Co-localization of Disturbed Flow Patterns and Occlusive Cardiac Allograft Vasculopathy Lesion Formation in Heart Transplant Patients

Abstract Cardiac allograft vasculopathy (CAV) is one of the leading causes of morbidity and morality in orthotopic heart transplant (HTx) patients. While disturbed flow patterns have been linked to the spatial localization of atherosclerosis, the role of hemodynamics in CAV development has not been...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Timmins, Lucas H. [verfasserIn] Gupta, Divya Corban, Michel T. Molony, David S. Oshinski, John N. Samady, Habib Giddens, Don P.

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	Cardiac allograft vasculopathy Cardiac transplant Wall shear stress Hemodynamics Computation fluid dynamics

Anmerkung:	© Biomedical Engineering Society 2014

Übergeordnetes Werk:	Enthalten in: Cardiovascular engineering and technology - New York, NY : Springer, 2010, 6(2014), 1 vom: 28. Okt., Seite 25-35
Übergeordnetes Werk:	volume:6 ; year:2014 ; number:1 ; day:28 ; month:10 ; pages:25-35

Links:	Volltext

DOI / URN:	10.1007/s13239-014-0198-2

Katalog-ID:	SPR03099585X

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100	1		\|a Timmins, Lucas H. \|e verfasserin \|4 aut
245	1	0	\|a Co-localization of Disturbed Flow Patterns and Occlusive Cardiac Allograft Vasculopathy Lesion Formation in Heart Transplant Patients
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520			\|a Abstract Cardiac allograft vasculopathy (CAV) is one of the leading causes of morbidity and morality in orthotopic heart transplant (HTx) patients. While disturbed flow patterns have been linked to the spatial localization of atherosclerosis, the role of hemodynamics in CAV development has not been examined. HTx patients (n = 5) requiring percutaneous coronary intervention (PCI) for a focal, epicardial lesion were studied. Angiographic images were retrospectively obtained from baseline (i.e., in the presence of no observed disease) and follow-up catheterizations (i.e., at the time of PCI; 12.4 ± 2.6 years post-HTx). Patient-specific computational models were created from baseline images. Computational fluid dynamic techniques were employed to quantify the hemodynamic environment, which was expressed as normalized time-averaged WSS ($ TAWSS_{norm} $; measure of temporal WSS magnitude) and normalized WSS angle deviation ($ WSSAD_{norm} $; measure of instantaneous WSS vector oscillation) values. Baseline hemodynamic and follow-up angiographic data were co-registered to investigate the association between WSS and subsequent occlusive CAV lesion location. Results indicate a high degree of co-localization between baseline low WSS data and follow-up occlusive CAV lesion. Local minima in $ TAWSS_{norm} $ were located 2.5 ± 0.6 mm from the site of PCI. Furthermore, local maxima in $ WSSAD_{norm} $ were located 3.9 ± 0.7 mm from the site of PCI. In 3 patients, the occlusive lesion formed in a region that was subjected to both low and oscillatory WSS at baseline. There was discernable spatial co-localization between baseline disturbed flow patterns and follow-up CAV lesions requiring PCI. These results suggest a role of fluid mechanics in the development of focal, flow-limiting CAV lesions.
