Investigating the haemodynamics of myocardial bridging
Myocardial bridging is a congenital anomaly wherein a segment of a coronary artery passes under a ‘bridge’ of heart muscle rather than resting upon the heart’s surface. Although it is usually benign, myocardial bridging has been associated with adverse clinical events including ischaemia, arrhythmia...
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Veröffentlicht in: | Experiments in fluids 2021-04, Vol.62 (4), Article 86 |
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creator | Vijayaratnam, P. R. S. Fulker, D. Kim, Y. C. Brandt, J. Yi, J. Yong, A. S. C. Kritharides, L. Simmons, A. Barber, T. J. |
description | Myocardial bridging is a congenital anomaly wherein a segment of a coronary artery passes under a ‘bridge’ of heart muscle rather than resting upon the heart’s surface. Although it is usually benign, myocardial bridging has been associated with adverse clinical events including ischaemia, arrhythmia and sudden death. Moreover, there is a tendency for atherosclerotic lesions to develop upstream of the bridge. These lesions may be the result of adverse fluid dynamic phenomena induced by the periodic compression of the artery by the overlying myocardial bridge. It is not possible to visualise these phenomena in vivo, and in this study we present an in vitro model capable of replicating the bridging conditions. This model is comprised of a pressure-measuring guide wire and catheter, a piston pump, a scaled artery model, and a ‘myocardial bridging mechanism’ which periodically compresses the artery model. A proportional-integral-derivative (PID) controller allowed the piston pump to recreate a patient-specific aortic pressure waveform upstream of the occluded artery model segment for each study. Stationary occlusions—achieved by placing 3D printed ‘stenosis inserts’ within the artery model—induced globally reduced pressures downstream of the stenosis when compared against the upstream pressure waveform. Conversely, the pressures downstream of the dynamic stenoses generated by the bridging mechanism closely matched the upstream pressures at all stages of the cardiac cycle except at the end of systole. This divergent pressure behaviour at the end of systole was similarly observed in vivo within a patient with a myocardial bridge. Flow visualisation using a laser sheet enabled dynamic flow structures to be observed, including recirculating flow regions, which may be precursors to arterial dysfunction.
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doi_str_mv | 10.1007/s00348-021-03185-9 |
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Graphic abstract</description><identifier>ISSN: 0723-4864</identifier><identifier>EISSN: 1432-1114</identifier><identifier>DOI: 10.1007/s00348-021-03185-9</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Aorta ; Arrhythmia ; Atherosclerosis ; Bridge loads ; Congenital anomalies ; Engineering ; Engineering Fluid Dynamics ; Engineering Thermodynamics ; Flow visualization ; Fluid- and Aerodynamics ; Guide wires ; Heat and Mass Transfer ; Hemodynamics ; In vivo methods and tests ; Inserts ; Ischemia ; Lesions ; Muscles ; Proportional integral derivative ; Research Article ; Segments ; Systole ; Three dimensional printing ; Upstream ; Veins & arteries ; Waveforms</subject><ispartof>Experiments in fluids, 2021-04, Vol.62 (4), Article 86</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2021</rights><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c307t-48082ce32e3a1e8f7e7719a875da406e529e7eabefaef0f89707cf76493bf4aa3</cites><orcidid>0000-0002-1219-0169</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00348-021-03185-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00348-021-03185-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids></links><search><creatorcontrib>Vijayaratnam, P. R. S.</creatorcontrib><creatorcontrib>Fulker, D.</creatorcontrib><creatorcontrib>Kim, Y. C.</creatorcontrib><creatorcontrib>Brandt, J.