all other groups. Abbreviations as in Figure 2.

	Discussion

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We demonstrated myocardial radial strain profile and transmural mechanics at the mid-LV posterior wall in humans using echocardiography for the first time. Our results indicate that in normal subjects the onset of myocardial relaxation in the subepicardium precedes that in the subendocardium at the mid-LV posterior wall, and that the transmural sequence is inverted in some patients with severely hypertrophied hearts.

Transmural mechanics assessed by echocardiography in normal human hearts.   We demonstrated that the onset of subepicardial relaxation precedes subendocardial relaxation at the mid-LV posterior wall in normal human hearts. The transmural heterogeneity of myocardial strain value in human hearts has been described previously using magnetic resonance imaging (14). However, the transmural sequence of myocardial relaxation has not been previously investigated in human hearts. The transmural sequence has been studied in normal animal hearts using sonomicrometry and in isolated myocytes (1–3); these results are consistent with our data of normal human hearts assessed by echocardiography.

We also found that subendocardial contraction at the mid-LV posterior wall sustained after AVC. During isovolumic relaxation, apical untwisting is accompanied by relaxation and expansion of LV apex (1). This generates a rapid base-to-apex reversal of isovolumic intracavitary pressure and blood flow (15,16). Because volume cannot change within isovolumic relaxation, subendocardial wall thickening at the basal to middle region might sustain after AVC with the apical expansion.

Transmural mechanics assessed by echocardiography in hypertrophied hearts.   We also demonstrated differences in the transmural sequence of myocardial relaxation between normal and severely hypertrophied left ventricles at the mid-LV posterior region. There was no significant difference in the transmural sequence of myocardial relaxation between Group N and Group HT, indicating that wall thickness itself may not be a major determinant of transmural difference in relaxation timing. However, the onset of subendocardial relaxation in Group AS-NT was earlier than that in Group HT. Although previous studies indicate that high LV pressure appears to affect myocardial strain value and LV segmental dyssynchrony (17,18), its effect on time-to-peak strain in the subendocardium has not been studied. The high LV pressure in end-systole may depress thickening of the subendocardium in patients with aortic stenosis resulting in a shortened duration of thickening.

The onset of subepicardial relaxation was delayed in Group AS-ST, compared with patients in Group AS-NT, and the transmural sequence of relaxation was inverted in some patients. It is known that transmural electrical heterogeneity exists in the myocardium and affects the ECG waveform (19). There are 3 types of gradient that are responsible for genesis of T-wave: 1) differences between the right and left ventricle; 2) differences between apex-base and anterior-posterior walls; and 3) transmural difference (20). In previous investigations, the presence of a repolarization gradient between the "mid-myocardial region" (M-cells) and subendocardial and subepicardial regions has been correlated with the genesis of upright T waves in ventricular wedge preparations (21). However, studies of intact hearts have failed to provide evidence for transmural differences in repolarization (22). Thus, the genesis of T-wave on surface ECG may be largely due to the base-to-apex gradient with minimum contribution from the transmural gradient (1). The presence of strain T-wave may be accompanied with significant change of the electrical property in the myocardial cells in the whole left ventricle, which generates not only base-to-apex gradient but also the transmural gradient to some extent in the hypertrophied hearts. Actually, a previous in vitro study (3) found that the action potential duration in the subepicardium and midcardium becomes longer as LV hypertrophy progresses, and that the time-to-peak cell shortening also becomes longer. In contrast, the action potential duration in the subendocardium becomes shorter and the time-to-peak cell shortening becomes shorter, although the degree is an insignificant amount. In the present study, we found that the onset of myocardial relaxation in the subendocardium and subepicardium at the mid-LV posterior wall was almost coincident, and that in some patients the onset of subendocardial relaxation preceded that of subepicardial relaxation. These findings are consistent with those of the earlier animal study (3).

Clinical implications.   The present study is the first report regarding the transmural mechanics in normal and hypertrophied myocardium under clinical conditions. There are a lot of conditions with T-wave alteration such as myocardial hypertrophy, ischemia, and cardiac arrhythmias including the Brugada syndrome and long QT syndrome. We believe that our present method should be useful to investigate transmural electromechanical sequence of relaxation, and also contraction, and could provide new insights into the pathophysiology of these conditions.

