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P-273: Arterial stiffness and gradient of blood pressure at essential hypertension
The two major causes of increased large artery stiffness are aging and high blood pressure. This study was designed to assess the modifications in large artery elastic properties and their hemodynamic resistance at essential hypertension (EH). The pulse wave velocity (PWV) was evaluated in the follo...
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Published in: | American journal of hypertension 2001-04, Vol.14 (S1), p.120A-120A |
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description | The two major causes of increased large artery stiffness are aging and high blood pressure. This study was designed to assess the modifications in large artery elastic properties and their hemodynamic resistance at essential hypertension (EH). The pulse wave velocity (PWV) was evaluated in the following distance: carotid-femoral artery, femoral-posterior tibial artery and carotid-radial artery by piezoelectric detectors. The gradient of arterial pressure (AP) was analyzed in the distance: brachial-finger artery and brachial-posterior tibial artery applying auscultatory method (using acoustic system), and, simultaneously, the gradient of systolic AP was evaluated according to volume oscillations. Data were analyzed in supine position, when intravascular pressure was modified by rising and lowering the extremity referring to the heart level, and when subjects was passively tilted up to 70° with and without unilateral thigh arterial occlusion for 5 min. Group of 78 patients with EH (38-57 yrs aged men) and 31 age and gender matched controls were studied. Antihypertensive treatment, if any, was interrupted 8 days before the examination. In EH pts mean AP gradient in the distance of brachial-finger artery was increased (14.1±1.4 vs. 8.7±1.7 mmHg; P |
doi_str_mv | 10.1016/S0895-7061(01)01443-1 |
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This study was designed to assess the modifications in large artery elastic properties and their hemodynamic resistance at essential hypertension (EH). The pulse wave velocity (PWV) was evaluated in the following distance: carotid-femoral artery, femoral-posterior tibial artery and carotid-radial artery by piezoelectric detectors. The gradient of arterial pressure (AP) was analyzed in the distance: brachial-finger artery and brachial-posterior tibial artery applying auscultatory method (using acoustic system), and, simultaneously, the gradient of systolic AP was evaluated according to volume oscillations. Data were analyzed in supine position, when intravascular pressure was modified by rising and lowering the extremity referring to the heart level, and when subjects was passively tilted up to 70° with and without unilateral thigh arterial occlusion for 5 min. Group of 78 patients with EH (38-57 yrs aged men) and 31 age and gender matched controls were studied. Antihypertensive treatment, if any, was interrupted 8 days before the examination. In EH pts mean AP gradient in the distance of brachial-finger artery was increased (14.1±1.4 vs. 8.7±1.7 mmHg; P<0.02), whereas systolic and pulse pressure on tibial artery comparing to brachial artery was increased (Franc's phenomenon) and this increase was more expressed in EH pts (35.2±5.4 vs. 18.5±2.3 mmHg; P<0.02) and related (r=0.63; P<0.01) to systemic AP level. Upper extremity lowering and subjects tilting was related with less than expected (calculated hydrostatic pressure) increase of AP in distal parts. This difference disappeared on background of unilateral reactive hyperemia. At upper extremity elevation, decrease of finger AP corresponded to expected hydrostatic pressure decrease in both groups. In all analyzed distances PWV values were increased in EH pts comparing to controls (P<0.001) and were related to systemic arterial (brachial) pressure level (r=0.51-0.59; P<0.01). Modifications in regional AP caused by hydrostatic effect was related with corresponding PWV changes (r=0.8 in EH pts and r=0.72 in controls). This study suggests that alongside increased wall stiffness the hemodynamic resistance of large arteries is increased at EH and modifications in smooth muscle tone maintain important role in systemic and regional hemodynamic reactions.</description><identifier>ISSN: 0895-7061</identifier><identifier>EISSN: 1941-7225</identifier><identifier>EISSN: 1879-1905</identifier><identifier>DOI: 10.1016/S0895-7061(01)01443-1</identifier><identifier>CODEN: AJHYE6</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>arterial pressure gradient ; hypertension ; pulse wave velocity</subject><ispartof>American journal of hypertension, 2001-04, Vol.14 (S1), p.120A-120A</ispartof><rights>Copyright Nature Publishing Group Apr 2001</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids></links><search><creatorcontrib>Vitols, A</creatorcontrib><title>P-273: Arterial stiffness and gradient of blood pressure at essential hypertension</title><title>American journal of hypertension</title><addtitle>AJH</addtitle><description>The two major causes of increased large artery stiffness are aging and high blood pressure. This study was designed to assess the modifications in large artery elastic properties and their hemodynamic resistance at essential hypertension (EH). The pulse wave velocity (PWV) was evaluated in the following distance: carotid-femoral artery, femoral-posterior tibial artery and carotid-radial artery by piezoelectric detectors. The gradient of arterial pressure (AP) was analyzed in the distance: brachial-finger artery and brachial-posterior tibial artery applying auscultatory method (using acoustic system), and, simultaneously, the gradient of systolic AP was evaluated according to volume oscillations. Data were analyzed in supine position, when intravascular pressure was modified by rising and lowering the extremity referring to the heart level, and when subjects was passively tilted up to 70° with and without unilateral thigh arterial occlusion for 5 min. Group of 78 patients with EH (38-57 yrs aged