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Assessment of Renal Artery Stenosis Severity by Pressure Gradient Measurements
Assessment of Renal Artery Stenosis Severity by Pressure Gradient Measurements Bernard De Bruyne, Ganesh Manoharan, Nico H. J. Pijls, Katia Verhamme, Juraj Madaric, Jozef Bartunek, Marc Vanderheyden, Guy R. Heyndrickx To define “significant” renal artery stenosis, graded stenoses were created by pro...
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Published in: | Journal of the American College of Cardiology 2006-11, Vol.48 (9), p.1851-1855 |
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description | Assessment of Renal Artery Stenosis Severity by Pressure Gradient Measurements
Bernard De Bruyne, Ganesh Manoharan, Nico H. J. Pijls, Katia Verhamme, Juraj Madaric, Jozef Bartunek, Marc Vanderheyden, Guy R. Heyndrickx
To define “significant” renal artery stenosis, graded stenoses were created by progressive balloon inflation after stenting of a mild renal stenosis. Stenosis was expressed as the ratio of distal pressure (Pd) to aortic pressure (Pa). Renin was measured in the aorta and in both renal veins. For a Pd/Paratio >0.90, renin did not increase. Only for Pd/Pa |
doi_str_mv | 10.1016/j.jacc.2006.05.074 |
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Bernard De Bruyne, Ganesh Manoharan, Nico H. J. Pijls, Katia Verhamme, Juraj Madaric, Jozef Bartunek, Marc Vanderheyden, Guy R. Heyndrickx
To define “significant” renal artery stenosis, graded stenoses were created by progressive balloon inflation after stenting of a mild renal stenosis. Stenosis was expressed as the ratio of distal pressure (Pd) to aortic pressure (Pa). Renin was measured in the aorta and in both renal veins. For a Pd/Paratio >0.90, renin did not increase. Only for Pd/Pa<0.90 was an increase in renin observed in the renal vein of the stenotic kidney. Renal artery stenoses with a Pd/Paratio <0.90 trigger the production of renin and are, therefore, likely to be responsible for renovascular hypertension.
The purpose of this study was to define “significant” renal artery stenosis (i.e., a stenosis able to induce arterial hypertension).
The degree of renal artery stenosis that justifies an attempt at revascularization is unknown.
In 15 patients, transstenotic pressure measurements were obtained before and after unilateral stenting. After stenting, graded stenoses were created in the stented segment by progressive inflation of a balloon catheter. Stenosis severity was expressed as the ratio of distal pressure (Pd) corrected for aortic pressure (Pa). Balloon inflation pressure was adjusted to create 6° of stenosis (Pd/Pafrom 1.0 to 0.5, each step during 10 min). Plasma renin concentration was measured at the end of each step in the aorta and in both renal veins.
For a Pd/Paratio >0.90, no significant change in plasma renin concentration was observed. However, when Pd/Pabecame <0.90, a significant increase in renin was observed in the renal vein of the stenotic kidney, finally reaching a maximal increase of 346 ± 145% for Pd/Paof 0.50 (p = 0.006). These values returned to baseline when the stenosis was relieved. In addition, plasma renin concentration increased significantly in the vein from the non-stenotic kidney (p = 0.02).
