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EFFECTIVE ARTERIAL ELASTANCE AS INDEX OF ARTERIAL VASCULAR LOAD IN HUMANS

Background. This study tested whether the simple ratio of ventricular end-systolic pressure to stroke volume, known as the effective arterial elastance (E(a)), provides a valid measure of arterial load in humans with normal and aged hypertensive vasculatures. Methods and Results. Ventricular pressur...

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Published in:Circulation (New York, N.Y.) N.Y.), 1992-08, Vol.86 (2), p.513-521
Main Authors: KELLY, RP, TING, CT, YANG, TM, LIU, CP, MAUGHAN, WL, CHANG, MS, KASS, DA
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TING, CT
YANG, TM
LIU, CP
MAUGHAN, WL
CHANG, MS
KASS, DA
description Background. This study tested whether the simple ratio of ventricular end-systolic pressure to stroke volume, known as the effective arterial elastance (E(a)), provides a valid measure of arterial load in humans with normal and aged hypertensive vasculatures. Methods and Results. Ventricular pressure-volume and invasive aortic pressure and flow were simultaneously determined in 10 subjects (four young normotensive and six older hypertensive). Measurements were obtained at rest, during mechanically reduced preload, and after pharmacological interventions. Two measures of arterial load were compared: One was derived from aortic input impedance and arterial compliance data using an algebraic expression based on a three-element Windkessel model of the arterial system [E(a)(Z)], and the other was more simply measured as the ratio of ventricular end-systolic pressure to stroke volume [E(a)(PV)]. Although derived from completely different data sources and despite the simplifying assumptions of E(a)(PV), both E(a)(Z) and E(a)(PV) were virtually identical over a broad range of altered conditions: E(a)(PV) = 0.97 . E(a)(Z) +0.17; n=33, r2=0.98, SEE=0.09, p
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This study tested whether the simple ratio of ventricular end-systolic pressure to stroke volume, known as the effective arterial elastance (E(a)), provides a valid measure of arterial load in humans with normal and aged hypertensive vasculatures. Methods and Results. Ventricular pressure-volume and invasive aortic pressure and flow were simultaneously determined in 10 subjects (four young normotensive and six older hypertensive). Measurements were obtained at rest, during mechanically reduced preload, and after pharmacological interventions. Two measures of arterial load were compared: One was derived from aortic input impedance and arterial compliance data using an algebraic expression based on a three-element Windkessel model of the arterial system [E(a)(Z)], and the other was more simply measured as the ratio of ventricular end-systolic pressure to stroke volume [E(a)(PV)]. Although derived from completely different data sources and despite the simplifying assumptions of E(a)(PV), both E(a)(Z) and E(a)(PV) were virtually identical over a broad range of altered conditions: E(a)(PV) = 0.97 . E(a)(Z) +0.17; n=33, r2=0.98, SEE=0.09, p&lt;0.0001. Whereas E(a)(PV) also correlated with mean arterial resistance, it exceeded resistance by as much as 25% in older hypertensive subjects (because of reduced compliance and wave reflections), which better indexed the arterial load effects on the ventricle. Simple methods to estimate E(a) (PV) from routine arterial pressures were tested and validated. Conclusions. E(a)(PV) provides a convenient, useful method to assess arterial load and its impact on the human ventricle. These results highlight effects of increased pulsatile load caused by aging or hypertension on the pressure-volume loop and indicate that this load and its effects on cardiac performance are often underestimated by mean arterial resistance but are better accounted for by E(a).</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.86.2.513</identifier><identifier>PMID: 1638719</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>PHILADELPHIA: Lippincott Williams &amp; Wilkins</publisher><subject>Adult ; Aorta - physiology ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiac &amp; Cardiovascular Systems ; Cardiology. Vascular system ; Cardiovascular System &amp; Cardiology ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Female ; Humans ; Hypertension - physiopathology ; Life Sciences &amp; Biomedicine ; Male ; Medical sciences ; Models, Cardiovascular ; Models, Theoretical ; Myocardial Contraction - physiology ; Peripheral Vascular Disease ; Pulsatile Flow - physiology ; Science &amp; Technology ; Space life sciences ; Stroke Volume - physiology ; Vascular Resistance - physiology ; Ventricular Function - physiology</subject><ispartof>Circulation (New York, N.Y.), 1992-08, Vol.86 (2), p.513-521</ispartof><rights>1992 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>640</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wosA1992JH00900021</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c514t-8717886c6bc6d92344b6b9df0585f31831d2bd038c4e64ff999dedefa71d4efc3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27225,27957,27958</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=5523878$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1638719$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KELLY, RP</creatorcontrib><creatorcontrib>TING, CT</creatorcontrib><creatorcontrib>YANG, TM</creatorcontrib><creatorcontrib>LIU, CP</creatorcontrib><creatorcontrib>MAUGHAN, WL</creatorcontrib><creatorcontrib>CHANG, MS</creatorcontrib><creatorcontrib>KASS, DA</creatorcontrib><title>EFFECTIVE ARTERIAL ELASTANCE AS INDEX OF ARTERIAL VASCULAR LOAD IN HUMANS</title><title>Circulation (New York, N.Y.)