CLINICAL STUDY: ECHOCARDIOGRAPHIC METHODS
Higher myocardial strain rates duringisovolumic relaxation phase than duringejection characterize acutely ischemic myocardium
Cristina Pislaru, MD*,*,
Peter C. Anagnostopoulos, MD ,
James B. Seward, MD, FACC,
James F. Greenleaf, PhD* and
Marek Belohlavek, MD, PhD, FACC
* Department of Physiology and Biophysics Rochester, Minnesota, USA
Division of Cardiovascular Diseases Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota, USA
Manuscript received November 26, 2001;
revised manuscript received May 30, 2002,
accepted July 2, 2002.
* Reprint requests and correspondence: Dr. Cristina Pislaru, Mayo Clinic, Ultrasound Research Laboratory, 200 First Street SW, Rochester, Minnesota 55905, USA.
Pislaru.Cristina{at}mayo.edu
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Abstract
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OBJECTIVES: The aim of this study was to define an index that can differentiate normal from ischemic myocardial segments that exhibit postsystolic shortening (PSS).
BACKGROUND: Identification of ischemia based on the reduction of regional systolic function is sometimes challenging because other factors such as normal nonuniformity in contraction between segments, tethering effect, pharmacologic agents, or alterations in loading conditions can also cause reduction in regional systolic deformation. The PSS (contraction after the end of systole) is a sensitive marker of ischemia; however, inconsistent patterns have also been observed in presumed normal myocardium.
METHODS: Twenty-eight open-chest pigs underwent echocardiographic study before and during acute myocardial ischemia induced by coronary artery occlusion. Ultrasound-derived myocardial longitudinal strain rates were calculated during systole (SSR), isovolumic relaxation (IVRSR), and rapid filling (ESR) phases in both ischemic and normal myocardium. Systolic strain ( sys) and postsystolic strain (ps) were calculated by integrating systolic and postsystolic strain rates, respectively.
RESULTS: During ischemia, SSR, ESR, and sys in ischemic segments were significantly lower (in magnitude) than in nonischemic segments or at baseline. However, some overlap occurred between ischemic and normal values for all three parameters. At baseline, 18 of 28 animals had negative IVRSR (i.e., PSS) in at least one segment. During coronary artery occlusion, IVRSR became negative and larger in magnitude than SSR in all ischemic segments. The IVRSR/SSR and ps best differentiated ischemic from nonischemic segments.
CONCLUSIONS: In the presence of reduced regional systolic deformation, a higher rate of PSS than systolic shortening identifies acutely ischemic myocardium.
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Abbreviations and Acronyms
| | ECG | | electrocardiogram | | ESR | | peak strain rate during early filling phase | | max | | maximum strain | | ps | | postsystolic strain | | sys | | systolic strain | | IVRSR | | peak strain rate during the isovolumic relaxation phase | | LAD | | left anterior descending coronary artery | | LCX | | left circumflex coronary artery | | LV | | left ventricle/ventricular | | PSS | | postsystolic shortening | | RCA | | right coronary artery | | SSR | | peak strain rate during ejection | | SRI | | strain rate imaging | | t-SSR | | time to the onset of longitudinal shortening |
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Reduced myocardial systolic strain (sys) (i.e., deformation) and strain rate (i.e., rate of deformation) occur during regional ischemia (1–5). However, alterations in regional strain were also found in normal myocardium adjacent to an infarct or even in remote segments (6,7). Loading conditions, inotropic agents, and impairment in global function can also affect regional strain and strain rates (8). Moreover, the normal heterogeneity in segmental contraction has to be taken into account. To discriminate normal from abnormal, a common solution relies on comparison of the measured parameter with the normal range of its values (9). An alternative strategy is to use a normalized measure, that is, an index that discriminates normal from ischemic myocardium even if regional or global systolic function is reduced.
