Real-time strain rate echocardiographic imaging: Temporal and spatial analysis of postsystolic compression in acutely ischemic myocardium

doi:10.1067/mje.2001.110786

Journal of the American Society of Echocardiography

Volume 14, Issue 5, May 2001, Pages 360-369

https://doi.org/10.1067/mje.2001.110786 Get rights and content

Abstract

Postsystolic compression (PSC) is a sensitive indicator of regional left ventricular ischemic diastolic dysfunction. Quantitative assessment of compression patterns by strain rate imaging could determine the presence and spatial extent of PSC for the detection and analysis of acute ischemic diastolic dysfunction. With the use of a segmental left ventricular model, we evaluated time to compression/expansion crossover (T-CEC) in standard apical views. Data at baseline and after acute left anterior descending coronary artery occlusion were collected from 18 open-chest pigs. We found significant mean prolongation of T-CEC, ranging from 43.9 ± 48.6 ms to 110.8 ± 73.8 ms, in all apical segments and in 2 midventricular (anterior and anteroseptal) segments. Analysis of variance demonstrated that the prolonged T-CEC is spatially consistent with perfusion defect. The temporal and spatial analysis of T-CEC with the use of strain rate imaging is a new noninvasive technique for identification and topographic quantitation of ischemic diastolic dysfunction expressed by PSC. (J Am Soc Echocardiogr 2001;14:360-9.)

Section snippets

Animal model of acute ischemia

The study protocol was approved by the Institutional Animal Care and Use Committee of the Mayo Clinic. Twenty-two pigs (mean weight of 31.3 ± 6.3 kg) were used in the study. Each animal was sedated with intramuscular ketamine hydrochloride (25 mg/kg) and xylazine hydrochloride (2.0 mg/kg); anesthetized with 4 mg/kg of ketamine hydrochloride, 0.04 mg/kg of fentanyl citrate, and 0.15 mg/kg of etomidate per hour in intravenous infusion; intubated; and mechanically ventilated with a respirator

Results

Of the 22 experimental animals, 3 pigs died prematurely because of ventricular fibrillation after LAD occlusion, and 1 animal was excluded because of abnormal baseline LV function. In the remaining 18 animals, 34 paired apical views (of 54 pairs possible) with 204 baseline/ischemia paired segments were deemed suitable for temporal and spatial characterization of T-CEC at baseline and during ischemia. The span of prolonged T-CEC across the segments was compared with the extent of the perfusion

Discussion

In the present study, we used real-time SRI and identified patterns of myocardial relaxation asynchrony associated with PSC. We introduced a new parameter, T-CEC, for quantitative temporal and spatial characterization of PSC, obtained by measuring the duration of T-CEC and the segmental span of the prolonged T-CEC, respectively. We demonstrated that PSC patterns during acute ischemia are reflected by statistically significant prolongation of T-CEC. We also showed that anatomic segments with the

Acknowledgements

We thank Dr Sorin Pislaru (University of Leuven, Belgium) for assisting with statistical analysis, Julie M. Patterson for preparation of illustrations, and Jamie R. Schmeling for handling the manuscript. This work was supported in part by a Clinical Research Grant from the Mayo Clinic and Foundation. The ultrasonographic scanner and experimental software were provided courtesy of GE Medical Systems, Milwaukee, Wis. The contrast medium was provided courtesy of Nycomed Imaging AS, Oslo, Norway.