</creatorcontrib><creatorcontrib>Yi, J.</creatorcontrib><creatorcontrib>Yong, A. S. C.</creatorcontrib><creatorcontrib>Kritharides, L.</creatorcontrib><creatorcontrib>Simmons, A.</creatorcontrib><creatorcontrib>Barber, T. J.</creatorcontrib><title>Investigating the haemodynamics of myocardial bridging</title><title>Experiments in fluids</title><addtitle>Exp Fluids</addtitle><description>Myocardial bridging is a congenital anomaly wherein a segment of a coronary artery passes under a ‘bridge’ of heart muscle rather than resting upon the heart’s surface. Although it is usually benign, myocardial bridging has been associated with adverse clinical events including ischaemia, arrhythmia and sudden death. Moreover, there is a tendency for atherosclerotic lesions to develop upstream of the bridge. These lesions may be the result of adverse fluid dynamic phenomena induced by the periodic compression of the artery by the overlying myocardial bridge. It is not possible to visualise these phenomena in vivo, and in this study we present an in vitro model capable of replicating the bridging conditions. This model is comprised of a pressure-measuring guide wire and catheter, a piston pump, a scaled artery model, and a ‘myocardial bridging mechanism’ which periodically compresses the artery model. A proportional-integral-derivative (PID) controller allowed the piston pump to recreate a patient-specific aortic pressure waveform upstream of the occluded artery model segment for each study. Stationary occlusions—achieved by placing 3D printed ‘stenosis inserts’ within the artery model—induced globally reduced pressures downstream of the stenosis when compared against the upstream pressure waveform. Conversely, the pressures downstream of the dynamic stenoses generated by the bridging mechanism closely matched the upstream pressures at all stages of the cardiac cycle except at the end of systole. This divergent pressure behaviour at the end of systole was similarly observed in vivo within a patient with a myocardial bridge. Flow visualisation using a laser sheet enabled dynamic flow structures to be observed, including recirculating flow regions, which may be precursors to arterial dysfunction.
Graphic abstract</description><subject>Aorta</subject><subject>Arrhythmia</subject><subject>Atherosclerosis</subject><subject>Bridge loads</subject><subject>Congenital anomalies</subject><subject>Engineering</subject><subject>Engineering Fluid Dynamics</subject><subject>Engineering Thermodynamics</subject><subject>Flow visualization</subject><subject>Fluid- and Aerodynamics</subject><subject>Guide wires</subject><subject>Heat and Mass Transfer</subject><subject>Hemodynamics</subject><subject>In vivo methods and tests</subject><subject>Inserts</subject><subject>Ischemia</subject><subject>Lesions</subject><subject>Muscles</subject><subject>Proportional integral derivative</subject><subject>Research Article</subject><subject>Segments</subject><subject>Systole</subject><subject>Three dimensional printing</subject><subject>Upstream</subject><subject>Veins & arteries</subject><subject>Waveforms</subject><issn>0723-4864</issn><issn>1432-1114</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp9kE1Lw0AURQdRsFb_gKuA6-ibj2RmllLUFgpudD28Jm_SlCapM6nQf-9oBHeu3ubcex-HsVsO9xxAP0QAqUwOgucguSlye8ZmXEmRc87VOZuBFjJXplSX7CrGHQAvLJgZK1f9J8WxbXBs-yYbt5RtkbqhPvXYtVXMBp91p6HCULe4zzahrZsEXrMLj_tIN793zt6fn94Wy3z9-rJaPK7zSoIe0yAYUZEUJJGT8Zq05haNLmpUUFIhLGnCDXkkD95YDbryulRWbrxClHN2N_UewvBxTI-63XAMfZp0ogBtjSmtTJSYqCoMMQby7hDaDsPJcXDfftzkxyU_7sePsykkp1BMcN9Q-Kv-J_UFtm5oYQ</recordid><startdate>20210401</startdate><enddate>20210401</enddate><creator>Vijayaratnam, P. R. S.</creator><creator>Fulker, D.</creator><creator>Kim, Y. C.</creator><creator>Brandt, J.</creator><creator>Yi, J.</creator><creator>Yong, A. S. C.</creator><creator>Kritharides, L.</creator><creator>Simmons, A.</creator><creator>Barber, T. J.