Postsystolic shortening (PSS), i.e., contraction after aortic valve closure, has long been described as a marker of ischemia (10–14) and potentially of viability (11,15,16). However, invasive or complex time-consuming methods for measurement of PSS have been used in those studies, thus limiting further clinical investigation. Doppler myocardial imaging and strain rate imaging (SRI) are new noninvasive techniques that can quantify regional motion and deformation rate, respectively, with high spatial and temporal resolution (17–19). Doppler-derived myocardial strain has been validated in vivo against sonomicrometry (4) and magnetic resonance imaging (20). Ischemic PSS has been identified using SRI as shortening occurring during the isovolumic relaxation phase (21). The extent of regions with ischemic PSS, as measured by SRI, has been shown to approximate the extent of the myocardium at risk (22). However, PSS has also been observed in presumably normal myocardium or adjacent to the ischemic area (11,23–26). The aim of this study was to define an index that can differentiate normal from ischemic myocardial segments that exhibit PSS.
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Methods
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Animal instrumentation.
Pigs weighing 30 to 60 kg were anesthetized with an infusion of ketamine, fentanyl, and amidate. Body temperature was kept constant with a heating pad. Following a median sternotomy, the heart was exposed in a pericardial cradle. All animals received intravenous heparin. After baseline echocardiographic measurements, total or subtotal coronary artery occlusion of the mid or distal portion of the left anterior descending (LAD), left circumflex (LCX), or right (RCA) coronary artery was induced by either ligation or using an angioplasty balloon catheter. Electrocardiograms (ECGs) and blood pressure were continuously monitored. Epicardial ultrasound scanning was performed at baseline and during acute ischemia. All animal experiments conformed to the Position of the American Heart Association on Research Animal Use. The study protocol was approved by the Institutional Animal Care and Use Committee of the Mayo Clinic.
Identification of the myocardium at ischemic risk
The location of the myocardium at ischemic risk was identified using either in vivo myocardial contrast echocardiography or dye staining of cardiac specimens. In 16 animals subjected to LAD ligature, contrast microbubbles (NC100100, Nycomed Imaging AS, Oslo, Norway) were infused intravenously, and ECG-gated end-diastolic frames were collected in three standard apical views using the second harmonic mode (1.7 MHz transmit/3.4 MHz receive, mechanical index 0.5). In the remaining animals, Evans blue solution was injected intravenously at the conclusion of the experiment with the coronary artery occlusion in place. In this way, myocardium at ischemic risk remained unstained while normally perfused myocardium stained blue.
After euthanasia, each heart was excised and cut orthogonal to the long axis of the left ventricle (LV) into 3 to 7-mm-thick slices. Slices were photographed using a digital camera, and the stained heart was reconstructed in the computer in three dimensions using dedicated software. The apical views were obtained from computer-generated sections through the heart (22).
Ultrasonic data acquisition and analysis
Tissue velocity data in three standard apical views (two-chamber, four-chamber, and apical long-axis) were collected from an epicardial approach using a commercial ultrasound scanner (GE Vingmed System FiVe, GE Medical Systems, Milwaukee, Wisconsin) and a 3.5-MHz transducer. Digital cineloops (>60 frames/s) of one to three cardiac cycles in sinus rhythm were collected at baseline and during occlusion. Data were transferred to a computer for offline analysis. Strain rate was calculated as the velocity difference between two points along the ultrasound beam divided by the distance between the points (5 mm in our analysis) (19). In our experiments assessing longitudinal deformation of the LV segments, negative strain rates reflected the rate of longitudinal shortening, and positive strain rates reflected the rate of longitudinal lengthening.
Guided by the location of the perfusion defect on either the stained cardiac specimen image or on the myocardial contrast echocardiography image, mean strain rate values were measured in two segments: 1) within the ischemic myocardium, and 2) within the normally perfused myocardium. Both segments were selected from the same LV wall (septal wall for LAD occlusions, inferior wall for RCA occlusions, and posterior wall for LCX occlusions). Care was taken to align the LV walls parallel with the ultrasound beam and to avoid the apex. The time of the aortic valve closure and mitral valve opening was identified from the underlying gray-scale images. End-diastole was considered at the peak R-wave of the ECG and end-systole at the time of the aortic valve closure. Peak strain rate values were measured during systolic (SSR), isovolumic relaxation (IVRSR), and early filling (ESR) phases (Fig. 1a). Peak SSR was measured during the ejection period, neglecting the occurrence of any early systolic bulging. The time to the onset of longitudinal shortening (t-SSR) was measured as the time from the ECG peak R-wave to the onset of SSR wave (Fig. 1a). Postsystolic-to-systolic strain rate ratio was obtained as IVRSR/SSR. This index was not calculated when the ischemic segments exhibited inverted (positive) SSR values (three animals). Strain was obtained by integrating strain rate values over time (19). The sys and maximum strain (max) were measured at end-systole and at the time of maximum deformation, respectively (Fig. 1b). Postsystolic strain (ps) was calculated as the difference between max and sys, and expressed as a percentage of max.
