Contribution of mitral annular dynamics to LV diastolic filling with alteration in preload and inotropic state
Departments of 1 Cardiothoracic Surgery and 2 Radiology, Stanford University School of Medicine, Stanford, and 3 Laboratory of Cardiovascular Physiology and Biophysics, Research Institute, Palo Alto Medical Foundation, Palo Alto, California; and 4 Department of Clinical Physiology, Linköping Univers...
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Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2007-09, Vol.293 (3), p.H1473-H1479 |
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creator | Carlhall, C Kindberg, K Wigstrom, L Daughters, G. T Miller, D. C Karlsson, M Ingels, N. B., Jr |
description | Departments of 1 Cardiothoracic Surgery and 2 Radiology, Stanford University School of Medicine, Stanford, and 3 Laboratory of Cardiovascular Physiology and Biophysics, Research Institute, Palo Alto Medical Foundation, Palo Alto, California; and 4 Department of Clinical Physiology, Linköping University Hospital, and 5 Department of Biomedical Engineering, Linköping University, Linköping, Sweden
Submitted 16 February 2007
; accepted in final form 6 May 2007
Mitral annular (MA) excursion during diastole encompasses a volume that is part of total left ventricular (LV) filling volume (LVFV). Altered excursion or area variation of the MA due to changes in preload or inotropic state could affect LV filling. We hypothesized that changes in LV preload and inotropic state would not alter the contribution of MA dynamics to LVFV. Six sheep underwent marker implantation in the LV wall and around the MA. After 7–10 days, biplane fluoroscopy was used to obtain three-dimensional marker dynamics from sedated, closed-chest animals during control conditions, inotropic augmentation with calcium (Ca), preload reduction with nitroprusside (N), and vena caval occlusion (VCO). The contribution of MA dynamics to total LVFV was assessed using volume estimates based on multiple tetrahedra defined by the three-dimensional marker positions. Neither the absolute nor the relative contribution of MA dynamics to LVFV changed with Ca or N, although MA area decreased (Ca, P < 0.01; and N, P < 0.05) and excursion increased (Ca, P < 0.01). During VCO, the absolute contribution of MA dynamics to LVFV decreased ( P < 0.001), based on a reduction in both area ( P < 0.001) and excursion ( P < 0.01), but the relative contribution to LVFV increased from 18 ± 4 to 45 ± 13% ( P < 0.001). Thus MA dynamics contribute substantially to LV diastolic filling. Although MA excursion and mean area change with moderate preload reduction and inotropic augmentation, the contribution of MA dynamics to total LVFV is constant with sizeable magnitude. With marked preload reduction (VCO), the contribution of MA dynamics to LVFV becomes even more important.
diastolic function; inotropic augmentation; mitral annular excursion; preload reduction; regional left ventricular filling properties
Address for reprint requests and other correspondence: N. B. Ingels, Jr., Laboratory of Cardiovascular Physiology and Biophysics, Research Inst., Palo Alto Medical Foundation, 795 El Camino Real, Palo Alto, CA 94301 (e-mail: ingels{ |
doi_str_mv | 10.1152/ajpheart.00208.2007 |
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Submitted 16 February 2007
; accepted in final form 6 May 2007
Mitral annular (MA) excursion during diastole encompasses a volume that is part of total left ventricular (LV) filling volume (LVFV). Altered excursion or area variation of the MA due to changes in preload or inotropic state could affect LV filling. We hypothesized that changes in LV preload and inotropic state would not alter the contribution of MA dynamics to LVFV. Six sheep underwent marker implantation in the LV wall and around the MA. After 7–10 days, biplane fluoroscopy was used to obtain three-dimensional marker dynamics from sedated, closed-chest animals during control conditions, inotropic augmentation with calcium (Ca), preload reduction with nitroprusside (N), and vena caval occlusion (VCO). The contribution of MA dynamics to total LVFV was assessed using volume estimates based on multiple tetrahedra defined by the three-dimensional marker positions. Neither the absolute nor the relative contribution of MA dynamics to LVFV changed with Ca or N, although MA area decreased (Ca, P < 0.01; and N, P < 0.05) and excursion increased (Ca, P < 0.01). During VCO, the absolute contribution of MA dynamics to LVFV decreased ( P < 0.001), based on a reduction in both area ( P < 0.001) and excursion ( P < 0.01), but the relative contribution to LVFV increased from 18 ± 4 to 45 ± 13% ( P < 0.001). Thus MA dynamics contribute substantially to LV diastolic filling. Although MA excursion and mean area change with moderate preload reduction and inotropic augmentation, the contribution of MA dynamics to total LVFV is constant with sizeable magnitude. With marked preload reduction (VCO), the contribution of MA dynamics to LVFV becomes even more important.
