EDITORIAL COMMENT
Non-ischemic infarct extension: A new type of infarct enlargement and a potential therapeutic target*
Mark B. Ratcliffe, MD*,*
* Division of Cardiothoracic Surgery, Department of Surgery, School of Medicine of the University of California–San Francisco and the San Francisco Veterans Affairs Medical Center, San Francisco, California, USA
* Reprint requests and correspondence: Dr. Mark B. Ratcliffe, VAMC Surgery 112D, San Francisco Veterans Affairs Medical Center, 4150 Clement Street, San Francisco, California 94121, USA.
mratcliffe{at}hotmail.com
In this issue of the Journal, Jackson et al. (1) describe infarct extension after anteroapical myocardial infarction (MI) in sheep that surprisingly occurs in the face of normal border zone (BZ) blood flow. Briefly, sheep were instrumented with an array of sonomicrometry crystals on a long-term basis. Crystals were placed within the area at risk, at the edge of the area at risk, and in the remote non-infarcted myocardium, and data were collected before and eight weeks after anteroapical MI (2). The BZ was defined as those chords that both remodeled (increase in chord length at end-systole) and had decreased function (decreased percent fractional shortening). Using these criteria, the BZ increased in size from 6 to 11 chords (of 20 total non-infarct chords) in the anterolateral left ventricular (LV) wall. Histology showed progressive fibrosis. This is demonstrated in Figure 6A of the Jackson et al. (1) article, in which tongues of fibrosis are seen infiltrating into the non-infarcted myocardium. At the edge of the advancing fibrosis were myocytes with pale cytoplasm and enlarged nuclei (myocytolysis) (Fig. 6C of Jackson et al. [1]) that the authors suggest are undergoing apoptosis.
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Non-ischemic infarct extension
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Infarct extension is secondary myocyte necrosis that occurs in the infarct BZ (3). Historically, the cause of infarct extension is BZ ischemia, and therapies have focused on reduction in myocardial energy expenditure (3). However, sheep do not have pre-formed intercoronary artery collaterals, and ligation of the left anterior descending (LAD) and second LAD diagonal causes a visually discrete, highly reproducible infarct (2). In the current study, Jackson et al. (1) confirmed the all-or-nothing nature of the BZ blood flow when, in a separate group of sheep, the authors showed blood flow in the BZ and infarct to be equal to remote and 25% of remote, respectively (Fig. 1 of Jackson et al. [1]). An enlarging area of BZ myocyte death, fibrosis, and dysfunction, taken together with a normal BZ blood supply, suggest that this is a new type of infarct enlargement that is neither expansion of the infarct proper nor further myocyte necrosis in an ischemic BZ. We suggest that this new entity be termed "non-ischemic infarct extension" (NIE). The NIE may contribute significantly to the development of ischemic cardiomyopathy. It may also be a target for new pharmacologic and surgical therapies. This is a remarkable finding that raises the following questions: - What are the mechanisms of non-ischemic BZ extension?
- Does non-ischemic BZ extension contribute to ischemic cardiomyopathy in humans?
- Are there possible drug and surgical therapies that might interrupt this process?
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Proposed mechanisms
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We suggest the following mechanism(s) for NIE (Fig. 1). Briefly, an increase in systolic BZ stress causes myocyte extension during isovolumic systole. This alteration in systolic strain initiates myocyte apoptosis and subsequently reduces BZ contractility. Alteration in systolic strain would also activate matrix metalloproteinases (MMP) and cause subsequent collagen breakdown and fibrosis. These latter effects contribute to thinning and stretching of the BZ wall. Border zone stress amplitude would increase, and the high stress zone would increase in size. The increase in high stress zone size progressively extends the infarct by drawing remote normally perfused myocardium into the BZ.
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Figure 1 Proposed mechanism of non-ischemic infarct extension. Dark gray = infarct; light gray = normal myocardium; transition = non-ischemic infarct extension. Note the progressive remodeling and infarction of the border zone (BZ) (normal blood flow). Note also the inverse effect of BZ contractility on stress. HTN = hypertension; LV = left ventricular; MI = myocardial infarction; MMP = matrix metalloproteinase.