</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><orcidid>https://orcid.org/0000-0002-1219-0169</orcidid></search><sort><creationdate>20210401</creationdate><title>Investigating the haemodynamics of myocardial bridging</title><author>Vijayaratnam, P. R. S. ; Fulker, D. ; Kim, Y. C. ; Brandt, J. ; Yi, J. ; Yong, A. S. C. ; Kritharides, L. ; Simmons, A. ; Barber, T. 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R. S.</creatorcontrib><creatorcontrib>Fulker, D.</creatorcontrib><creatorcontrib>Kim, Y. C.</creatorcontrib><creatorcontrib>Brandt, J.</creatorcontrib><creatorcontrib>Yi, J.</creatorcontrib><creatorcontrib>Yong, A. S. C.</creatorcontrib><creatorcontrib>Kritharides, L.</creatorcontrib><creatorcontrib>Simmons, A.</creatorcontrib><creatorcontrib>Barber, T. J.</creatorcontrib><collection>CrossRef</collection><jtitle>Experiments in fluids</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vijayaratnam, P. R. S.</au><au>Fulker, D.</au><au>Kim, Y. C.</au><au>Brandt, J.</au><au>Yi, J.</au><au>Yong, A. S. C.</au><au>Kritharides, L.</au><au>Simmons, A.</au><au>Barber, T. J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Investigating the haemodynamics of myocardial bridging</atitle><jtitle>Experiments in fluids</jtitle><stitle>Exp Fluids</stitle><date>2021-04-01</date><risdate>2021</risdate><volume>62</volume><issue>4</issue><artnum>86</artnum><issn>0723-4864</issn><eissn>1432-1114</eissn><abstract>Myocardial bridging is a congenital anomaly wherein a segment of a coronary artery passes under a ‘bridge’ of heart muscle rather than resting upon the heart’s surface. Although it is usually benign, myocardial bridging has been associated with adverse clinical events including ischaemia, arrhythmia and sudden death. Moreover, there is a tendency for atherosclerotic lesions to develop upstream of the bridge. These lesions may be the result of adverse fluid dynamic phenomena induced by the periodic compression of the artery by the overlying myocardial bridge. It is not possible to visualise these phenomena in vivo, and in this study we present an in vitro model capable of replicating the bridging conditions. This model is comprised of a pressure-measuring guide wire and catheter, a piston pump, a scaled artery model, and a ‘myocardial bridging mechanism’ which periodically compresses the artery model. A proportional-integral-derivative (PID) controller allowed the piston pump to recreate a patient-specific aortic pressure waveform upstream of the occluded artery model segment for each study. Stationary occlusions—achieved by placing 3D printed ‘stenosis inserts’ within the artery model—induced globally reduced pressures downstream of the stenosis when compared against the upstream pressure waveform. Conversely, the pressures downstream of the dynamic stenoses generated by the bridging mechanism closely matched the upstream pressures at all stages of the cardiac cycle except at the end of systole. This divergent pressure behaviour at the end of systole was similarly observed in vivo within a patient with a myocardial bridge. Flow visualisation using a laser sheet enabled dynamic flow structures to be observed, including recirculating flow regions, which may be precursors to arterial dysfunction.
Graphic abstract</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><doi>10.1007/s00348-021-03185-9</doi><orcidid>https://orcid.org/0000-0002-1219-0169</orcidid></addata></record> |
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subjects | Aorta Arrhythmia Atherosclerosis Bridge loads Congenital anomalies Engineering Engineering Fluid Dynamics Engineering Thermodynamics Flow visualization Fluid- and Aerodynamics Guide wires Heat and Mass Transfer Hemodynamics In vivo methods and tests Inserts Ischemia Lesions Muscles Proportional integral derivative Research Article Segments Systole Three dimensional printing Upstream Veins & arteries Waveforms |
title | Investigating the haemodynamics of myocardial bridging |
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