diastolic function; inotropic augmentation; mitral annular excursion; preload reduction; regional left ventricular filling properties
Address for reprint requests and other correspondence: N. B. Ingels, Jr., Laboratory of Cardiovascular Physiology and Biophysics, Research Inst., Palo Alto Medical Foundation, 795 El Camino Real, Palo Alto, CA 94301 (e-mail: ingels{at}stanford.edu )]]></description><identifier>ISSN: 0363-6135</identifier><identifier>ISSN: 1522-1539</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.00208.2007</identifier><identifier>PMID: 17496217</identifier><identifier>CODEN: AJPPDI</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Animals ; Blood vessels ; Calcium - pharmacology ; Heart ; Heart rate ; Male ; Mitral Valve - drug effects ; Mitral Valve - physiology ; Myocardial Contraction - drug effects ; Myocardial Contraction - physiology ; Nitroprusside - pharmacology ; Sheep ; TECHNOLOGY ; TEKNIKVETENSKAP ; Vasodilator Agents - pharmacology ; Ventricular Function, Left - drug effects ; Ventricular Function, Left - physiology ; Ventricular Pressure</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2007-09, Vol.293 (3), p.H1473-H1479</ispartof><rights>Copyright American Physiological Society Sep 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c459t-9a17ffa5ede53bdc2ba48996f4352e5e23b7269b3227104b784d9306ec042fdd3</citedby><cites>FETCH-LOGICAL-c459t-9a17ffa5ede53bdc2ba48996f4352e5e23b7269b3227104b784d9306ec042fdd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,777,781,882,3026,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17496217$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-41883$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Carlhall, C</creatorcontrib><creatorcontrib>Kindberg, K</creatorcontrib><creatorcontrib>Wigstrom, L</creatorcontrib><creatorcontrib>Daughters, G. T</creatorcontrib><creatorcontrib>Miller, D. C</creatorcontrib><creatorcontrib>Karlsson, M</creatorcontrib><creatorcontrib>Ingels, N. B., Jr</creatorcontrib><title>Contribution of mitral annular dynamics to LV diastolic filling with alteration in preload and inotropic state</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description><![CDATA[Departments of 1 Cardiothoracic Surgery and 2 Radiology, Stanford University School of Medicine, Stanford, and 3 Laboratory of Cardiovascular Physiology and Biophysics, Research Institute, Palo Alto Medical Foundation, Palo Alto, California; and 4 Department of Clinical Physiology, Linköping University Hospital, and 5 Department of Biomedical Engineering, Linköping University, Linköping, Sweden
Submitted 16 February 2007
; accepted in final form 6 May 2007
Mitral annular (MA) excursion during diastole encompasses a volume that is part of total left ventricular (LV) filling volume (LVFV). Altered excursion or area variation of the MA due to changes in preload or inotropic state could affect LV filling. We hypothesized that changes in LV preload and inotropic state would not alter the contribution of MA dynamics to LVFV. Six sheep underwent marker implantation in the LV wall and around the MA. After 7–10 days, biplane fluoroscopy was used to obtain three-dimensional marker dynamics from sedated, closed-chest animals during control conditions, inotropic augmentation with calcium (Ca), preload reduction with nitroprusside (N), and vena caval occlusion (VCO). The contribution of MA dynamics to total LVFV was assessed using volume estimates based on multiple tetrahedra defined by the three-dimensional marker positions. Neither the absolute nor the relative contribution of MA dynamics to LVFV changed with Ca or N, although MA area decreased (Ca, P < 0.01; and N, P < 0.05) and excursion increased (Ca, P < 0.01). During VCO, the absolute contribution of MA dynamics to LVFV decreased ( P < 0.001), based on a reduction in both area ( P < 0.001) and excursion ( P < 0.01), but the relative contribution to LVFV increased from 18 ± 4 to 45 ± 13% ( P < 0.001). Thus MA dynamics contribute substantially to LV diastolic filling. Although MA excursion and mean area change with moderate preload reduction and inotropic augmentation, the contribution of MA dynamics to total LVFV is constant with sizeable magnitude. With marked preload reduction (VCO), the contribution of MA dynamics to LVFV becomes even more important.