In renal artery stenoses, a Pd/Paratio of 0.90 can be considered a threshold value below which the stenosis is likely responsible for an up-regulation of renin production and, thus, for renovascular hypertension. These findings might contribute to better patient selection for renal angioplasty.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/j.jacc.2006.05.074</identifier><identifier>PMID: 17084261</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Aged ; Angioplasty ; Blood Pressure - physiology ; Cardiology ; Cardiovascular disease ; Catheterization - methods ; Coronary vessels ; Female ; Flow velocity ; Humans ; Hypertension ; Hypertension, Renovascular - diagnosis ; Hypertension, Renovascular - physiopathology ; Intubation ; Male ; Medical imaging ; Patients ; Plasma ; Renal Artery Obstruction - diagnosis ; Renal Artery Obstruction - physiopathology ; Severity of Illness Index ; Ultrasonography, Doppler, Color - methods</subject><ispartof>Journal of the American College of Cardiology, 2006-11, Vol.48 (9), p.1851-1855</ispartof><rights>2006 American College of Cardiology Foundation</rights><rights>Copyright Elsevier Limited Nov 7, 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c461t-7de7ace52d64d6f461b1356b067612330e6d938e0591b3fecd37884cd7cb46853</citedby><cites>FETCH-LOGICAL-c461t-7de7ace52d64d6f461b1356b067612330e6d938e0591b3fecd37884cd7cb46853</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17084261$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>De Bruyne, Bernard</creatorcontrib><creatorcontrib>Manoharan, Ganesh</creatorcontrib><creatorcontrib>Pijls, Nico H.J.</creatorcontrib><creatorcontrib>Verhamme, Katia</creatorcontrib><creatorcontrib>Madaric, Juraj</creatorcontrib><creatorcontrib>Bartunek, Jozef</creatorcontrib><creatorcontrib>Vanderheyden, Marc</creatorcontrib><creatorcontrib>Heyndrickx, Guy R.</creatorcontrib><title>Assessment of Renal Artery Stenosis Severity by Pressure Gradient Measurements</title><title>Journal of the American College of Cardiology</title><addtitle>J Am Coll Cardiol</addtitle><description>Assessment of Renal Artery Stenosis Severity by Pressure Gradient Measurements
Bernard De Bruyne, Ganesh Manoharan, Nico H. J. Pijls, Katia Verhamme, Juraj Madaric, Jozef Bartunek, Marc Vanderheyden, Guy R. Heyndrickx
To define “significant” renal artery stenosis, graded stenoses were created by progressive balloon inflation after stenting of a mild renal stenosis. Stenosis was expressed as the ratio of distal pressure (Pd) to aortic pressure (Pa). Renin was measured in the aorta and in both renal veins. For a Pd/Paratio >0.90, renin did not increase. Only for Pd/Pa<0.90 was an increase in renin observed in the renal vein of the stenotic kidney. Renal artery stenoses with a Pd/Paratio <0.90 trigger the production of renin and are, therefore, likely to be responsible for renovascular hypertension.
The purpose of this study was to define “significant” renal artery stenosis (i.e., a stenosis able to induce arterial hypertension).
The degree of renal artery stenosis that justifies an attempt at revascularization is unknown.
In 15 patients, transstenotic pressure measurements were obtained before and after unilateral stenting. After stenting, graded stenoses were created in the stented segment by progressive inflation of a balloon catheter. Stenosis severity was expressed as the ratio of distal pressure (Pd) corrected for aortic pressure (Pa). Balloon inflation pressure was adjusted to create 6° of stenosis (Pd/Pafrom 1.0 to 0.5, each step during 10 min). Plasma renin concentration was measured at the end of each step in the aorta and in both renal veins.
For a Pd/Paratio >0.90, no significant change in plasma renin concentration was observed. However, when Pd/Pabecame <0.90, a significant increase in renin was observed in the renal vein of the stenotic kidney, finally reaching a maximal increase of 346 ± 145% for Pd/Paof 0.50 (p = 0.006). These values returned to baseline when the stenosis was relieved. In addition, plasma renin concentration increased significantly in the vein from the non-stenotic kidney (p = 0.02).