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650		4	\|a Cardiac transplant \|7 (dpeaa)DE-He213
650		4	\|a Wall shear stress \|7 (dpeaa)DE-He213
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650		4	\|a Computation fluid dynamics \|7 (dpeaa)DE-He213
700	1		\|a Gupta, Divya \|4 aut
700	1		\|a Corban, Michel T. \|4 aut
700	1		\|a Molony, David S. \|4 aut
700	1		\|a Oshinski, John N. \|4 aut
700	1		\|a Samady, Habib \|4 aut
700	1		\|a Giddens, Don P. \|4 aut
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author_variant	l h t lh lht d g dg m t c mt mtc d s m ds dsm j n o jn jno h s hs d p g dp dpg
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allfields	10.1007/s13239-014-0198-2 doi (DE-627)SPR03099585X (SPR)s13239-014-0198-2-e DE-627 ger DE-627 rakwb eng Timmins, Lucas H. verfasserin aut Co-localization of Disturbed Flow Patterns and Occlusive Cardiac Allograft Vasculopathy Lesion Formation in Heart Transplant Patients 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Biomedical Engineering Society 2014 Abstract Cardiac allograft vasculopathy (CAV) is one of the leading causes of morbidity and morality in orthotopic heart transplant (HTx) patients. While disturbed flow patterns have been linked to the spatial localization of atherosclerosis, the role of hemodynamics in CAV development has not been examined. HTx patients (n = 5) requiring percutaneous coronary intervention (PCI) for a focal, epicardial lesion were studied. Angiographic images were retrospectively obtained from baseline (i.e., in the presence of no observed disease) and follow-up catheterizations (i.e., at the time of PCI; 12.4 ± 2.6 years post-HTx). Patient-specific computational models were created from baseline images. Computational fluid dynamic techniques were employed to quantify the hemodynamic environment, which was expressed as normalized time-averaged WSS ($ TAWSS_{norm} $; measure of temporal WSS magnitude) and normalized WSS angle deviation ($ WSSAD_{norm} $; measure of instantaneous WSS vector oscillation) values. Baseline hemodynamic and follow-up angiographic data were co-registered to investigate the association between WSS and subsequent occlusive CAV lesion location. Results indicate a high degree of co-localization between baseline low WSS data and follow-up occlusive CAV lesion. Local minima in $ TAWSS_{norm} $ were located 2.5 ± 0.6 mm from the site of PCI. Furthermore, local maxima in $ WSSAD_{norm} $ were located 3.9 ± 0.7 mm from the site of PCI. In 3 patients, the occlusive lesion formed in a region that was subjected to both low and oscillatory WSS at baseline. There was discernable spatial co-localization between baseline disturbed flow patterns and follow-up CAV lesions requiring PCI. These results suggest a role of fluid mechanics in the development of focal, flow-limiting CAV lesions. Cardiac allograft vasculopathy (dpeaa)DE-He213 Cardiac transplant (dpeaa)DE-He213 Wall shear stress (dpeaa)DE-He213 Hemodynamics (dpeaa)DE-He213 Computation fluid dynamics (dpeaa)DE-He213 Gupta, Divya aut Corban, Michel T. aut Molony, David S. aut Oshinski, John N. aut Samady, Habib aut Giddens, Don P. aut Enthalten in Cardiovascular engineering and technology New York, NY : Springer, 2010 6(2014), 1 vom: 28. Okt., Seite 25-35 (DE-627)620775289 (DE-600)2543111-0 1869-4098 nnns volume:6 year:2014 number:1 day:28 month:10 pages:25-35 https://dx.doi.org/10.1007/s13239-014-0198-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 6 2014 1 28 10 25-35
