Postinfarction rupture of the left ventricular free wall: Clinicopathologic correlates in 100 consecutive autopsy cases

Batts, Kenneth P.; Ackermann, D. Michael; Edwards, William D.

doi:10.1016/0046-8177(90)90010-3

Cited by 131 publications

(63 citation statements)

References 39 publications

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“…In vivo, most infarct ruptures occur in the first few days after infarction (25)(26)(27), whereas our earliest time point was 1 week. However, structural heterogeneity in healing myocardial infarcts certainly has at least one other important implication in this era of emerging cardiac regenerative therapies: cardiomyocytes have been shown to align with preexisting matrix (28), and heterogeneity in regenerated myocyte alignment could impair both electrical and mechanical functions of the myocardium.…”

Section: Structural Heterogeneity In Healing Rat Infarctsmentioning

confidence: 91%

Emergence of Collagen Orientation Heterogeneity in Healing Infarcts and an Agent-Based Model

Richardson

Holmes

2016

Biophysical Journal

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Spatial heterogeneity of matrix structure can be an important determinant of tissue function. Although bulk properties of collagen structure in healing myocardial infarcts have been characterized previously, regional heterogeneity in infarct structure has received minimal attention. Herein, we quantified regional variations of collagen and nuclear orientations over the initial weeks of healing after infarction in rats, and employed a computational model of infarct remodeling to test potential explanations for the heterogeneity we observed in vivo. Fiber and cell orientation maps were generated from infarct samples acquired previously at 1, 2, 3, and 6 weeks postinfarction in a rat ligation model. We analyzed heterogeneity by calculating the dot product of each fiber or cell orientation vector with every other fiber or cell orientation vector, and plotting that dot product versus distance between the fibers or cells. This analysis revealed prominent regional heterogeneity, with alignment of both fibers and cell nuclei in local pockets far exceeding the global average. Using an agent-based model of fibroblast-mediated collagen remodeling, we found that similar levels of heterogeneity can spontaneously emerge from initially isotropic matrix via locally reinforcing cell-matrix interactions. Specifically, cells that sensed fiber orientation at a distance or remodeled fibers at a distance by traction-mediated reorientation or aligned deposition gave rise to regionally heterogeneous structures. However, only the simulations in which cells deposited collagen fibers aligned with their own orientation reproduced experimentally measured patterns of heterogeneity across all time points. These predictions warrant experimental follow-up to test the role of such mechanisms in vivo and identify opportunities to control heterogeneity for therapeutic benefit.

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Section: Structural Heterogeneity In Healing Rat Infarctsmentioning

confidence: 91%

Emergence of Collagen Orientation Heterogeneity in Healing Infarcts and an Agent-Based Model

Richardson

Holmes

2016

Biophysical Journal

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“…Postinfarction VSD occurs in the apicoseptal wall more frequently after anterior infarction [8]. In addition, approximately 70 to 85 percent of LV aneurysms occurring following AMI with total occlusion of LAD are located in the apical or anterior walls [9,10].…”

Section: Discussionmentioning

confidence: 99%

Transcatheter Closure of a Large Postinfarction Ventricular Septal Defect Complicated With Perforation of Ventricular Aneurysm

Tai¹,

Wu²,

Lin³

et al. 2015

J Clin Exp Cardiolog

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Ventricular septal defect concurrent with left ventricular aneurysm is unusual in postinfarction patients. The complex anatomy is challenging for occluder deployment in transcatheter closure and associated with high risk of aneurysm perforation. We present a case of transcatheter closure of a large postinfarction ventricular septal defect with an Amplatzer septal occluder in a 71-year-old woman, complicated with aneurysm rupture and cardiac tamponade and corrected with surgical repair.

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“…В экспериментах доказано, что миокард восстанавли-вает свою нормальную прочность на 7-8-е сутки после ОИМ [10,12]. Это объясняет тот факт, что разрыв мио-карда, постинфарктный дефект межжелудочковой пере-городки (ДМЖП), отрыв сосочковой мышцы, РССЛЖ чаще всего возникают в указанные выше сроки.…”

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“…Ранний РССЛЖ развивается в течение первых 48 ч ОИМ и составляет 40-50% всех РССЛЖ [4,5,13], но ис-тинный процент более высокий, поскольку включает в себя и пациентов, умерших внезапно на догоспитальном этапе [12]. Поздний РССЛЖ возникает в сроки более 48 ч у пациентов, менее склонных к артериальной гипертонии (АГ), но испытывающих значительные физические на-грузки (кашель, рвота, чрезмерные усилия), что может яв-ляться основным триггером для возникновения дефекта миокарда [4].…”

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Successful experience of surgical treatment of postinfarction rupture of left ventricular free wall (brief literature review, case report)

Zybin¹,

Semagin²,

Хохлунов³

et al. 2015

Kardiol. serdechno-sosud. khir.

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Postinfarction rupture of the left ventricular free wall: Clinicopathologic correlates in 100 consecutive autopsy cases

Cited by 131 publications

References 39 publications

Emergence of Collagen Orientation Heterogeneity in Healing Infarcts and an Agent-Based Model

Emergence of Collagen Orientation Heterogeneity in Healing Infarcts and an Agent-Based Model

Transcatheter Closure of a Large Postinfarction Ventricular Septal Defect Complicated With Perforation of Ventricular Aneurysm

Successful experience of surgical treatment of postinfarction rupture of left ventricular free wall (brief literature review, case report)

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