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An artificial neural network (ANN) is one type of these methods that adapts itself based on input signals and expected outcomes. As echocardiographic images depicting strain rate and strain have gone from a research tool [1–4] to their use in clinical practice [5–13], a number of different parameters have been suggested to assess myocardial functional status. These parameters include measurements of peak magnitudes of strain rates and strains [14,15] or of time intervals [16–18] during selected phases of the cardiac cycle, and can differentiate myocardial motion in a normal and ischemic heart, for example.
Echocardiographic strain waveforms are highly variable, so their interpretation is experience-dependent and subjective. We tested whether an artificial neural network (ANN) can distinguish between strain waveforms obtained at baseline and during experimentally induced acute ischemia. An open-chest model of coronary occlusion and acute ischemia was used in 14 adult pigs. Strain waveforms were obtained using a GE Vivid 7 ultrasound system. An ANN design was implemented in ${MATLAB}^{®}$ , and backpropagation and “leave-one-out” processes were used to train and test it. Specificity of 86% and sensitivity of 87% suggest that ANNs could aid in diagnostic prescreening of echocardiographic strain waveforms.
Mechanisms of Postsystolic Thickening in Ischemic Myocardium: Mathematical Modelling and Comparison With Experimental Ischemic Substrates
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Since the introduction of echocardiographic deformation (strain-rate) imaging, there has been a renewed interest in regional deformation of the myocardium in various ischemic pathologic conditions (D’hooge et al. 2000; Sutherland et al. 2006). The high temporal resolution of this technique makes it possible to identify fast events in thickening/lengthening of the myocardium (Kukulski et al. 2002; Belohlavek et al. 2001). A specific feature that has been described in several pathologies, as well as in normal individuals, under certain circumstances, is postsystolic deformation.
In the setting of regional ischemia, the “at-risk” myocardium exhibits a flow-related reduction in systolic thickening with a concomitant development of abnormal thickening after aortic valve closure (postsystolic thickening [PST]). With the introduction of high time–resolution ultrasonic-based strain/strain-rate imaging, this short lived phenomenon can be measured accurately in the clinical setting. The mechanisms underlying this ischemia-related PST are poorly understood and both active and passive etiologies have been proposed. This study aims at elucidating the potential mechanisms behind PST in the intact heart. A theoretical model, describing active force development, elasticity and segment interaction has been developed to simulate radial deformation during systole and iso-volumetric relaxation. Simulation results have been compared with experimental deformation curves obtained from postero-basal segments of a pig model undergoing varying controlled ischemic challenges. Three forms of regional ischemia could be simulated by varying the model parameters of the ischemic segments: (i) chronic regional hypo-perfusion (reduced and prolonged active force development; preserved elasticity); (ii) acute short-lived ischemia—temporary vessel occlusion (no active force development; preserved elasticity); and (iii) chronic myocardial infarction (no active force development; decreased elasticity). For all ischemic substrates, the simulated curves closely correlate to the deformation measured in the corresponding porcine models without the need for active force development during the occurrence of PST. This suggests that segment interaction is the key determinant in the development of PST. Thus, in all instances, at the time of its manifestation, ischemia-related PST could be explained in a unified way as a passive phenomenon that was the result of elastic segment interaction. Its occurrence originates from the end-systolic inhomogeneous state where neighboring segments have a different wall thickness. The occurrence of these differences at end-systole depends on the presence of regional differences within the ventricle in the magnitude and duration of the developed contraction force during the first part of systole, the elasticity of the ischemic segment and the left-ventricular pressure. (E-mail: [email protected])
Effect of Medical Therapy for Heart Failure on Segmental Myocardial Function in Patients With Ischemic Cardiomyopathy
2007, American Journal of Cardiology
Citation Excerpt :
Thus, the average time interval between segments contracting during systole and those with postsystolic shortening decreased by >50% (from 136 to 61 ms). Postsystolic shortening is detrimental to LV function because it fails to contribute to stroke volume and also interferes with early diastolic LV filling.5 In addition, segments that start contracting late in systole (usually ischemic and dysfunctional) contract against an augmented pressure produced by the earlier contraction of normal segments, and this may also be detrimental to their contraction.
The adjustment of medications and dosages to the needs of individual patients with heart failure is mostly intuitive, but even when their effect on global myocardial function is measured by classic indexes, their effect on segmental function is overlooked. This study was conducted to assess the feasibility of using echocardiographic myocardial strain imaging to evaluate the effect of medication on global and segmental function in 21 ambulatory patients with heart failure (mean age 65 ± 11 years) who had echocardiographic studies performed before and 2 hours after ingesting their regular morning medications. The ejection fraction, global and regional strain, and time to regional peak strain were compared between the 2 examinations. Medication induced no significant changes in mean ejection fraction (28.6 ± 7.8% to 27.5 ± 9.9%) and mean global strain (−9.5 ± 3.6% to −9.8 ± 3.2%). Changes in segmental strain depended on baseline function: normal segments (peak strain more negative than −12%) deteriorated (−15.5 ± 2.7% to −13.7 ± 4.6%, p <0.0001), but dysfunctional segments (peak strain less negative than −8%) improved (−5.3 ± 2.0% to −7.4 ± 4.3%, p <0.0001). Medication also improved segmental synchronization: average time to peak strain of segments in which peak strain was attained before aortic valve closure increased (325 ± 69 to 375 ± 100 ms, p <0.0001), but that of segments with postsystolic shortening at baseline decreased (451 ± 93 to 435 ± 93 ms, p <0.006). Thus, the time interval between time to peak strain of segments with systolic and post-systolic shortening at baseline was halved after medication. In conclusion, medications for heart failure induced an increase in the echocardiographically determined peak strain of myocardial segments with impaired function at baseline but decreased the peak strain of normally contracting segments. Medications also improved the synchronization of myocardial contraction. Neither the global ejection fraction nor global strain reflected these changes. Thus, medication tended to improve the homogeneity of left ventricular contraction.
Analysis of Postsystolic Myocardial Thickening Work in Selective Myocardial Layers During Progressive Myocardial Ischemia
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Citation Excerpt :
In recent years, strain rate echocardiography based on myocardial velocities was used to detect psT. Using an experimental model of acute ischemia, we previously reported that the topographic extent of delayed relaxation matches the extent of perfusion defect,28 and that a higher strain rate during the IVRT interval, ie, higher postsystolic strain rate, than systolic strain rate characterizes acutely ischemic myocardium.29 Some investigators used the ratio of postsystolic strain to peak systolic strain to quantify psT and the transmurality of ischemic necrosis.26,30
Myocardial function is transmurally heterogeneous. Postsystolic work may functionally reflect ischemic but viable myocardium. We calculated systolic and postsystolic regional myocardial work index (RMWi) in subendocardial and subepicardial layers of myocardium supplied by a slowly occluding coronary artery.
Progressive stenosis of the left anterior descending coronary artery lasting 11 ± 5 days (end point) was induced in 10 dogs, and pressure-strain loops were obtained from subendocardial and subepicardial layers of apical and middle anterior segments by intracardiac ultrasound.
At baseline, the RMWi was significantly higher (P < .05) in the subendocardial layer. At the end point, there was no significant change in the RMWi in ischemic myocardium; however, the postsystolic RMWi was higher (P < .05) in the subendocardial layer and accompanied a decrease in subendocardial myocardial blood flow, although viability was largely maintained.
A significant subendocardial postsystolic RMWi at rest suggests an impending ischemic injury in coronary artery disease when segmental function is still preserved.
Detection of Significant Stenotic Lesions in the Left Anterior Descending Coronary Artery Using Adenosine Triphosphate Stress Strain Imaging: Comparison with Coronary Flow Velocity Reserve Measurement Using Transthoracic Doppler Echocardiography
2006, Journal of the American Society of Echocardiography
To evaluate the usefulness of adenosine triphosphate stress strain imaging for detecting significant coronary artery disease in the left anterior descending coronary artery (LAD), 34 patients underwent coronary flow velocity reserve measurement in the distal LAD and adenosine triphosphate stress strain imaging simultaneously. Time to peak strain (TPS) was measured in the apical septal segment. TPS ratio was obtained as the ratio between TPS at adenosine triphosphate stress and at baseline. TPS ratio in 11 patients with LAD lesions was significantly greater than that in 23 patients without LAD lesions (1.24 ± 0.17 vs 0.92 ± 0.12, respectively, P < .0001). With a cut-off value greater than or equal to 1.1 for the TPS ratio and less than 2.0 for the coronary flow velocity reserve, diagnostic accuracy for the presence of significant LAD lesions were 88% and 82%, respectively. In conclusion, strain imaging can differentiate ischemic and nonischemic myocardium accurately comparable with coronary flow velocity reserve measurement.