diastolic function; inotropic augmentation; mitral annular excursion; preload reduction; regional left ventricular filling properties
Address for reprint requests and other correspondence: N. B. Ingels, Jr., Laboratory of Cardiovascular Physiology and Biophysics, Research Inst., Palo Alto Medical Foundation, 795 El Camino Real, Palo Alto, CA 94301 (e-mail: ingels{at}stanford.edu )]]></description><subject>Animals</subject><subject>Blood vessels</subject><subject>Calcium - pharmacology</subject><subject>Heart</subject><subject>Heart rate</subject><subject>Male</subject><subject>Mitral Valve - drug effects</subject><subject>Mitral Valve - physiology</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocardial Contraction - physiology</subject><subject>Nitroprusside - pharmacology</subject><subject>Sheep</subject><subject>TECHNOLOGY</subject><subject>TEKNIKVETENSKAP</subject><subject>Vasodilator Agents - pharmacology</subject><subject>Ventricular Function, Left - drug effects</subject><subject>Ventricular Function, Left - physiology</subject><subject>Ventricular Pressure</subject><issn>0363-6135</issn><issn>1522-1539</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU2PEyEAhonRuHX1F5gY4sGT0-VjBoZ42lTXNWniZd0rYQamQ0NhBCbd_nvZba3GRC6E8DwvHy8AbzFaYtyQK7WdRqNiXiJEULskCPFnYFF2SIUbKp6DBaKMVgzT5gK8SmmLEGo4oy_BBea1YATzBfCr4HO03Zxt8DAMcGdzVA4q72enItQHr3a2TzAHuL6H2qqUg7M9HKxz1m_g3uYRKpdNVE8R1sMpGheULhm6LEOOYSpCyiqb1-DFoFwyb07zJfhx8-VudVutv3_9trpeV33diFwJhfkwqMZo09BO96RTdSsEG2raENMYQjtOmOgoIRyjuuNtrQVFzPSoJoPW9BJ8POamvZnmTk7R7lQ8yKCs_Gzvr2WIG-nsLGvctrTgH474FMPP2aQsdzb1xjnlTZiTZC2hgrO6gO__Abdhjr48RRJSvrQMViB6hPoYUopmOB-PkXysTv6uTj5VJx-rK9a7U_Tc7Yz-45y6KsCnIzDazbi30chpPCQbXNgc5M3s3J15yOdoIqik8hbXnMpJD8W--r99vs9fFv0FklG-0Q</recordid><startdate>20070901</startdate><enddate>20070901</enddate><creator>Carlhall, C</creator><creator>Kindberg, K</creator><creator>Wigstrom, L</creator><creator>Daughters, G. T</creator><creator>Miller, D. C</creator><creator>Karlsson, M</creator><creator>Ingels, N. B., Jr</creator><general>American Physiological Society</general><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>7QP</scope><scope>7QR</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>DG8</scope></search><sort><creationdate>20070901</creationdate><title>Contribution of mitral annular dynamics to LV diastolic filling with alteration in preload and inotropic state</title><author>Carlhall, C ; Kindberg, K ; Wigstrom, L ; Daughters, G. T ; Miller, D. C ; Karlsson, M ; Ingels, N. B., Jr</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c459t-9a17ffa5ede53bdc2ba48996f4352e5e23b7269b3227104b784d9306ec042fdd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Blood vessels</topic><topic>Calcium - pharmacology</topic><topic>Heart</topic><topic>Heart rate</topic><topic>Male</topic><topic>Mitral Valve - drug effects</topic><topic>Mitral Valve - physiology</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocardial Contraction - physiology</topic><topic>Nitroprusside - pharmacology</topic><topic>Sheep</topic><topic>TECHNOLOGY</topic><topic>TEKNIKVETENSKAP</topic><topic>Vasodilator Agents - pharmacology</topic><topic>Ventricular Function, Left - drug effects</topic><topic>Ventricular Function, Left - physiology</topic><topic>Ventricular Pressure</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Carlhall, C</creatorcontrib><creatorcontrib>Kindberg, K</creatorcontrib><creatorcontrib>Wigstrom, L</creatorcontrib><creatorcontrib>Daughters, G. T</creatorcontrib><creatorcontrib>Miller, D. C</creatorcontrib><creatorcontrib>Karlsson, M</creatorcontrib><creatorcontrib>Ingels, N. 