Background: The role of posterior papillary muscle anchoring (PPMA) in the management of chronic ischemic mitral regurgitation (CIMR) is controversial. We studied the effect of anchoring point direction and relocation displacement on left ventricular (LV) regional myofiber stress and pump function.
Methods: Previously described finite element models of sheep 16 weeks after posterolateral myocardial infarction (MI) were used. True-sized mitral annuloplasty (MA) ring insertion plus different PPM anchoring techniques were simulated. Anchoring points tested included both commissures and the central anterior mitral annulus; relocation displacement varied from 10% to 40% of baseline diastolic distance from the PPM to the anchor points on the annulus. For each reconstruction scenario, myofiber stress in the MI, border zone, and remote myocardium as well as pump function were calculated.
Results: PPMA caused reductions in myofiber stress at end-diastole and end-systole in all regions of the left ventricle that were proportional to the relocation displacement. Although stress reduction was greatest in the MI region, it also occurred in the remote region. The maximum 40% displacement caused a slight reduction in LV pump function. However, with the correction of regurgitation by MA plus PPMA, there was an overall increase in forward stroke volume. Finally, anchoring point direction had no effect on myofiber stress or pump function.
Conclusions: PPMA reduces remote myofiber stress, which is proportional to the absolute distance of relocation and independent of anchoring point. Aggressive use of PPMA techniques to reduce remote myofiber stress may accelerate reverse LV remodeling without impairing LV function.
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http://dx.doi.org/10.1016/j.athoracsur.2014.04.077 | DOI Listing |
Front Physiol
December 2024
Emergency Center, Hubei Clinical Research Center for Emergency and Resuscitaion, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Background: Skeletal muscle atrophy significantly affects quality of life and has socio-economic and health implications. This study evaluates the effects of entacapone (ENT) on skeletal muscle atrophy linked with oxidative stress and proteolysis.
Methods: C2C12 cells were treated with dexamethasone (Dex) to simulate muscle atrophy.
Front Physiol
December 2024
Institute of Biochemistry and Cell Biology, National Research Council (CNR), Monterotondo (RM), Italy.
Duchenne muscular dystrophy (DMD) is caused by mutations in the gene encoding dystrophin, a subsarcolemmal protein whose absence results in increased susceptibility of the muscle fiber membrane to contraction-induced injury. This results in increased calcium influx, oxidative stress, and mitochondrial dysfunction, leading to chronic inflammation, myofiber degeneration, and reduced muscle regenerative capacity. Fast glycolytic muscle fibers have been shown to be more vulnerable to mechanical stress than slow oxidative fibers in both DMD patients and DMD mouse models.
View Article and Find Full Text PDFFood Funct
December 2024
Research Center of Translational Medicine, Jinan Central Hospital, Shandong University, No. 105 Jiefang Road, Jinan, Shandong, 250013, China.
Sarcopenia frequently occurs with aging and leads to major adverse impacts in elderly individuals. The protective effects of omega-3 polyunsaturated fatty acids against aging-related sarcopenia have been demonstrated; however, the effect and underlying mechanism of EPA or DHA alone remain inconclusive. Hence, the present study was aimed to clarify the differential effects and possible mechanisms of EPA and DHA on aging-related sarcopenia.
View Article and Find Full Text PDFBiochem Soc Trans
December 2024
Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, U.S.A.
Skeletal muscle cells (myofibers) require multiple nuclei to support a cytoplasmic volume that is larger than other mononuclear cell types. It is dogmatic that mammalian resident myonuclei rely on stem cells (specifically satellite cells) for adding new DNA to muscle fibers to facilitate cytoplasmic expansion that occurs during muscle growth. In this review, we discuss the relationship between cell size and supporting genetic material.
View Article and Find Full Text PDFiScience
December 2024
Institute of Muscle Biology and Cachexia, University of Houston College of Pharmacy, Houston, TX 77204, USA.
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