We demonstrated the difference in the onset of myocardial relaxation between the subendocardium and subepicardium using echocardiography, without opening the chest and implanting crystals, as has been performed in some reports that focused on transmural mechanics using sonomicrometry with open-chest animals (1,2). The invasive method cannot be applied to humans. Moreover, the implantation of the crystals may cause local scarring and induce abnormal wall motion not only due to the implantation procedure, but also due to their weight and inertial properties. The thoracotomy itself can alter the temperature of the epicardial surface and change its action potential duration and T-wave polarity (23). Opening the pericardium could affect the whole cardiac motion and regional myocardial deformation. In contrast, the recent development of echocardiography has enabled the investigation of the transmural myocardial deformation in clinical settings (5,10–12).

We assumed that earlier myocardial relaxation of the subepicardium might facilitate the following relaxation of the subendocardium so that the early LV filling occurs efficiently. However, unfortunately, in this study, we could not find a significant association of the difference in TP- between the subendocardium and subepicardium with transmitral E-wave velocity (r = 0.011, p = 0.940). Further study will be needed using more sophisticated indexes of LV filling or relaxation.

Study limitations.   In the present study, we assessed myocardial strain only at the mid-posterior wall; therefore, our results may not apply to the other LV segments. Our findings may not relate to aortic stenosis, but may reflect the consequences of LV pressure load. We did not measure actual LV pressure when we obtained the echocardiographic data. The LV pressure and wall stress affect the myocardial strain profile. The difference in the onset of myocardial relaxation among the 4 groups may be caused by differences in the hemodynamic condition rather than differences in electrical properties, especially in the subendocardium. Despite these limitations, we consider that our method is a successful noninvasive technique for demonstrating the transmural sequence of myocardial relaxation.

We set the initial length to obtain instantaneous radial strain at 2 mm. A longer length would be advantageous for obtaining peak radial strain but a smaller length would be better for obtaining regional information. In the present study, we measured time-to-peak strain, which might be less affected by noise than peak strain even with a smaller initial length.

	Conclusions

Top Abstract Methods Results Discussion Conclusions REFERENCES

 
Myocardial relaxation of the subepicardium precedes that of the subendocardium at the mid-LV posterior wall in the normal human myocardium. In the hypertrophied myocardium with aortic stenosis, the onset of myocardial relaxation in the subendocardium is earlier than that in normal myocardium at the mid-LV posterior wall, whereas the onset in the subepicardium is later than that in the normal myocardium. In some patients with severe hypertrophy and strain T-wave, there is an inversion of the transmural sequence of the myocardial relaxation, compared with that in normal subjects.

^_* Reprint requests and correspondence: Dr. Satoshi Nakatani, Division of Functional Diagnostics, Department of Health Sciences, Osaka University Graduate School of Medicine, 1-7 Yamada-oka, Suita, Osaka 565-0871, Japan (Email: nakatani{at}sahs.med.osaka-u.ac.jp).

Manuscript received June 19, 2008; revised manuscript received November 6, 2008, accepted November 16, 2008.