Statistical analysis
Statistical analysis was performed with SAS software (27). Differences between ischemic and nonischemic segments and between baseline and occlusion were compared using paired t tests and applying Bonferroni correction for multiple comparisons. The performance of strain and strain rate parameters, and the optimal cutoff points for detection of ischemia, were analyzed using receiver operating characteristic analysis. The normal distribution was tested and confirmed using the Shapiro-Wilk statistic. The results are presented as mean ± SD.
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Results
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A total of 35 experiments were performed; 7 animals died immediately after coronary artery occlusion. The remaining 28 pigs were subjected to LAD (n = 18), LCX (n = 5), or RCA (n = 5) occlusion. The average time from occlusion to the echocardiographic study was 20 ± 18 min. Mean heart rate did not change between baseline and occlusion (88 ± 19 beats/min and 90 ± 20 beats/min, respectively, p = 0.42), while mean blood pressure slightly decreased (100 ± 16 mm Hg and 91 ± 18 mm Hg, respectively; p < 0.05).
Strain and strain rate parameters during acute ischemia.
Figure 1 shows representative strain rate and strain curves in ischemic and nonischemic segments before and after LAD occlusion. Mean strain rate values in each cardiac phase from ischemic and nonischemic segments are shown in Table 1. During coronary artery occlusion, SSR and ESR were significantly reduced (in magnitude) in the ischemic but not in the nonischemic segments. Some overlap between values in nonischemic and ischemic segments was found for all parameters (Fig. 2). For instance, SSR varied between –1.69 s–1 and –0.51 s–1 at baseline and between –0.81 s–1 and 0.21 s–1during occlusion. The t-SSR significantly increased (with >25 ms) in the ischemic segment during occlusion in 25 animals and remained unchanged in the rest of the animals (Table 1).
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Figure 2 Regional strain rate parameters during baseline and acute ischemia. A significant change in regional peak strain rate during ejection (SSR), isovolumic relaxation (IVRSR) and early filling (ESR) occurred in the ischemic segments (solid square) but not in normally perfused segments (open circle). No overlap between normal and ischemic was found for IVRSR/SSR ratio. Values from all 28 animals and all three perfusion territories are displayed, except for IVRSR/SSR (25 animals).
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Baseline IVRSR was either positive (10 animals) or negative (18 animals). The segments that exhibited negative IVRSR (i.e., PSS) at baseline were apical septal (8 animals), apical inferior (2 animals), apical posterior (2 animals), basal septal (10 animals), basal posterior (5 animals), and basal inferior segments (2 animals). During occlusion, IVRSR in the ischemic segments changed from positive to negative (Fig. 1a) or increased in magnitude in those animals with negative IVRSR at baseline. The IVRSR/SSR was <1 at baseline in all segments. During occlusion, this index was consistently >1 in the ischemic but not in the nonischemic segments (Fig. 2). No differences in SSR, ESR, and IVRSR were observed at baseline between the apical and basal segments (p = 0.11, 0.13, and 0.91, respectively).
Strain parameters at baseline and during coronary artery occlusion are shown in Table 2 and Figure 3. As expected, sys was severely reduced (in magnitude) or even reversed (positive values), while ps significantly increased in the ischemic segments. The ps varied between 0% and 36% in normally perfused segments, and between 18% and 330% in ischemic segments.
Using the receiver operating characteristic analysis, the highest values for area under the curve were obtained for IVRSR/SSR (0.99), ps (0.99), and SSR(0.95). A cutoff value of 0.74 s–1 for SSR, 1.01 for IVRSR/SSR, and 41% for ps had 93%, 98%, and 96% sensitivity, and 87%, 100%, and 100% specificity to detect acute ischemia.