spelling	10.1007/s13239-014-0198-2 doi (DE-627)SPR03099585X (SPR)s13239-014-0198-2-e DE-627 ger DE-627 rakwb eng Timmins, Lucas H. verfasserin aut Co-localization of Disturbed Flow Patterns and Occlusive Cardiac Allograft Vasculopathy Lesion Formation in Heart Transplant Patients 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Biomedical Engineering Society 2014 Abstract Cardiac allograft vasculopathy (CAV) is one of the leading causes of morbidity and morality in orthotopic heart transplant (HTx) patients. While disturbed flow patterns have been linked to the spatial localization of atherosclerosis, the role of hemodynamics in CAV development has not been examined. HTx patients (n = 5) requiring percutaneous coronary intervention (PCI) for a focal, epicardial lesion were studied. Angiographic images were retrospectively obtained from baseline (i.e., in the presence of no observed disease) and follow-up catheterizations (i.e., at the time of PCI; 12.4 ± 2.6 years post-HTx). Patient-specific computational models were created from baseline images. Computational fluid dynamic techniques were employed to quantify the hemodynamic environment, which was expressed as normalized time-averaged WSS ($ TAWSS_{norm} $; measure of temporal WSS magnitude) and normalized WSS angle deviation ($ WSSAD_{norm} $; measure of instantaneous WSS vector oscillation) values. Baseline hemodynamic and follow-up angiographic data were co-registered to investigate the association between WSS and subsequent occlusive CAV lesion location. Results indicate a high degree of co-localization between baseline low WSS data and follow-up occlusive CAV lesion. Local minima in $ TAWSS_{norm} $ were located 2.5 ± 0.6 mm from the site of PCI. Furthermore, local maxima in $ WSSAD_{norm} $ were located 3.9 ± 0.7 mm from the site of PCI. In 3 patients, the occlusive lesion formed in a region that was subjected to both low and oscillatory WSS at baseline. There was discernable spatial co-localization between baseline disturbed flow patterns and follow-up CAV lesions requiring PCI. These results suggest a role of fluid mechanics in the development of focal, flow-limiting CAV lesions. Cardiac allograft vasculopathy (dpeaa)DE-He213 Cardiac transplant (dpeaa)DE-He213 Wall shear stress (dpeaa)DE-He213 Hemodynamics (dpeaa)DE-He213 Computation fluid dynamics (dpeaa)DE-He213 Gupta, Divya aut Corban, Michel T. aut Molony, David S. aut Oshinski, John N. aut Samady, Habib aut Giddens, Don P. aut Enthalten in Cardiovascular engineering and technology New York, NY : Springer, 2010 6(2014), 1 vom: 28. Okt., Seite 25-35 (DE-627)620775289 (DE-600)2543111-0 1869-4098 nnns volume:6 year:2014 number:1 day:28 month:10 pages:25-35 https://dx.doi.org/10.1007/s13239-014-0198-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 6 2014 1 28 10 25-35
allfields_unstemmed	10.1007/s13239-014-0198-2 doi (DE-627)SPR03099585X (SPR)s13239-014-0198-2-e DE-627 ger DE-627 rakwb eng Timmins, Lucas H. verfasserin aut Co-localization of Disturbed Flow Patterns and Occlusive Cardiac Allograft Vasculopathy Lesion Formation in Heart Transplant Patients 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Biomedical Engineering Society 2014 Abstract Cardiac allograft vasculopathy (CAV) is one of the leading causes of morbidity and morality in orthotopic heart transplant (HTx) patients. While disturbed flow patterns have been linked to the spatial localization of atherosclerosis, the role of hemodynamics in CAV development has not been examined. HTx patients (n = 5) requiring percutaneous coronary intervention (PCI) for a focal, epicardial lesion were studied. Angiographic images were retrospectively obtained from baseline (i.e., in the presence of no observed disease) and follow-up catheterizations (i.e., at the time of PCI; 12.4 ± 2.6 years post-HTx). Patient-specific computational models were created from baseline images. Computational fluid dynamic techniques were employed to quantify the hemodynamic environment, which was expressed as normalized time-averaged WSS ($ TAWSS_{norm} $; measure of temporal WSS magnitude) and normalized WSS angle deviation ($ WSSAD_{norm} $; measure of instantaneous WSS vector oscillation) values. Baseline hemodynamic and follow-up angiographic data were co-registered to investigate the association between WSS and subsequent occlusive CAV lesion location. Results indicate a high degree of co-localization between baseline low WSS data and follow-up occlusive CAV lesion. Local minima in $ TAWSS_{norm} $ were located 2.5 ± 0.6 mm from the