men) and 31 age and gender matched controls were studied. Antihypertensive treatment, if any, was interrupted 8 days before the examination. In EH pts mean AP gradient in the distance of brachial-finger artery was increased (14.1±1.4 vs. 8.7±1.7 mmHg; P<0.02), whereas systolic and pulse pressure on tibial artery comparing to brachial artery was increased (Franc's phenomenon) and this increase was more expressed in EH pts (35.2±5.4 vs. 18.5±2.3 mmHg; P<0.02) and related (r=0.63; P<0.01) to systemic AP level. Upper extremity lowering and subjects tilting was related with less than expected (calculated hydrostatic pressure) increase of AP in distal parts. This difference disappeared on background of unilateral reactive hyperemia. At upper extremity elevation, decrease of finger AP corresponded to expected hydrostatic pressure decrease in both groups. In all analyzed distances PWV values were increased in EH pts comparing to controls (P<0.001) and were related to systemic arterial (brachial) pressure level (r=0.51-0.59; P<0.01). Modifications in regional AP caused by hydrostatic effect was related with corresponding PWV changes (r=0.8 in EH pts and r=0.72 in controls). This study suggests that alongside increased wall stiffness the hemodynamic resistance of large arteries is increased at EH and modifications in smooth muscle tone maintain important role in systemic and regional hemodynamic reactions.</description><subject>arterial pressure gradient</subject><subject>hypertension</subject><subject>pulse wave velocity</subject><issn>0895-7061</issn><issn>1941-7225</issn><issn>1879-1905</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><recordid>eNpFjkFLAzEQhYMoWKs_QQh40UN0kmySjbda1CpVi_YgvYRsk7Vb6-6abMH-eyMVPc0w73vvDULHFM4pUHnxArkWRIGkp0DPgGYZJ3QH9ajOKFGMiV3U-0P20UGMSwDIpKQ99DwhTPFLPAidD5Vd4dhVZVn7GLGtHX4L1lW-7nBT4mLVNA63IWnr4LHtcNqS9uNabFqfEupYNfUh2ivtKvqj39lH05vr6XBExk-3d8PBmFSaAnGZtDmbW8F1AdwpoQtFVca8k5Qx6QVzZckyqzTkzBa68K5I9zn3OZUu17yPTraxbWg-1z52ZtmsQ50aDQUmJdO5gEThLVXbLn1t2lB92LAxdrlgAFRInhCyRarY-a9_IrwbqbgSZvQ6M5PJjN8_PF6ZnH8DJPZrwg</recordid><startdate>200104</startdate><enddate>200104</enddate><creator>Vitols, A</creator><general>Oxford University Press</general><scope>BSCLL</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope></search><sort><creationdate>200104</creationdate><title>P-273: Arterial stiffness and gradient of blood pressure at essential hypertension</title><author>Vitols, A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i910-d46a82ca539b03d759b71742ed61226e52dff24a79082ab9bedb226c3e816d893</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>arterial pressure gradient</topic><topic>hypertension</topic><topic>pulse wave velocity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vitols, A</creatorcontrib><collection>Istex</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><jtitle>American journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vitols, A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>P-273: Arterial stiffness and gradient of blood pressure at essential hypertension</atitle><jtitle>American journal of hypertension</jtitle><addtitle>AJH</addtitle><date>2001-04</date><risdate>2001</risdate><volume>14</volume><issue>S1</issue><spage>120A</spage><epage>120A</epage><pages>120A-120A</pages><issn>0895-7061</issn><eissn>1941-7225</eissn><eissn>1879-1905</eissn><coden>AJHYE6</coden><abstract>The two major causes of increased large artery stiffness are aging and high blood pressure. This study was designed to assess the modifications in large artery elastic properties and their hemodynamic resistance at essential hypertension (EH). The pulse wave velocity (PWV) was evaluated in the following distance: carotid-femoral artery, femoral-posterior tibial artery and carotid-radial artery by piezoelectric detectors. The gradient of arterial pressure (AP) was analyzed in the distance: brachial-finger artery and brachial-posterior tibial artery applying auscultatory method (using acoustic system), and, simultaneously, the gradient of systolic AP was evaluated according to volume oscillations. Data were analyzed in supine position, when intravascular pressure was modified by rising and lowering the extremity referring to the heart level, and when subjects was passively tilted up to 70° with and without unilateral thigh arterial occlusion for 5 min. Group of 78 patients with EH (38-57 yrs aged men) and 31 age and gender matched controls were studied. Antihypertensive treatment, if any, was interrupted 8 days before the examination. In EH pts mean AP gradient in the distance of brachial-finger artery was increased (14.1±1.4 vs. 8.7±1.7 mmHg; P<0.02), whereas systolic and pulse pressure on tibial artery comparing to brachial artery was increased (Franc's phenomenon) and this increase was more expressed in EH pts (35.2±5.4 vs. 18.5±2.3 mmHg; P<0.02) and related (r=0.63; P<0.01) to systemic AP level. Upper extremity lowering and subjects tilting was related with less than expected (calculated hydrostatic pressure) increase of AP in distal parts. This difference disappeared on background of unilateral reactive hyperemia. At upper extremity elevation, decrease of finger AP corresponded to expected hydrostatic pressure decrease in both groups. In all analyzed distances PWV values were increased in EH pts comparing to controls (P<0.001) and were related to systemic arterial (brachial) pressure level (r=0.51-0.59; P<0.01). Modifications in regional AP caused by hydrostatic effect was related with corresponding PWV changes (r=0.8 in EH pts and r=0.72 in controls). This study suggests that alongside increased wall stiffness the hemodynamic resistance of large arteries is increased at EH and modifications in smooth muscle tone maintain important role in systemic and regional hemodynamic reactions.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><doi>10.1016/S0895-7061(01)01443-1</doi></addata></record> |
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title | P-273: Arterial stiffness and gradient of blood pressure at essential hypertension |
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