File:Myocardial-contractility-in-the-stress-echo-lab-from-pathophysiological-toy-to-clinical-tool-1476-7120-11-41-S4.ogv
Myocardial-contractility-in-the-stress-echo-lab-from-pathophysiological-toy-to-clinical-tool-1476-7120-11-41-S4.ogv (Ogg multiplexed audio/video file, Theora/Vorbis, length 2 min 8 s, 648 × 486 pixels, 3.4 Mbps overall, file size: 51.92 MB)
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[edit]DescriptionMyocardial-contractility-in-the-stress-echo-lab-from-pathophysiological-toy-to-clinical-tool-1476-7120-11-41-S4.ogv |
English: Dilated Cardiomyopathy: Actin-myosin contraction. Contraction is the result a sliding of actin and myosin fibers, due to the activity of the myosin cycle: this cycle is active in the presence of Calcium, which mediates transmission of signal to both the actin and myosin fibers, via other accessory proteins. The activity requires energy, in the form of ATP (not shown). When Calcium has been removed, the myosin heads detach from the actin fibers and the muscle can relax. In the DCM heart calcium re-uptake is incomplete: this leads to a constant contraction which, on one hand requires more energy (hence the enlarged mitochondria) and on the other impedes full extension of the heart fibers during relaxation, thus limiting the amount of incoming blood. The problem is even worse under stress conditions. Note that due to the excess work and the lack of total relaxation, the actin and myosin fibers of the dilated heart are not regularly aligned and the overall structure of the myofiber is slightly disorganized. (The full quality video can be accessed at this link: https://vimeo.com/79085977). |
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Source | Bombardini T, Zoppe M, Ciampi Q, Cortigiani L, Agricola E, Salvadori S, Loni T, Pratali L, Picano E (2013). "Myocardial contractility in the stress echo lab: from pathophysiological toy to clinical tool". Cardiovascular Ultrasound. DOI:10.1186/1476-7120-11-41. PMID 24246005. PMC: 3875530. | ||
Author | Bombardini T, Zoppe M, Ciampi Q, Cortigiani L, Agricola E, Salvadori S, Loni T, Pratali L, Picano E | ||
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current | 03:35, 1 January 2014 | 2 min 8 s, 648 × 486 (51.92 MB) | Open Access Media Importer Bot (talk | contribs) | Automatically uploaded media file from Open Access source. Please report problems or suggestions here. |
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Short title | Additional file 4 |
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Author | Bombardini T, Zoppe M, Ciampi Q, Cortigiani L, Agricola E, Salvadori S, Loni T, Pratali L, Picano E |
Usage terms | http://creativecommons.org/licenses/by/2.0/ |
Image title | Dilated Cardiomyopathy: Actin-myosin contraction. Contraction is the result a sliding of actin and myosin fibers, due to the activity of the myosin cycle: this cycle is active in the presence of Calcium, which mediates transmission of signal to both the actin and myosin fibers, via other accessory proteins. The activity requires energy, in the form of ATP (not shown). When Calcium has been removed, the myosin heads detach from the actin fibers and the muscle can relax. In the DCM heart calcium re-uptake is incomplete: this leads to a constant contraction which, on one hand requires more energy (hence the enlarged mitochondria) and on the other impedes full extension of the heart fibers during relaxation, thus limiting the amount of incoming blood. The problem is even worse under stress conditions. Note that due to the excess work and the lack of total relaxation, the actin and myosin fibers of the dilated heart are not regularly aligned and the overall structure of the myofiber is slightly disorganized. (The full quality video can be accessed at this link: https://vimeo.com/79085977). |
Software used | |
Date and time of digitizing | 2013 |