site of PCI. Furthermore, local maxima in $ WSSAD_{norm} $ were located 3.9 ± 0.7 mm from the site of PCI. In 3 patients, the occlusive lesion formed in a region that was subjected to both low and oscillatory WSS at baseline. There was discernable spatial co-localization between baseline disturbed flow patterns and follow-up CAV lesions requiring PCI. These results suggest a role of fluid mechanics in the development of focal, flow-limiting CAV lesions. Cardiac allograft vasculopathy (dpeaa)DE-He213 Cardiac transplant (dpeaa)DE-He213 Wall shear stress (dpeaa)DE-He213 Hemodynamics (dpeaa)DE-He213 Computation fluid dynamics (dpeaa)DE-He213 Gupta, Divya aut Corban, Michel T. aut Molony, David S. aut Oshinski, John N. aut Samady, Habib aut Giddens, Don P. aut Enthalten in Cardiovascular engineering and technology New York, NY : Springer, 2010 6(2014), 1 vom: 28. Okt., Seite 25-35 (DE-627)620775289 (DE-600)2543111-0 1869-4098 nnns volume:6 year:2014 number:1 day:28 month:10 pages:25-35 https://dx.doi.org/10.1007/s13239-014-0198-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 6 2014 1 28 10 25-35
allfieldsGer	10.1007/s13239-014-0198-2 doi (DE-627)SPR03099585X (SPR)s13239-014-0198-2-e DE-627 ger DE-627 rakwb eng Timmins, Lucas H. verfasserin aut Co-localization of Disturbed Flow Patterns and Occlusive Cardiac Allograft Vasculopathy Lesion Formation in Heart Transplant Patients 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Biomedical Engineering Society 2014 Abstract Cardiac allograft vasculopathy (CAV) is one of the leading causes of morbidity and morality in orthotopic heart transplant (HTx) patients. While disturbed flow patterns have been linked to the spatial localization of atherosclerosis, the role of hemodynamics in CAV development has not been examined. HTx patients (n = 5) requiring percutaneous coronary intervention (PCI) for a focal, epicardial lesion were studied. Angiographic images were retrospectively obtained from baseline (i.e., in the presence of no observed disease) and follow-up catheterizations (i.e., at the time of PCI; 12.4 ± 2.6 years post-HTx). Patient-specific computational models were created from baseline images. Computational fluid dynamic techniques were employed to quantify the hemodynamic environment, which was expressed as normalized time-averaged WSS ($ TAWSS_{norm} $; measure of temporal WSS magnitude) and normalized WSS angle deviation ($ WSSAD_{norm} $; measure of instantaneous WSS vector oscillation) values. Baseline hemodynamic and follow-up angiographic data were co-registered to investigate the association between WSS and subsequent occlusive CAV lesion location. Results indicate a high degree of co-localization between baseline low WSS data and follow-up occlusive CAV lesion. Local minima in $ TAWSS_{norm} $ were located 2.5 ± 0.6 mm from the site of PCI. Furthermore, local maxima in $ WSSAD_{norm} $ were located 3.9 ± 0.7 mm from the site of PCI. In 3 patients, the occlusive lesion formed in a region that was subjected to both low and oscillatory WSS at baseline. There was discernable spatial co-localization between baseline disturbed flow patterns and follow-up CAV lesions requiring PCI. These results suggest a role of fluid mechanics in the development of focal, flow-limiting CAV lesions. Cardiac allograft vasculopathy (dpeaa)DE-He213 Cardiac transplant (dpeaa)DE-He213 Wall shear stress (dpeaa)DE-He213 Hemodynamics (dpeaa)DE-He213 Computation fluid dynamics (dpeaa)DE-He213 Gupta, Divya aut Corban, Michel T. aut Molony, David S. aut Oshinski, John N. aut Samady, Habib aut Giddens, Don P. aut Enthalten in Cardiovascular engineering and technology New York, NY : Springer, 2010 6(2014), 1 vom: 28. Okt., Seite 25-35 (DE-627)620775289 (DE-600)2543111-0 1869-4098 nnns volume:6 year:2014 number:1 day:28 month:10 pages:25-35 https://dx.doi.org/10.1007/s13239-014-0198-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 6 2014 1 28 10 25-35