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Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Carlhall, C</au><au>Kindberg, K</au><au>Wigstrom, L</au><au>Daughters, G. T</au><au>Miller, D. C</au><au>Karlsson, M</au><au>Ingels, N. B., Jr</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Contribution of mitral annular dynamics to LV diastolic filling with alteration in preload and inotropic state</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2007-09-01</date><risdate>2007</risdate><volume>293</volume><issue>3</issue><spage>H1473</spage><epage>H1479</epage><pages>H1473-H1479</pages><issn>0363-6135</issn><issn>1522-1539</issn><eissn>1522-1539</eissn><coden>AJPPDI</coden><abstract><![CDATA[Departments of 1 Cardiothoracic Surgery and 2 Radiology, Stanford University School of Medicine, Stanford, and 3 Laboratory of Cardiovascular Physiology and Biophysics, Research Institute, Palo Alto Medical Foundation, Palo Alto, California; and 4 Department of Clinical Physiology, Linköping University Hospital, and 5 Department of Biomedical Engineering, Linköping University, Linköping, Sweden
Submitted 16 February 2007
; accepted in final form 6 May 2007
Mitral annular (MA) excursion during diastole encompasses a volume that is part of total left ventricular (LV) filling volume (LVFV). Altered excursion or area variation of the MA due to changes in preload or inotropic state could affect LV filling. We hypothesized that changes in LV preload and inotropic state would not alter the contribution of MA dynamics to LVFV. Six sheep underwent marker implantation in the LV wall and around the MA. After 7–10 days, biplane fluoroscopy was used to obtain three-dimensional marker dynamics from sedated, closed-chest animals during control conditions, inotropic augmentation with calcium (Ca), preload reduction with nitroprusside (N), and vena caval occlusion (VCO). The contribution of MA dynamics to total LVFV was assessed using volume estimates based on multiple tetrahedra defined by the three-dimensional marker positions. Neither the absolute nor the relative contribution of MA dynamics to LVFV changed with Ca or N, although MA area decreased (Ca, P < 0.01; and N, P < 0.05) and excursion increased (Ca, P < 0.01). During VCO, the absolute contribution of MA dynamics to LVFV decreased ( P < 0.001), based on a reduction in both area ( P < 0.001) and excursion ( P < 0.01), but the relative contribution to LVFV increased from 18 ± 4 to 45 ± 13% ( P < 0.001). Thus MA dynamics contribute substantially to LV diastolic filling. Although MA excursion and mean area change with moderate preload reduction and inotropic augmentation, the contribution of MA dynamics to total LVFV is constant with sizeable magnitude. With marked preload reduction (VCO), the contribution of MA dynamics to LVFV becomes even more important.
diastolic function; inotropic augmentation; mitral annular excursion; preload reduction; regional left ventricular filling properties
Address for reprint requests and other correspondence: N. B. Ingels, Jr., Laboratory of Cardiovascular Physiology and Biophysics, Research Inst., Palo Alto Medical Foundation, 795 El Camino Real, Palo Alto, CA 94301 (e-mail: ingels{at}stanford.edu )]]></abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>17496217</pmid><doi>10.1152/ajpheart.00208.2007</doi></addata></record> |
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source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
subjects | Animals Blood vessels Calcium - pharmacology Heart Heart rate Male Mitral Valve - drug effects Mitral Valve - physiology Myocardial Contraction - drug effects Myocardial Contraction - physiology Nitroprusside - pharmacology Sheep TECHNOLOGY TEKNIKVETENSKAP Vasodilator Agents - pharmacology Ventricular Function, Left - drug effects Ventricular Function, Left - physiology Ventricular Pressure |
title | Contribution of mitral annular dynamics to LV diastolic filling with alteration in preload and inotropic state |
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