For practical application of our method, we developed custom software to generate parametric displays (28) of regional function based on both systolic and diastolic SRI parameters. Examples from two animals are shown in Figure 4. The SSR and IVRSR/SSR ratio were calculated for each segment and the results color-coded and overlaid on the gray-scale image. Ischemic myocardium is delineated as an area with low SSR and IVRSR/SSR >1.
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Figure 4 Parametric images generated from strain rate data in two animals, one subjected to left anterior descending (LAD) and the other to right coronary artery (RCA) occlusion. Each manually delineated left ventricular wall (a and e) was divided into 10 segments (to increase the spatial resolution). Peak systolic strain rates (SSR) (b and f) and postsystolic-to-systolic strain rate ratio (IVRSR/SSR) (c and g) were calculated and used to generate corresponding parametric images. Ischemic myocardium was outlined as the region with reduced SSR, and IVRSR/SSR >1. Note the reduced systolic strain rates in the border zones, while the IVRSR/SSR is <1 in these segments. Panels d and h show the extent of perfusion defect at myocardial contrast echocardiography or postmortem staining.
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Discussion
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This study demonstrates that myocardial segments with reduced systolic deformation caused by severe ischemia exhibit a higher rate of shortening during the isovolumic relaxation phase than during the ejection phase.
PSS in normal myocardium.
In our experiments, small magnitudes of shortening after the aortic valve closure were found in normal segments in apical and basal segments in 18 of 28 animals. This pattern of prolonged shortening (i.e., PSS) after the end of the mechanical systole may be due to physiologic asynchrony in depolarization and repolarization between segments (29) or to intersegmental interaction in contraction and relaxation rates (30). Similar delays in wall motion in basal segments have been observed using ultrasonic crystals and digitized cine-ventriculograms (11,23–26). The magnitude of PSS measured in those studies and considered normal varied between 6% and 15% of total systolic shortening. In our data, using 15% as a cutoff value for ps, five normal segments at baseline and two nonischemic segments during ischemia would be erroneously classified as ischemic (Fig. 3).
Changes in regional systolic parameters during acute ischemia
A significant reduction in SSR was found in the ischemic segments, which agrees with previous studies using SRI (1,2,5). In those studies and in our present study, there was an overlap between the SSR values for normal and ischemic segments, thereby limiting the sensitivity and specificity of this parameter for identifying regional ischemia in individual cases. The measured range and cutoff values of SSR for identifying ischemia will likely depend on the loading conditions (4), myocardial contractility state (8), segment analyzed (9), and type of strain measured (i.e., longitudinal, radial, or circumferential) (31). Widespread SSR values indicated that this parameter alone cannot reliably detect ischemia.
The delayed onset of systolic shortening, another objective marker of asynchrony during regional ischemia (32), was readily quantified by SRI. Although all ischemic segments presented PSS, not all manifested this asynchrony in the onset of contraction. This finding agrees with previous studies showing that PSS may be accounted for without invoking asynchrony of activation (30). The preserved onset of SSR may be related to the persistence of regional isovolumic contraction if the ischemic insult is less severe (33,34).
Changes in diastolic parameters during ischemia
Simultaneously with the reduction in SSR, there was a prominent increase in IVRSR in the ischemic segment in all animals and all ischemic segments. High IVRSR (generally >0.5 s–1) indicated that shortening of the ischemic segment occured at a faster rate than in a normal segment favored by the LV pressure fall and, consequently, segment unloading (35). Our finding of a significant increase in magnitude of ps during acute ischemia agrees with sonomicrometry studies (10,11,13). In addition, we now show that rates of deformation during PSS can be used to identify acute ischemia. Still, IVRSR alone did not discriminate normal from ischemic in all cases. Further studies are required to test the influence of loading on IVRSR. The mechanism of ischemic PSS is still under debate; altered local activation or electromechanical coupling, delayed myocardial relaxation, and passive elastic recoil have been proposed as potential mechanisms (11,30).
Postsystolic-to-systolic strain rate ratio.