allfieldsSound	10.1007/s13239-014-0198-2 doi (DE-627)SPR03099585X (SPR)s13239-014-0198-2-e DE-627 ger DE-627 rakwb eng Timmins, Lucas H. verfasserin aut Co-localization of Disturbed Flow Patterns and Occlusive Cardiac Allograft Vasculopathy Lesion Formation in Heart Transplant Patients 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Biomedical Engineering Society 2014 Abstract Cardiac allograft vasculopathy (CAV) is one of the leading causes of morbidity and morality in orthotopic heart transplant (HTx) patients. While disturbed flow patterns have been linked to the spatial localization of atherosclerosis, the role of hemodynamics in CAV development has not been examined. HTx patients (n = 5) requiring percutaneous coronary intervention (PCI) for a focal, epicardial lesion were studied. Angiographic images were retrospectively obtained from baseline (i.e., in the presence of no observed disease) and follow-up catheterizations (i.e., at the time of PCI; 12.4 ± 2.6 years post-HTx). Patient-specific computational models were created from baseline images. Computational fluid dynamic techniques were employed to quantify the hemodynamic environment, which was expressed as normalized time-averaged WSS ($ TAWSS_{norm} $; measure of temporal WSS magnitude) and normalized WSS angle deviation ($ WSSAD_{norm} $; measure of instantaneous WSS vector oscillation) values. Baseline hemodynamic and follow-up angiographic data were co-registered to investigate the association between WSS and subsequent occlusive CAV lesion location. Results indicate a high degree of co-localization between baseline low WSS data and follow-up occlusive CAV lesion. Local minima in $ TAWSS_{norm} $ were located 2.5 ± 0.6 mm from the site of PCI. Furthermore, local maxima in $ WSSAD_{norm} $ were located 3.9 ± 0.7 mm from the site of PCI. In 3 patients, the occlusive lesion formed in a region that was subjected to both low and oscillatory WSS at baseline. There was discernable spatial co-localization between baseline disturbed flow patterns and follow-up CAV lesions requiring PCI. These results suggest a role of fluid mechanics in the development of focal, flow-limiting CAV lesions. Cardiac allograft vasculopathy (dpeaa)DE-He213 Cardiac transplant (dpeaa)DE-He213 Wall shear stress (dpeaa)DE-He213 Hemodynamics (dpeaa)DE-He213 Computation fluid dynamics (dpeaa)DE-He213 Gupta, Divya aut Corban, Michel T. aut Molony, David S. aut Oshinski, John N. aut Samady, Habib aut Giddens, Don P. aut Enthalten in Cardiovascular engineering and technology New York, NY : Springer, 2010 6(2014), 1 vom: 28. Okt., Seite 25-35 (DE-627)620775289 (DE-600)2543111-0 1869-4098 nnns volume:6 year:2014 number:1 day:28 month:10 pages:25-35 https://dx.doi.org/10.1007/s13239-014-0198-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 6 2014 1 28 10 25-35
language	English
source	Enthalten in Cardiovascular engineering and technology 6(2014), 1 vom: 28. Okt., Seite 25-35 volume:6 year:2014 number:1 day:28 month:10 pages:25-35
sourceStr	Enthalten in Cardiovascular engineering and technology 6(2014), 1 vom: 28. Okt., Seite 25-35 volume:6 year:2014 number:1 day:28 month:10 pages:25-35
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Cardiac allograft vasculopathy Cardiac transplant Wall shear stress Hemodynamics Computation fluid dynamics
isfreeaccess_bool	false
container_title	Cardiovascular engineering and technology
authorswithroles_txt_mv	Timmins, Lucas H. @@aut@@ Gupta, Divya @@aut@@ Corban, Michel T. @@aut@@ Molony, David S. @@aut@@ Oshinski, John N. @@aut@@ Samady, Habib @@aut@@ Giddens, Don P. @@aut@@
publishDateDaySort_date	2014-10-28T00:00:00Z
hierarchy_top_id	620775289
id	SPR03099585X
language_de	englisch
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author	Timmins, Lucas H.
spellingShingle	Timmins, Lucas H. misc Cardiac allograft vasculopathy misc Cardiac transplant misc Wall shear stress misc Hemodynamics misc Computation fluid dynamics Co-localization of Disturbed Flow Patterns and Occlusive Cardiac Allograft Vasculopathy Lesion Formation in Heart Transplant Patients
authorStr	Timmins, Lucas H.