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^*: This work was supported in part by a Clinical Research Grant from the Mayo Clinic and Foundation. The ultrasonographic scanner and experimental software were provided courtesy of GE Medical Systems, Milwaukee, Wis. The contrast medium was provided courtesy of Nycomed Imaging AS, Oslo, Norway.

^**: Reprint requests: Dr Marek Belohlavek, Translational Ultrasound Research, Mayo Clinic and Foundation, 200 First Street SW, Rochester, Minn 55905 (E-mail: [email protected]).

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Original ArticlesReal-time strain rate echocardiographic imaging: Temporal and spatial analysis of postsystolic compression in acutely ischemic myocardium*,**

Abstract

Section snippets

Animal model of acute ischemia

Results

Discussion

Acknowledgements

J Am Soc Echocardiogr

J Am Soc Echocardiogr

J Am Soc Echocardiogr

Am Heart J

J Am Soc Echocardiogr

J Am Coll Cardiol

Post-systolic shortening: a marker of potential for early recovery of acutely ischemic myocardium in the dog

Cardiovasc Res

The influence of preload on post-systolic shortening in ischemic myocardium

Eur J Anaesthesiol

Post-ejection wall thickening as a marker of successful short term hibernation

Cardiovasc Res

Transmural myocardial deformation in the ischemic canine left ventricle

Circ Res

Diastolic dysfunction on myocardial energetics

Eur Heart J

Energetic basis for reduced contractile reserve in isolated rat hearts

Am J Physiol

Diastolic dysfunction in hypertensive heart disease is associated with altered myocardial metabolism

Circulation

Impact of ischemia on diastolic function: clinical relevance and recent Doppler echocardiographic insights

Eur J Anaesthesiol

Digital subtraction high-frame-rate echocardiography in detecting delayed onset of regional left ventricular relaxation in ischemic heart disease

Circulation

Echocardiographic functional images based on tissue velocity information

Herz

Original Articles
Real-time strain rate echocardiographic imaging: Temporal and spatial analysis of postsystolic compression in acutely ischemic myocardium*,**