In renal artery stenoses, a Pd/Paratio of 0.90 can be considered a threshold value below which the stenosis is likely responsible for an up-regulation of renin production and, thus, for renovascular hypertension. These findings might contribute to better patient selection for renal angioplasty.</description><subject>Aged</subject><subject>Angioplasty</subject><subject>Blood Pressure - physiology</subject><subject>Cardiology</subject><subject>Cardiovascular disease</subject><subject>Catheterization - methods</subject><subject>Coronary vessels</subject><subject>Female</subject><subject>Flow velocity</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Hypertension, Renovascular - diagnosis</subject><subject>Hypertension, Renovascular - physiopathology</subject><subject>Intubation</subject><subject>Male</subject><subject>Medical imaging</subject><subject>Patients</subject><subject>Plasma</subject><subject>Renal Artery Obstruction - diagnosis</subject><subject>Renal Artery Obstruction - physiopathology</subject><subject>Severity of Illness Index</subject><subject>Ultrasonography, Doppler, Color - methods</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNp9kF1LwzAUhoMobk7_gBdSELxrTZomacGbMXQK8wOn16FNTqFlXTWnHfTfm7KB4IVXB16e94XzEHLJaMQok7d1VOfGRDGlMqIioio5IlMmRBpykaljMqWKi5DRTE3IGWJNPZiy7JRMmKJpEks2JS9zREBsYNsFbRm8wzbfBHPXgRuCdQfbFisM1rADV3VDUAzBm_N47yBYutxWY-0Z8jEYJ_CcnJT5BuHicGfk8-H-Y_EYrl6XT4v5KjSJZF2oLKjcgIitTKwsfVYwLmRBpZIs5pyCtBlPgYqMFbwEY7lK08RYZYpEpoLPyM1-98u13z1gp5sKDWw2-RbaHrX_k_E4VR68_gPWbe_8k6iZoJKpLE5GKt5TxrWIDkr95aomd4NmVI-uda1H13p0ranQ3rUvXR2m-6IB-1s5yPXA3R4Ab2JXgdNovDEDtnJgOm3b6r_9H74CjwU</recordid><startdate>20061107</startdate><enddate>20061107</enddate><creator>De Bruyne, Bernard</creator><creator>Manoharan, Ganesh</creator><creator>Pijls, Nico H.J.</creator><creator>Verhamme, Katia</creator><creator>Madaric, Juraj</creator><creator>Bartunek, Jozef</creator><creator>Vanderheyden, Marc</creator><creator>Heyndrickx, Guy R.</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20061107</creationdate><title>Assessment of Renal Artery Stenosis Severity by Pressure Gradient Measurements</title><author>De Bruyne, Bernard ; 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Bernard De Bruyne, Ganesh Manoharan, Nico H. J. Pijls, Katia Verhamme, Juraj Madaric, Jozef Bartunek, Marc Vanderheyden, Guy R. Heyndrickx
To define “significant” renal artery stenosis, graded stenoses were created by progressive balloon inflation after stenting of a mild renal stenosis. Stenosis was expressed as the ratio of distal pressure (Pd) to aortic pressure (Pa). Renin was measured in the aorta and in both renal veins. For a Pd/Paratio >0.90, renin did not increase. Only for Pd/Pa<0.90 was an increase in renin observed in the renal vein of the stenotic kidney. Renal artery stenoses with a Pd/Paratio <0.90 trigger the production of renin and are, therefore, likely to be responsible for renovascular hypertension.
The purpose of this study was to define “significant” renal artery stenosis (i.e., a stenosis able to induce arterial hypertension).
The degree of renal artery stenosis that justifies an attempt at revascularization is unknown.
In 15 patients, transstenotic pressure measurements were obtained before and after unilateral stenting. After stenting, graded stenoses were created in the stented segment by progressive inflation of a balloon catheter. Stenosis severity was expressed as the ratio of distal pressure (Pd) corrected for aortic pressure (Pa). Balloon inflation pressure was adjusted to create 6° of stenosis (Pd/Pafrom 1.0 to 0.5, each step during 10 min). Plasma renin concentration was measured at the end of each step in the aorta and in both renal veins.
For a Pd/Paratio >0.90, no significant change in plasma renin concentration was observed. However, when Pd/Pabecame <0.90, a significant increase in renin was observed in the renal vein of the stenotic kidney, finally reaching a maximal increase of 346 ± 145% for Pd/Paof 0.50 (p = 0.006). These values returned to baseline when the stenosis was relieved. In addition, plasma renin concentration increased significantly in the vein from the non-stenotic kidney (p = 0.02).
In renal artery stenoses, a Pd/Paratio of 0.90 can be considered a threshold value below which the stenosis is likely responsible for an up-regulation of renin production and, thus, for renovascular hypertension. These findings might contribute to better patient selection for renal angioplasty.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>17084261</pmid><doi>10.1016/j.jacc.2006.05.074</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aged Angioplasty Blood Pressure - physiology Cardiology Cardiovascular disease Catheterization - methods Coronary vessels Female Flow velocity Humans Hypertension Hypertension, Renovascular - diagnosis Hypertension, Renovascular - physiopathology Intubation Male Medical imaging Patients Plasma Renal Artery Obstruction - diagnosis Renal Artery Obstruction - physiopathology Severity of Illness Index Ultrasonography, Doppler, Color - methods |
title | Assessment of Renal Artery Stenosis Severity by Pressure Gradient Measurements |
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