Regional Cardiac Dilatation after Acute Myocardial Infarction

Eaton, Leland W.; Weiss, James L.; Bulkley, Bernadine H.; Garrison, John B.; Weisfeldt, Myron L.

doi:10.1056/nejm197901113000202

Cited by 552 publications

(108 citation statements)

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“…29 There was no significant *To test reproducibility of landmark localization only, the computer produced 128 equally spaced points around the left ventricular circumference, not 16. intra-reader variation for segment length or myocardial thickness, or inter-reader variation for segment length.…”

Section: Analysis Of Datamentioning

confidence: 99%

Two-dimensional echocardiography and infarct size: relationship of regional wall motion and thickening to the extent of myocardial infarction in the dog.

Lieberman¹,

Weiss²,

Jugdutt³

et al. 1981

Circulation

527

136

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SUMMARY To study endocardial wall motion and thickness as indexes of infarction, we used two-dimensional echocardiography to examine regional percentages of systolic wall thickening (%Th) and endocardial motion (%EM) in infarcted canine hearts. Thirteen dogs were studied 48 hours after occlusion of the circumflex or left anterior descending coronary artery. Two-dimensional echocardiographic cross sections obtained every 16 msec at 1-cm intervals from apex to base in an open-chest, anesthetized preparation were analyzed with a computer-aided contouring system for quantification of segmental %EM and %Th at 16 equally spaced points per slice. Slices corresponding to each two-dimensional echocardiographic cross section were examined pathologically for evidence of infarction.Comparing histologically infarcted with distant normal zones in each slice, %Th and %EM both yielded clear separation with little overlap (-12.5% infarcted vs 37.4% normal for thickness; -11.3 vs 25.7% for motion, p << 0.001 for both). Endocardial motion was less precise than thickening, however, in distinguishing infarct from either distant normal zones or zones directly adjacent to infarct.Although wall thickening was useful in separating out true subendocardial infarct, change in systolic thickening was not accurate in detecting the transmural extent of infarction. In 827 individual two-dimensional echocardiographic segments with varying degrees of transmural involvement, segments with 1-20% extent of transmural infarction showed reduced thickening compared with noninfarcted segments (39.9 vs 15.2%, p < 0.001), whereas myocardial segments with 21-100% transmural infarction showed systolic thinning (-8.9 to -13.3%). There was no significant augmentation in the severity of systolic thinning as the extent of transmural infarction increased from 21% to 100%.We conclude that: (1) Wall motion abnormalities are less precise than thickening in discriminating between infarcted and noninfarcted zones and could lead to overestimation of infarct size. (2) There is an abrupt deterioration in systolic thickening in segments containing more than 20% transmural extent of infarction. (3) There is no significant augmentation in the degree of systolic thinning as the transmural extent of infarct increases from 21% to 100%. This "threshold" phenomenon may therefore preclude accurate estimation of infarct size by two-dimensional echocardiography. (4

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Section: Analysis Of Datamentioning

confidence: 99%

Two-dimensional echocardiography and infarct size: relationship of regional wall motion and thickening to the extent of myocardial infarction in the dog.

Lieberman¹,

Weiss²,

Jugdutt³

et al. 1981

Circulation

527

136

View full text Add to dashboard Cite

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“…Early infarct expansion or stretching has been associated with poor long-term prognosis [2][3][4] and has been identified as the mechanical phenomenon that initiates and sustains the process of adverse post-MI LV remodeling that leads to heart failure [5][6][7][8][9][10]. Infarct expansion causes abnormal stress distributions in myocardial regions outside the infarction, especially in the adjacent border zone (BZ) region, putting this region at a mechanical disadvantage.…”