The most important finding of this study was that although the SSR value was significantly reduced, the IVRSR was consistently higher than SSR in the acutely ischemic segments. Seven ischemic segments had SSR value higher (in magnitude) than the range of SSR values measured at baseline (Fig. 2); however, all those segments had IVRSR/SSR >1. The combined systolic and diastolic parameters (IVRSR/SSR and ps) had higher sensitivities and specificities than systolic parameters alone (such as SSR and sys) to detect ischemia.
Implications
Conventional assessment of wall motion abnormalities is subjective and experience-dependent. New high frame-rate quantitative methods, such as Doppler myocardial imaging and SRI, can measure regional function, thus avoiding errors induced by subjective visual evaluation. Moreover, the time of aortic valve closure is of critical importance when quantifying local function, because maximum shortening may be mistakenly reported as systolic shortening, although a substantial proportion may occur after the end of ejection. This correct timing can only be achieved by using high frame rates (at least 80 frames/s) (18). Clearly, shortening after the aortic valve closure will contribute nothing to ejection but can interfere with early filling. Early systolic bulging and PSS are markers of regional asynchrony and were easily identified and quantified using this high frame-rate quantitative method. Measurement of only end-systolic and end-diastolic wall thickness may mask important information available from the entire cardiac cycle (32,36). Although current quantitation with SRI is time-consuming, by using semiautomatic myocardial edge detection and constructing parametric displays of regional dysfunction, the ischemic region can be more objectively defined with less user interaction.
It has been suggested that the detection of regional diastolic abnormalities during demand ischemia may become a new paradigm in stress echocardiography for detection of coronary artery disease (37). Because dynamic and opposite changes in systolic shortening and PSS gradually progress during regional ischemia (5,10,13), their ratio should emphasize this transition. The utility of this index to detect inducible ischemia in patients needs to be further tested.
The PSS has been related to myocardial viability in animal and human studies (11,15,16). Whether our index could be a measure for regional viability remains to be tested. Our preliminary results suggest that IVRSR values decrease in magnitude during the progression from ischemic to transmural infarct (38).
Limitations
Strain rate is prone to noise because it is a gradient of velocities. Similar to other Doppler measurements, strain rate values are affected by the angle between the ultrasound beam and direction of wall motion; our index is a ratio and, therefore, the angle dependency may be markedly reduced. Myocardial blood flow was not measured in this study, and the mild reduction in SSR observed in some animals may be the result of persistent collateral blood flow or incomplete coronary artery occlusion. However, this limitation does not invalidate our findings. It has been shown that open-chest preparation (employed in this study for optimal imaging) may reduce diastolic strain rates (during early and late LV filling) but not SSR (39); however, similar findings on PSS were previously described in a closed-chest preparation (3,5). The effect of loading on strain rate parameters has to be further tested; we anticipate that loading will alter the strain rate ratio, predominantly by changes induced in the sys rates and strain (4,13). Whether our findings apply to a multivessel disease model needs to be confirmed. Finally, conditions associated with delayed local activation not necessary induced by ischemia, can also exhibit patterns of PSS (40).
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Conclusions
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This study demonstrates that acutely ischemic segments exhibit a higher rate of regional deformation during the isovolumic relaxation phase than during the ejection phase. Although significant reduction in systolic strain rate and strain parameters occurred during ischemia, some overlap between ischemic and normal values was observed. Similarly, the presence of PSS does not always identify ischemia because normal segments occasionally exhibit PSS of small magnitude. Therefore, a decision based solely on a single parameter alone is not always straightforward. The combination of both systolic and diastolic parameters best differentiated normal from ischemic segments.
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Acknowledgments
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The authors thank Sorin V. Pislaru, MD, PhD, for help with the statistical analysis, and Jennifer Milliken for her secretarial assistance.
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Footnotes
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Supported in part by grants from the National Institutes of Health (HL41046) and GE Medical Systems (Milwaukee, Wisconsin).
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J. G. Barra, A. J. Crottogini, P. Willshaw, E. C. Lascano, and R. H. Pichel
Contribution of myocardium hydraulic skeleton to left ventricular wall interaction and synergy in dogs
Am J Physiol Heart Circ Physiol,
August 1, 2004;
287(2):
H896 - H904.
[Abstract]
[Full Text]
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Abstract
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