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Increased BZ stress
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Ventricular wall stress, which cannot be directly measured, has traditionally been estimated with LaPlace’s law. However, localized shape change in and around the infarct, and regional changes in systolic and diastolic material properties (4), make the infarcted LV a mechanically complex structure. The use of LaPlace’s law is, therefore, not appropriate. On the other hand, the infarcted LV can now be accurately simulated with finite element models. For instance, Guccione et al. (5) recently constructed a three-dimensional finite element model from multiple short- and long-axis MRI slices of the sheep LV after anteroapical infarction. Midwall fiber strain and stress were predicted throughout the LV wall during isovolumic systole, while active stress development (contractility) in the BZ region and aneurysm stiffness were varied. Of note, when the aneurysm in this model had normal diastolic material properties, BZ contractility had to be reduced to 50% of that in regions remote from the aneurysm in order to reproduce stretching of BZ fibers during isovolumic systole (5). Finally, fiber stresses in the anterior and posterior BZs were increased by 50% and 65%, respectively (5).
With the exception of the study by Guccione et al. (5), the relative effects of cavity pressure, infarct, and BZ material properties and regional and global geometry on BZ wall stress are unknown. In general, reduction of cavity pressure and preservation of BZ wall thickness would be expected to reduce stress. The application of finite element techniques to hearts with differing infarct sizes, infarct locations, and amounts of remodeling has not been performed to date.
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Altered BZ strain
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We also know that BZ strain is altered after anteroapical MI. Moulton et al. (6) used MRI tissue tagging to study mechanical dysfunction in the BZ of the anteroapical sheep infarct model (2). Regional ventricular wall strains (8 to 12 weeks after transmural infarction) were calculated in BZ regions and regions remote from the aneurysm and compared with strains measured in corresponding regions from normal control sheep. The results demonstrated significant positive circumferential strains (lengthening) in the BZ regions during isovolumic systole. In a similar study, Kramer et al. (7) demonstrated that mechanical dysfunction in the BZ of LV aneurysms persists up to six months after transmural infarction.
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Apoptosis and collagen turnover
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Apoptosis is increased in the BZ of both humans and animals (8,9). Although BZ apoptosis may be multifactorial, there is mounting evidence that myocyte apoptosis can be initiated by mechanical stretch. Briefly, high-amplitude myocyte stretch in vivo is associated with myocyte apoptosis (10), increase in angiotensin II (Ang II), and up-regulation of Ang II receptors on the myocyte surface (11); and administration of the Ang II receptor 1 (AT1) blocker losartan inhibits myocyte apoptosis (12). Furthermore, amplitude-dependent myocyte stretch in vivo increases superoxide production, and the addition of reactive oxygen species (ROS) scavenger blocks the associated myocyte apoptosis (10).
Border zone hydroxyproline is increased fourfold (13), and collagen is increased 20-fold (6), after MI in sheep. The fact that MMP-1 and MMP-2 are increased between four- and eightfold in the BZ after MI (13) suggests a dynamic balance between collagen degradation and new collagen deposition. Although the pattern and type of collagen synthesis is influenced by local hormones and autacoids (tumor necrosis factor-alpha, Ang II, and endothelin-1), there is increasing evidence that mechanical stretch affects collagen turnover and the amount and type of collagen deposition. For instance, mechanical stretch of cardiac fibroblasts in vivo increases the ratio of type 3 to type 1 collagen (14). Mechanical stretch of cardiac fibroblasts in vivo also increases membrane-type MMP activity (15), and administration of a broad-spectrum MMP inhibitor attenuates early LV dilation after experimental MI in mice (16). These data suggest that collagen turnover, regulated by MMP activity, may be directly controlled by ventricular remodeling and wall stress.
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Importance to human ischemic cardiomyopathy
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Infarct extension occurs in 8.4% of patients after acute MI and has a hospital mortality more than four times higher than MI without extension (3). On the other hand, the incidence and risk associated with NIE is unknown. For example, NIE is likely to occur later than ischemic extension and to involve chronic and potentially undetectable levels of enzyme release. Separation of the infarct proper from new cell death with conventional imaging techniques may be impossible, although scans targeted at apoptosis show promise (17).
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Therapy
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Pharmacology.
