Dysoxia

Robin, Eugene D.

doi:10.1001/archinte.1977.03630190059015

Cited by 28 publications

(2 citation statements)

References 8 publications

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“…After coronary artery blockage, the downstream cardiomyocytes die and lead to myocardial infarction (MI), commonly known as heart attack [2 -4]. This subsequently results in expansion of the infarcted region, formation of scar tissues, left ventricular wall thinning and dilatation, loss of cardiac function, and eventually fatal heart failure (HF) [5][6][7][8][9][10][11][12]. Current therapies for HF provide modest symptom relief but fail in preventing dilation and improving long-term survival outcomes [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

“…However, they still face challenges with respect to limited reverse LV remodelling and long-term ventricular function or survival [17 -19]. Improvements in elastic support device development and their modes of application can only be done once ventricular mechanics and its post-MI alteration are better understood [5][6][7][8][9][10][11][12][17][18][19].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Epicardial prestrained confinement and residual stresses: a newly observed heart ventricle confinement interface

Shi

Liu

Copeland

et al. 2019

J. R. Soc. Interface.

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The heart epicardial layer, with elastin as the dominant component, has not been well investigated, specifically on how it contributes to ventricular biomechanics. In this study, we revealed and quantitatively assessed the overall status of prestraining and residual stresses exerted by the epicardial layer on the heart left ventricle (LV). During porcine heart wall dissection, we discovered that bi-layered LV surface strips, consisting of an epicardial layer and cardiac muscle, always curled towards the epicardial side due to epicardial residual stresses. We hence developed a curling angle characterization technique to intuitively and qualitatively reveal the location-dependency and direction-dependency of epicardial residual stresses. Moreover, by combining prestrain measurement and biaxial mechanical testing, we were able to quantify the epicardial prestrains and residual stresses on the unpressurized intact LV. To investigate the potential mechanical effect of epicardial prestraining, a finite-element (FE) model has been constructed, and we demonstrate that it is the prestraining of the epicardial layer, not the epicardial layer alone, providing an additional resistance mechanism during LV diastolic expansion and ventricular wall protection by reducing myocardial stress. In short, our study on healthy, native porcine hearts has revealed an important phenomenon—the epicardial layer, rich in elastin, acts like a prestrained ‘balloon’ that wraps around the heart and functions as an extra confinement and protection interface. The obtained knowledge fills a gap in ventricular biomechanics and will help design novel biomimicking materials or prosthetic devices to target the maintenance/recreation of this ventricle confinement interface.

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