Section: Introductionmentioning

confidence: 99%

Injectable Acellular Hydrogels for Cardiac Repair

Tous

Purcell

Ifkovits

et al. 2011

J. of Cardiovasc. Trans. Res.

152

136

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Injectable hydrogels are being developed as potential translatable materials to influence the cascade of events that occur after myocardial infarction. These hydrogels, consisting of both synthetic and natural materials, form through numerous chemical crosslinking and assembly mechanisms and can be used as bulking agents or for the delivery of biological molecules. Specifically, a range of materials are being applied that alter the resulting mechanical and biological signals after infarction and have shown success in reducing stresses in the myocardium and limiting the resulting adverse left ventricular (LV) remodeling. Additionally, the delivery of molecules from injectable hydrogels can influence cellular processes such as apoptosis and angiogenesis in cardiac tissue or can be used to recruit stem cells for repair. There is still considerable work to be performed to elucidate the mechanisms of these injectable hydrogels and to optimize their various properties (e.g., mechanics and degradation profiles). Furthermore, although the experimental findings completed to date in small animals are promising, future work needs to focus on the use of large animal models in clinically relevant scenarios. Interest in this therapeutic approach is high due to the potential for developing percutaneous therapies to limit LV remodeling and to prevent the onset of congestive heart failure that occurs with loss of global LV function. This review focuses on recent efforts to develop these injectable and acellular hydrogels to aid in cardiac repair.

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“…Early infarct expansion or stretching has been associated with poor long-term prognosis (2)(3)(4) and has been identified as the mechanical phenomenon that initiates and sustains the process of adverse post-MI LV remodeling that leads to heart failure (5-10). Infarct expansion causes abnormal stress distribution in myocardial regions outside the infarction, especially in the adjacent borderzone region, putting this region at a mechanical disadvantage.…”

mentioning

confidence: 99%

Injectable hydrogel properties influence infarct expansion and extent of postinfarction left ventricular remodeling in an ovine model

Ifkovits

Tous

Minakawa

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

276

273

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A recent trend has emerged that involves myocardial injection of biomaterials, containing cells or acellular, following myocardial infarction (MI) to influence the remodeling response through both biological and mechanical effects. Despite the number of different materials injected in these approaches, there has been little investigation into the importance of material properties on therapeutic outcomes. This work focuses on the investigation of injectable hyaluronic acid (MeHA) hydrogels that have tunable mechanics and gelation behavior. Specifically, two MeHA formulations that exhibit similar degradation and tissue distribution upon injection but have differential moduli (∼8 versus ∼43 kPa) were injected into a clinically relevant ovine MI model to evaluate the associated salutary effect of intramyocardial hydrogel injection on the remodeling response based on hydrogel mechanics. Treatment with both hydrogels significantly increased the wall thickness in the apex and basilar infarct regions compared with the control infarct. However, only the higher-modulus (MeHA High) treatment group had a statistically smaller infarct area compared with the control infarct group. Moreover, reductions in normalized end-diastolic and end-systolic volumes were observed for the MeHA High group. This group also tended to have better functional outcomes (cardiac output and ejection fraction) than the low-modulus (MeHA Low) and control infarct groups. This study provides fundamental information that can be used in the rational design of therapeutic materials for treatment of MI.L eft ventricular (LV) remodeling caused by a myocardial infarction (MI) is responsible for almost 70% of the 5 million cases of heart failure that have occurred in the United States in recent years (1). Early infarct expansion or stretching has been associated with poor long-term prognosis (2-4) and has been identified as the mechanical phenomenon that initiates and sustains the process of adverse post-MI LV remodeling that leads to heart failure (5-10). Infarct expansion causes abnormal stress distribution in myocardial regions outside the infarction, especially in the adjacent borderzone region, putting this region at a mechanical disadvantage. With time, increased regional stress is the impetus for several maladaptive biologic processes, such as myocyte apoptosis and matrix metalloproteinase activation, that inherently alter the contractile properties of normally perfused myocardium (11,12). Once initiated, these maladaptive processes lead to a heart failure phenotype that is difficult to reverse by medical or surgical means.We have demonstrated that ventricular restraint early after MI reduces infarct expansion and limits long-term global LV remodeling in large-animal infarction models (10, 13-16). To circumvent the surgical placement of restraining devices early post-MI, our group and others have begun to explore the use of injectable materials to limit infarct expansion and normalize the regional stress distribution (17-26). Such an approach offers th...

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Regional Cardiac Dilatation after Acute Myocardial Infarction

Cited by 552 publications

References 0 publications

Two-dimensional echocardiography and infarct size: relationship of regional wall motion and thickening to the extent of myocardial infarction in the dog.

Two-dimensional echocardiography and infarct size: relationship of regional wall motion and thickening to the extent of myocardial infarction in the dog.

Injectable Acellular Hydrogels for Cardiac Repair

Injectable hydrogel properties influence infarct expansion and extent of postinfarction left ventricular remodeling in an ovine model

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