	REFERENCES

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1. Sengupta PP, Khandheria BK, Korinek J, et al. Apex-to-base dispersion in regional timing of left ventricular shortening and lengthening J Am Coll Cardiol 2006;47:163-172.[Abstract/Free Full Text]
2. Ashikaga H, Coppola BA, Hopenfeld B, et al. Transmural dispersion of myofiber mechanics: implications for electrical heterogeneity in vivo J Am Coll Cardiol 2007;49:909-916.[Abstract/Free Full Text]
3. Bryant SM, Shipsey SJ, Hart G. Regional differences in electrical and mechanical properties of myocytes from guinea-pig hearts with mild left ventricular hypertrophy Cardiovasc Res 1997;35:315-323.[Abstract/Free Full Text]
4. Ashikaga H, Mickelsen SR, Ennis DB, et al. Electromechanical analysis of infarct border zone in chronic myocardial infarction Am J Physiol Heart Circ Physiol 2005;289:H1099-H1105.[Abstract/Free Full Text]
5. Maruo T, Nakatani S, Jin Y, et al. Evaluation of transmural distribution of viable muscle by myocardial strain profile and dobutamine stress echocardiography Am J Physiol Heart Circ Physiol 2007;292:H921-H927.[Abstract/Free Full Text]
6. Lang RM, Bierig M, Devereux RB, et al. Chamber Quantification Writing Group, American Society of Echocardiography's Guidelines and Standards Committee, European Association of Echocardiography Recommendations for chamber quantification: a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology J Am Soc Echocardiogr 2005;18:1440-1463.[CrossRef][Web of Science][Medline]
7. Quinones MA, Waggoner AD, Reduto LA, et al. A new, simplified and accurate method for determining ejection fraction with two-dimensional echocardiography Circulation 1981;64:744-753.[Abstract/Free Full Text]
8. Devereux RB, Alonso DR, Lutas EM, et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings Am J Cardiol 1986;57:450-458.[CrossRef][Web of Science][Medline]
9. Quinones MA, Otto CM, Stoddard M, et al. Doppler Quantification Task Force of the Nomenclature and Standards Committee of the American Society of Echocardiography Recommendations for quantification of Doppler echocardiography: a report from the Doppler Quantification Task Force of the Nomenclature and Standards Committee of the American Society of Echocardiography J Am Soc Echocardiogr 2002;15:167-184.[CrossRef][Web of Science][Medline]
10. Tanaka N, Tone T, Ono S, et al. Predominant inner-half wall thickening of left ventricle is attenuated in dilated cardiomyopathy: an application of tissue Doppler tracking technique J Am Soc Echocardiogr 2001;14:97-103.[CrossRef][Web of Science][Medline]
11. Sade LE, Severyn DA, Kanzaki H, et al. Second-generation tissue Doppler with angle-corrected color-coded wall displacement for quantitative assessment of regional left ventricular function Am J Cardiol 2003;92:554-560.[CrossRef][Web of Science][Medline]
12. Dohi K, Pinsky MR, Kanzaki H, et al. Effects of radial left ventricular dyssynchrony on cardiac performance using quantitative tissue Doppler radial strain imaging J Am Soc Echocardiogr 2006;19:475-482.[CrossRef][Web of Science][Medline]
13. Urheim S, Edvardsen T, Torp H, et al. Myocardial strain by Doppler echocardiography. Validation of a new method to quantify regional myocardial function. Circulation 2000;102:1158-1164.[Abstract/Free Full Text]
14. Bogaert J, Rademakers FE. Regional nonuniformity of normal adult human left ventricle Am J Physiol Heart Circ Physiol 2001;280:H610-H620.[Abstract/Free Full Text]
15. Goetz WA, Lansac E, Lim HS, et al. Left ventricular endocardial longitudinal and transverse changes during isovolumic contraction and relaxation: a challenge Am J Physiol Heart Circ Physiol 2005;289:H196-H201.[Abstract/Free Full Text]
16. Sengupta PP, Khandheria BK, Korinek J, et al. Left ventricular isovolumic flow sequence during sinus and paced rhythms: new insights from use of high-resolution Doppler and ultrasonic digital particle imaging velocimetry J Am Coll Cardiol 2007;49:899-908.[Abstract/Free Full Text]
17. Biederman RW, Doyle M, Yamrozik J, et al. Physiologic compensation is supranormal in compensated aortic stenosis: does it return to normal after aortic valve replacement or is it blunted by coexistent coronary artery disease?. An intramyocardial magnetic resonance imaging study. Circulation 2005;112:I429-I436.[Web of Science][Medline]
18. Park TH, Lakkis NM, Middleton KJ, et al. Acute effect of nonsurgical septal reduction therapy on regional left ventricular asynchrony in patients with hypertrophic obstructive cardiomyopathy Circulation 2002;106:412-415.[Abstract/Free Full Text]
19. Wilson FN, Macleod AG, Barker PS, Johnston FD. The determination and the significance of the areas of the ventricular deflections of the electrocardiogram Am Heart J 1934;10:46-61.[CrossRef][Web of Science]
20. Opthof T. In vivo dispersion in repolarization and arrhythmias in the human heart Am J Physiol Heart Circ Physiol 2006;290:H77-H78.[Free Full Text]
21. Antzelevitch C. Transmural dispersion of repolarization and the T wave Cardiovasc Res 2001;50:426-431.[Free Full Text]
22. Janse MJ, Sosunov EA, Coronel R, et al. Repolarization gradients in the canine left ventricle before and after induction of short-term cardiac memory Circulation 2005;112:1711-1718.[Abstract/Free Full Text]
23. Inoue M, Hori M, Kajiya F, et al. Theoretical analysis of T-wave polarity based on a model of cardiac electrical activity J Electrocardiol 1978;11:171-180.[CrossRef][Web of Science][Medline]

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