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topic_title	Co-localization of Disturbed Flow Patterns and Occlusive Cardiac Allograft Vasculopathy Lesion Formation in Heart Transplant Patients Cardiac allograft vasculopathy (dpeaa)DE-He213 Cardiac transplant (dpeaa)DE-He213 Wall shear stress (dpeaa)DE-He213 Hemodynamics (dpeaa)DE-He213 Computation fluid dynamics (dpeaa)DE-He213
topic	misc Cardiac allograft vasculopathy misc Cardiac transplant misc Wall shear stress misc Hemodynamics misc Computation fluid dynamics
topic_unstemmed	misc Cardiac allograft vasculopathy misc Cardiac transplant misc Wall shear stress misc Hemodynamics misc Computation fluid dynamics
topic_browse	misc Cardiac allograft vasculopathy misc Cardiac transplant misc Wall shear stress misc Hemodynamics misc Computation fluid dynamics
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title	Co-localization of Disturbed Flow Patterns and Occlusive Cardiac Allograft Vasculopathy Lesion Formation in Heart Transplant Patients
ctrlnum	(DE-627)SPR03099585X (SPR)s13239-014-0198-2-e
title_full	Co-localization of Disturbed Flow Patterns and Occlusive Cardiac Allograft Vasculopathy Lesion Formation in Heart Transplant Patients
author_sort	Timmins, Lucas H.
journal	Cardiovascular engineering and technology
journalStr	Cardiovascular engineering and technology
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author_browse	Timmins, Lucas H. Gupta, Divya Corban, Michel T. Molony, David S. Oshinski, John N. Samady, Habib Giddens, Don P.
container_volume	6
format_se	Elektronische Aufsätze
author-letter	Timmins, Lucas H.
doi_str_mv	10.1007/s13239-014-0198-2
title_sort	co-localization of disturbed flow patterns and occlusive cardiac allograft vasculopathy lesion formation in heart transplant patients
title_auth	Co-localization of Disturbed Flow Patterns and Occlusive Cardiac Allograft Vasculopathy Lesion Formation in Heart Transplant Patients
abstract	Abstract Cardiac allograft vasculopathy (CAV) is one of the leading causes of morbidity and morality in orthotopic heart transplant (HTx) patients. While disturbed flow patterns have been linked to the spatial localization of atherosclerosis, the role of hemodynamics in CAV development has not been examined. HTx patients (n = 5) requiring percutaneous coronary intervention (PCI) for a focal, epicardial lesion were studied. Angiographic images were retrospectively obtained from baseline (i.e., in the presence of no observed disease) and follow-up catheterizations (i.e., at the time of PCI; 12.4 ± 2.6 years post-HTx). Patient-specific computational models were created from baseline images. Computational fluid dynamic techniques were employed to quantify the hemodynamic environment, which was expressed as normalized time-averaged WSS ($ TAWSS_{norm} $; measure of temporal WSS magnitude) and normalized WSS angle deviation ($ WSSAD_{norm} $; measure of instantaneous WSS vector oscillation) values. Baseline hemodynamic and follow-up angiographic data were co-registered to investigate the association between WSS and subsequent occlusive CAV lesion location. Results indicate a high degree of co-localization between baseline low WSS data and follow-up occlusive CAV lesion. Local minima in $ TAWSS_{norm} $ were located 2.5 ± 0.6 mm from the site of PCI. Furthermore, local maxima in $ WSSAD_{norm} $ were located 3.9 ± 0.7 mm from the site of PCI. In 3 patients, the occlusive lesion formed in a region that was subjected to both low and oscillatory WSS at baseline. There was discernable spatial co-localization between baseline disturbed flow patterns and follow-up CAV lesions requiring PCI. These results suggest a role of fluid mechanics in the development of focal, flow-limiting CAV lesions. © Biomedical Engineering Society 2014