A full discussion of how pharmacologic inhibitors of apoptosis, MMP activity, and fibrosis might affect non-ischemic infarct extension is well beyond the scope of this editorial. However, inhibition of AT1 with losartan and the use of ROS scavengers would seem reasonable. Also, broad MMP inhibitors, such as PD166793, that have successfully attenuated remodeling in the pacing tachycardia model of dilated cardiomyopathy would seem reasonable (18). Finally, any intervention that reduces afterload would decrease stress and strain within the BZ.
Surgery: Dor and Surgical Anterior Ventricular Endocardial Restoration (SAVER) LVremodeling operations.
Surgery may interrupt the development of NIE by reducing BZ stress. For instance, Dor (19) has used synthetic patches (patch aneurysmorraphy) sewn to the edges of the aneurysm neck after the perimeter was reduced by a pursestring suture. More recently, Athanasuleas et al. (20) have suggested that exclusion of non-contracting "akinetic" but potentially viable segments in dilated hearts after anterior MI is also beneficial (SAVER operation). There are several reports that document an increase in LV ejection fraction with aneurysm repair (21–23). Di Donato et al. (23) found that ejection fraction increased from 17% to 37% after patch aneurysmorraphy in patients with severely depressed preoperative ventricular function. However, ejection fraction is not a reliable measure of LV function (24), especially in operations that surgically remodel the LV (25,26).
Border zone stress may decrease, remain the same, or increase after aneurysm repair. For instance, Savage et al. (27) used the method of sonomicrometry array localization to measure regional deformation after aneurysm plication. Although longitudinal stress was not measured, Savage et al. (27) did note an increase in longitudinal dimensions and suggested that longitudinal stress was increased. Infarct plication may impose a high constant closing or residual stress. In addition, the suture line of the linear repair may act as a tether of potentially greater magnitude than the infarct itself and thereby create high local afterload against which the BZ must contract. It is possible that aneurysm plication fails to significantly reduce stress in the infarct BZ and that BZ function may therefore not recover.
Surgery: passive constraint operations.
Passive epicardial constraint of the infarcted myocardium may prevent BZ remodeling. Presumably, infarct constraint prevents infarct expansion and subsequent high BZ stress. The NIE fails to occur. Kelly et al. (28) demonstrated that a patch placed over the infarct area at risk one week before infarction will largely prevent infarct expansion and subsequent ventricular remodeling but will increase collagen content and decrease MMP-1 and MMP-2 activity in the BZ (13). These studies prove, in concept, that passive constraint may significantly affect BZ remodeling. However, the therapeutic window (time after infarct) has yet to be worked out. Radiofrequency (RF) infarct shrinking and infarct patch application have recently been shown to reduce and stabilize LV volume in sheep (29). These techniques, which have been used safely in humans (30), may reduce BZ stress and prevent infarct extension. However, a stress analysis of RF infarct heating has not been performed. Alternatively, the entire epicardial surface can be constrained. For instance, the ACORN (Acorn Cardiovascular Inc., St. Paul, Minnesota) cardiac support device has recently been shown to reduce LV volume and infarct area in an animal model of dilated cardiomyopathy when applied one week after infarction (31).
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Conclusions
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Non-ischemic infarct extension is a newly recognized type of infarct enlargement. We propose a mechanism in which increased systolic fiber stress causes myocyte extension (altered strain) during isovolumic systole. Altered strain induces neurohumoral and cytokine expression, activates MMPs, and initiates apoptosis, leading to decreased BZ contractility and BZ remodeling. As a consequence, stress amplitude is increased, and the size of the high-stress zone is increased. The increase in the high-stress-zone area progressively extends the infarct by drawing remote normally perfused myocardium into the BZ.
The importance of NIE is unclear but potentially significant. However, investigation in humans may be difficult, granted that separation of the infarct proper from new cell death with conventional imaging techniques may be impossible, although scans targeted at apoptosis show promise. Investigations in the sheep infarct model may hold the most promise in the short term.
In addition to conventional antihypertensive therapy, antiapoptotic and antifibrotic drug therapies hold promise. Also, both surgical infarct remodeling and passive constraint procedures may prevent non-ischemic extension.
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Footnotes
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This work has been supported by NIH R01 HL63348.
* 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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Top
Non-ischemic infarct extension
Proposed mechanisms