</title><addtitle>CIRCULATION</addtitle><addtitle>Circulation</addtitle><description>Background. This study tested whether the simple ratio of ventricular end-systolic pressure to stroke volume, known as the effective arterial elastance (E(a)), provides a valid measure of arterial load in humans with normal and aged hypertensive vasculatures. Methods and Results. Ventricular pressure-volume and invasive aortic pressure and flow were simultaneously determined in 10 subjects (four young normotensive and six older hypertensive). Measurements were obtained at rest, during mechanically reduced preload, and after pharmacological interventions. Two measures of arterial load were compared: One was derived from aortic input impedance and arterial compliance data using an algebraic expression based on a three-element Windkessel model of the arterial system [E(a)(Z)], and the other was more simply measured as the ratio of ventricular end-systolic pressure to stroke volume [E(a)(PV)]. Although derived from completely different data sources and despite the simplifying assumptions of E(a)(PV), both E(a)(Z) and E(a)(PV) were virtually identical over a broad range of altered conditions: E(a)(PV) = 0.97 . E(a)(Z) +0.17; n=33, r2=0.98, SEE=0.09, p&lt;0.0001. Whereas E(a)(PV) also correlated with mean arterial resistance, it exceeded resistance by as much as 25% in older hypertensive subjects (because of reduced compliance and wave reflections), which better indexed the arterial load effects on the ventricle. Simple methods to estimate E(a) (PV) from routine arterial pressures were tested and validated. Conclusions. E(a)(PV) provides a convenient, useful method to assess arterial load and its impact on the human ventricle. These results highlight effects of increased pulsatile load caused by aging or hypertension on the pressure-volume loop and indicate that this load and its effects on cardiac performance are often underestimated by mean arterial resistance but are better accounted for by E(a).</description><subject>Adult</subject><subject>Aorta - physiology</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiac &amp; Cardiovascular Systems</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular System &amp; Cardiology</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Female</subject><subject>Humans</subject><subject>Hypertension - physiopathology</subject><subject>Life Sciences &amp; Biomedicine</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Models, Cardiovascular</subject><subject>Models, Theoretical</subject><subject>Myocardial Contraction - physiology</subject><subject>Peripheral Vascular Disease</subject><subject>Pulsatile Flow - physiology</subject><subject>Science &amp; Technology</subject><subject>Space life sciences</subject><subject>Stroke Volume - physiology</subject><subject>Vascular Resistance - physiology</subject><subject>Ventricular Function - physiology</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EZCTM</sourceid><recordid>eNqNkc9r2zAUx8XY6NJu554KPoxdil09yZKlo3CcxcNLID_KbsKWJfBI7NZyGP3vq5HQXncST9_Pew8-D6FbwAkAhwcMSV5uEsETkjCgH9AMGEnjlFH5Ec0wxjLOKCGf0bX3f0LJacau0BVwKjKQM1QWi0WR78rHIlKbXbEpVRUVldru1CoPX9uoXM2L39F68R4_qm2-r9QmqtZqHvJouf-lVtsv6JOrD95-vbw3aL8odvkyrtY_ylxVsWGQTnFYmwnBDW8MbyWhadrwRrYOM8EcBUGhJU2LqTCp5alzUsrWttbVGbSpdYbeoO_nuU_j8HyyftLHzht7ONS9HU5eZxTLoEYG8OEMmnHwfrROP43dsR5fNGD9T57GoIM8LbgmOsgLHXeX0afmaNt3_mwr5N8uee1NfXBj3ZvOv2GMkcCJgN2fsb-2GZw3ne2NfaMUSEl-LsNlwjkIBFr8P513Uz11Q58Pp36ir1O0kHg</recordid><startdate>19920801</startdate><enddate>19920801</enddate><creator>KELLY, RP</creator><creator>TING, CT</creator><creator>YANG, TM</creator><creator>LIU, CP</creator><creator>MAUGHAN, WL</creator><creator>CHANG, MS</creator><creator>KASS, DA</creator><general>Lippincott Williams &amp; Wilkins</general><scope>BLEPL</scope><scope>DTL</scope><scope>EZCTM</scope><scope>IQODW</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>7X8</scope></search><sort><creationdate>19920801</creationdate><title>EFFECTIVE ARTERIAL ELASTANCE AS INDEX OF ARTERIAL VASCULAR LOAD IN HUMANS</title><author>KELLY, RP ; TING, CT ; YANG, TM ; LIU, CP ; MAUGHAN, WL ; CHANG, MS ; KASS, DA</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-8717886c6bc6d92344b6b9df0585f31831d2bd038c4e64ff999dedefa71d4efc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Adult</topic><topic>Aorta - physiology</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiac &amp; Cardiovascular Systems</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular System &amp; Cardiology</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Female</topic><topic>Humans</topic><topic>Hypertension - physiopathology</topic><topic>Life Sciences &amp; Biomedicine</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Models, Cardiovascular</topic><topic>Models, Theoretical</topic><topic>Myocardial Contraction - physiology</topic><topic>Peripheral Vascular Disease</topic><topic>Pulsatile Flow - physiology</topic><topic>Science &amp; Technology</topic><topic>Space life sciences</topic><topic>Stroke Volume - physiology</topic><topic>Vascular Resistance - physiology</topic><topic>Ventricular Function - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KELLY, RP</creatorcontrib><creatorcontrib>TING, CT</creatorcontrib><creatorcontrib>YANG, TM</creatorcontrib><creatorcontrib>LIU, CP</creatorcontrib><creatorcontrib>MAUGHAN, WL</creatorcontrib><creatorcontrib>CHANG, MS</creatorcontrib><creatorcontrib>KASS, DA</creatorcontrib><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Web of Science - Science Citation Index Expanded - 1992</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KELLY, RP</au><au>TING, CT</au><au>YANG, TM</au><au>LIU, CP</au><au>MAUGHAN, WL</au><au>CHANG, MS</au><au>KASS, DA</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>EFFECTIVE ARTERIAL ELASTANCE AS INDEX OF ARTERIAL VASCULAR LOAD IN HUMANS</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><stitle>CIRCULATION</stitle><addtitle>Circulation</addtitle><date>1992-08-01</date><risdate>1992</risdate><volume>86</volume><issue>2</issue><spage>513</spage><epage>521</epage><pages>513-521</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><notes>Medline</notes><notes>NIH RePORTER</notes><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Background. This study tested whether the simple ratio of ventricular end-systolic pressure to stroke volume, known as the effective arterial elastance (E(a)), provides a valid measure of arterial load in humans with normal and aged hypertensive vasculatures. Methods and Results. Ventricular pressure-volume and invasive aortic pressure and flow were simultaneously determined in 10 subjects (four young normotensive and six older hypertensive). Measurements were obtained at rest, during mechanically reduced preload, and after pharmacological interventions. Two measures of arterial load were compared: One was derived from aortic input impedance and arterial compliance data using an algebraic expression based on a three-element Windkessel model of the arterial system [E(a)(Z)], and the other was more simply measured as the ratio of ventricular end-systolic pressure to stroke volume [E(a)(PV)]. Although derived from completely different data sources and despite the simplifying assumptions of E(a)(PV), both E(a)(Z) and E(a)(PV) were virtually identical over a broad range of altered conditions: E(a)(PV) = 0.97 . E(a)(Z) +0.17; n=33, r2=0.98, SEE=0.09, p&lt;0.0001. Whereas E(a)(PV) also correlated with mean arterial resistance, it exceeded resistance by as much as 25% in older hypertensive subjects (because of reduced compliance and wave reflections), which better indexed the arterial load effects on the ventricle. Simple methods to estimate E(a) (PV) from routine arterial pressures were tested and validated. Conclusions. E(a)(PV) provides a convenient, useful method to assess arterial load and its impact on the human ventricle. These results highlight effects of increased pulsatile load caused by aging or hypertension on the pressure-volume loop and indicate that this load and its effects on cardiac performance are often underestimated by mean arterial resistance but are better accounted for by E(a).</abstract><cop>PHILADELPHIA</cop><pub>Lippincott Williams &amp; Wilkins</pub><pmid>1638719</pmid><doi>10.1161/01.CIR.86.2.513</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
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source Web of Science - Science Citation Index Expanded - 1992<img src="https://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" />; EZB Electronic Journals Library
subjects Adult
Aorta - physiology
Arterial hypertension. Arterial hypotension
Biological and medical sciences
Blood and lymphatic vessels
Cardiac & Cardiovascular Systems
Cardiology. Vascular system
Cardiovascular System & Cardiology
Clinical manifestations. Epidemiology. Investigative techniques. Etiology
Female
Humans
Hypertension - physiopathology
Life Sciences & Biomedicine
Male
Medical sciences
Models, Cardiovascular
Models, Theoretical
Myocardial Contraction - physiology
Peripheral Vascular Disease
Pulsatile Flow - physiology
Science & Technology
Space life sciences
Stroke Volume - physiology
Vascular Resistance - physiology
Ventricular Function - physiology
title EFFECTIVE ARTERIAL ELASTANCE AS INDEX OF ARTERIAL VASCULAR LOAD IN HUMANS
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