abstractGer	Abstract Cardiac allograft vasculopathy (CAV) is one of the leading causes of morbidity and morality in orthotopic heart transplant (HTx) patients. While disturbed flow patterns have been linked to the spatial localization of atherosclerosis, the role of hemodynamics in CAV development has not been examined. HTx patients (n = 5) requiring percutaneous coronary intervention (PCI) for a focal, epicardial lesion were studied. Angiographic images were retrospectively obtained from baseline (i.e., in the presence of no observed disease) and follow-up catheterizations (i.e., at the time of PCI; 12.4 ± 2.6 years post-HTx). Patient-specific computational models were created from baseline images. Computational fluid dynamic techniques were employed to quantify the hemodynamic environment, which was expressed as normalized time-averaged WSS ($ TAWSS_{norm} $; measure of temporal WSS magnitude) and normalized WSS angle deviation ($ WSSAD_{norm} $; measure of instantaneous WSS vector oscillation) values. Baseline hemodynamic and follow-up angiographic data were co-registered to investigate the association between WSS and subsequent occlusive CAV lesion location. Results indicate a high degree of co-localization between baseline low WSS data and follow-up occlusive CAV lesion. Local minima in $ TAWSS_{norm} $ were located 2.5 ± 0.6 mm from the site of PCI. Furthermore, local maxima in $ WSSAD_{norm} $ were located 3.9 ± 0.7 mm from the site of PCI. In 3 patients, the occlusive lesion formed in a region that was subjected to both low and oscillatory WSS at baseline. There was discernable spatial co-localization between baseline disturbed flow patterns and follow-up CAV lesions requiring PCI. These results suggest a role of fluid mechanics in the development of focal, flow-limiting CAV lesions. © Biomedical Engineering Society 2014
abstract_unstemmed	Abstract Cardiac allograft vasculopathy (CAV) is one of the leading causes of morbidity and morality in orthotopic heart transplant (HTx) patients. While disturbed flow patterns have been linked to the spatial localization of atherosclerosis, the role of hemodynamics in CAV development has not been examined. HTx patients (n = 5) requiring percutaneous coronary intervention (PCI) for a focal, epicardial lesion were studied. Angiographic images were retrospectively obtained from baseline (i.e., in the presence of no observed disease) and follow-up catheterizations (i.e., at the time of PCI; 12.4 ± 2.6 years post-HTx). Patient-specific computational models were created from baseline images. Computational fluid dynamic techniques were employed to quantify the hemodynamic environment, which was expressed as normalized time-averaged WSS ($ TAWSS_{norm} $; measure of temporal WSS magnitude) and normalized WSS angle deviation ($ WSSAD_{norm} $; measure of instantaneous WSS vector oscillation) values. Baseline hemodynamic and follow-up angiographic data were co-registered to investigate the association between WSS and subsequent occlusive CAV lesion location. Results indicate a high degree of co-localization between baseline low WSS data and follow-up occlusive CAV lesion. Local minima in $ TAWSS_{norm} $ were located 2.5 ± 0.6 mm from the site of PCI. Furthermore, local maxima in $ WSSAD_{norm} $ were located 3.9 ± 0.7 mm from the site of PCI. In 3 patients, the occlusive lesion formed in a region that was subjected to both low and oscillatory WSS at baseline. There was discernable spatial co-localization between baseline disturbed flow patterns and follow-up CAV lesions requiring PCI. These results suggest a role of fluid mechanics in the development of focal, flow-limiting CAV lesions. © Biomedical Engineering Society 2014
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container_issue	1
title_short	Co-localization of Disturbed Flow Patterns and Occlusive Cardiac Allograft Vasculopathy Lesion Formation in Heart Transplant Patients
url	https://dx.doi.org/10.1007/s13239-014-0198-2
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author2	Gupta, Divya Corban, Michel T. Molony, David S. Oshinski, John N. Samady, Habib Giddens, Don P.
author2Str	Gupta, Divya Corban, Michel T. Molony, David S. Oshinski, John N. Samady, Habib Giddens, Don P.
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doi_str	10.1007/s13239-014-0198-2
up_date	2024-07-03T21:22:38.733Z
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Co-localization of Disturbed Flow Patterns and Occlusive Cardiac Allograft Vasculopathy Lesion Formation in Heart Transplant Patients

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