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J Am Coll Cardiol, 2004; 44:1672-1674, doi:10.1016/j.jacc.2004.07.024 © 2004 by the American College of Cardiology Foundation |
Department of Cardiology, St. George's Hospital, London, United Kingdom
* Reprint requests and correspondence: Prof. George R. Sutherland, Department of Cardiology, Atkinson Morley Wing, St. George's Hospital, Blackshaw Road, London, SW17 0QT, United Kingdom (Email: george.sutherland{at}stgeorges.nhs.uk).
)/strain rate (SR) imaging has been shown to be a more sensitive technique for quantifying regional myocardial deformation compared with other standard cardiac imaging modalities. With its high sampling rate (typically >200 samples/s), it can resolve two parameters that represent systolic deformation: regional strain and SR (1). These clinical data sets offer the equivalent of the high-resolution deformation information that usually is obtainable only by implanting intramyocardial microcrystals in the experimental environment. Thus, it should not be surprising that this new ultrasound technique is being used to transfer the concepts of flow related-changes in regional deformation, first described in animal models (2–4), to the clinic. The experimental article by Yip et al. (5) published in this issue of the Journal adds important new data to the rapidly growing literature, confirming the validity of using this new ultrasound technique to detect both resting and stress-induced abnormalities in deformation that characterize each ischemic substrate and its flow reserve (using a low-dose dobutamine infusion). Before discussing the clinical implications of the article by Yip et al. (5), it is perhaps best to review the previous work (both experimental and clinical) that also supports the clinical use of ultrasound-based deformation imaging in defining an ischemic substrate.
For normal myocardium, peak systolic SR may be used to represent regional contractile function, whereas end-systolic strain (although related to contractility) is a more load-dependent parameter (6). In fact, regional peak systolic SR currently is the closest approximation to local contractility that is measurable in the clinical setting because this represents the rate of wall thickening during early contraction when loading is optimal. In previous experimental studies, Derumeaux et al. (7), Jamal et al. (8,9), and Weidemann et al. (10) have demonstrated for normal myocardium, the complex interaction of acute modulations in regional flow with changes in deformation. In this regard, the findings of Yip et al. (5) complement and extend those of Jamal et al. (8), who examined the complex interaction of changes in deformation and flow in post-ischemic myocardial segments with differing flow reserves.
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Acute ischemia: Experimental findings |
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 Top Acute ischemia: Experimental... Unmasking the ischemic...Deformation in infarcted...Transferring experimental...References |
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. After aortic valve closure, acutely ischemic myocardium continued to thicken, resulting in the phenomenon of delayed peak thickening (post-systolic thickening [PST]). Occlusion release after 30 s allowed deformation indices to normalize. Subsequent experimental studies have shown that the distribution of ischemic PST is spatially consistent with the myocardium at risk (11,12). However, debate exists whether such ischemia-induced PST represents an active or passive event. Skulstad et al. (13) have claimed that ischemic PST represented actively contracting myocardium and, therefore, potentially viable myocardium. However, Claus et al. (14), by combining mathematical modeling with experimental data, suggested that ischemic PST is a purely passive phenomenon as a result of the interaction of ischemic with surrounding nonischemic segments. The findings of Bito et al. (15), who examined contractile dysfunction in hibernating cells, would further support the explanation of PST proposed by Claus et al. (14). |
Unmasking the ischemic substrate: The role of an incremental dobutamine challenge |
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TopAcute ischemia: Experimental...Unmasking the ischemic...Deformation in infarcted...Transferring experimental...References |
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/SR parameters, demonstrated that as regional flow was progressively decreased, systolic thickening was progressively reduced whereas PST concomitantly increased, thus confirming that changes in regional systolic SR and parameters paralleled stepwise reductions in coronary flow. In this model, (with no inherent flow reserve), an incremental infusion of dobutamine failed to induce an increase in end-systolic , whereas PST values increased progressively.
In the same model, the response of two ischemic substrates (stunned vs. chronic ischemia) to an incremental dobutamine infusion was compared. At rest, stunned segments (i.e., post-ischemic segments with flow reserve) had the same abnormal deformation characteristics as segments with ongoing ischemia (ischemic segments with reduced resting flow and very limited or no flow reserve). Thus, both chronically ischemic and "stunned" segments were characterized by a decrease in the magnitude of systolic and an increase in PST. However, the response to an incremental low-dose dobutamine infusion differentiated stunned from ischemic myocardium. During the incremental infusion, stunned myocardium tended to normalize the abnormal resting strain curve. "Normalization" was characterized by a return in end-systolic strain to normal or near-normal values with a concomitant reduction in the percentage of PST. This tendency toward normalizing the curve was indicative of adequate (or near-adequate flow reserve). In contrast, chronically ischemic myocardium with inadequate flow reserve was characterized by a further reduction in end-systolic strain during the infusion and an increase in percentage of PST. These latter findings would indicate a worsening of the ischemia during the dobutamine challenge.
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Deformation in infarcted segments |
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TopAcute ischemia: Experimental...Unmasking the ischemic...Deformation in infarcted...Transferring experimental...References |
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Transferring experimental findings to clinical practice |
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TopAcute ischemia: Experimental...Unmasking the ischemic...Deformation in infarcted...Transferring experimental...References |
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However, although in clinical practice the close correlation of changes in regional perfusion with changes in regional deformation holds good for acute and chronic regional ischemia, both at rest and during a dobutamine infusion, the same does not hold true for either regional hibernation or for myocardium that has been acutely infarcted (either transmurally or partially) but reperfused by primary angioplasty. In the latter situation, acute wall edema will prevent the expression of any residual contractile function because intramural edema is incompressible. In regional hibernation, the myocardium has chronically depressed function, which is unrelated to flow. In both these substrates, changes in deformation are not tightly linked to changes in flow, and both parameters must be measured to define the ischemic substrate. In contrast, in all other ischemic substrates, regional perfusion can be inferred by measuring the combination of resting deformation parameters and their response to a dobutamine infusion.
Thus, the article by Yip et al. (5) further confirms and extends existing data. It confirms the findings of Jamal et al. (8,9) but differs in that Yip et al. (5) used microspheres to determine changes in flow induced by a dobutamine infusion in the presence of a nonocclusive coronary narrowing, which in turn adds more weight to the concept that in clinical practice it may be more appropriate to measure functional, rather than perfusion, indices to define an ischemic substrate. Ultrasonic deformation imaging can now be used in the clinic to determine the nature of an ischemic substrate, the adequacy of its flow reserve, and the resolution of the ischemic changes after appropriate therapy. However, it must be remembered that deformation indices should only be used in those ischemic substrates where function and perfusion remain tightly coupled.
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Footnotes |
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* Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. 
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References |
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TopAcute ischemia: Experimental...Unmasking the ischemic...Deformation in infarcted...Transferring experimental...References |
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