Transcatheter Replacement of Stenotic Aortic Valve Normalizes Cardiac–Coronary Interaction by Restoration of Systolic Coronary Flow Dynamics as Assessed by Wave Intensity Analysis

BACKGROUND—Aortic valve stenosis (AS) can cause angina despite unobstructed coronary arteries, which may be related to increased compression of the intramural microcirculation, especially at the subendocardium. We assessed coronary wave intensity and phasic flow velocity patterns to unravel changes...

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Veröffentlicht in:Circulation. Cardiovascular interventions 2016-04, Vol.9 (4), p.e002356-e002356
Hauptverfasser: Rolandi, M Cristina, Wiegerinck, Esther M.A, Casadonte, Lorena, Yong, Ze-Yie, Koch, Karel T, Vis, Marije, Piek, Jan J, Baan, Jan, Spaan, Jos A.E, Siebes, Maria
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container_end_page e002356
container_issue 4
container_start_page e002356
container_title Circulation. Cardiovascular interventions
container_volume 9
creator Rolandi, M Cristina
Wiegerinck, Esther M.A
Casadonte, Lorena
Yong, Ze-Yie
Koch, Karel T
Vis, Marije
Piek, Jan J
Baan, Jan
Spaan, Jos A.E
Siebes, Maria
description BACKGROUND—Aortic valve stenosis (AS) can cause angina despite unobstructed coronary arteries, which may be related to increased compression of the intramural microcirculation, especially at the subendocardium. We assessed coronary wave intensity and phasic flow velocity patterns to unravel changes in cardiac–coronary interaction because of transcatheter aortic valve implantation (TAVI). METHODS AND RESULTS—Intracoronary pressure and flow velocity were measured at rest and maximal hyperemia in undiseased vessels in 15 patients with AS before and after TAVI and in 12 control patients. Coronary flow reserve, systolic and diastolic velocity time integrals, and the energies of forward (aorta-originating) and backward (microcirculatory-originating) coronary waves were determined. Coronary flow reserve was 2.8±0.2 (mean±SEM) in control and 1.8±0.1 in AS (P30%. The increase in forward compression wave with TAVI was related to an increase in systolic velocity time integral. AS or TAVI did not alter diastolic velocity time integral. CONCLUSIONS—Reduced coronary forward wave energy and systolic velocity time integral imply a compromised systolic flow velocity with AS that is restored after TAVI, suggesting an acute relief of excess compression in systole that likely benefits subendocardial perfusion. Vasodilation is observed to be a major determinant of backward waves.
doi_str_mv 10.1161/CIRCINTERVENTIONS.114.002356
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We assessed coronary wave intensity and phasic flow velocity patterns to unravel changes in cardiac–coronary interaction because of transcatheter aortic valve implantation (TAVI). METHODS AND RESULTS—Intracoronary pressure and flow velocity were measured at rest and maximal hyperemia in undiseased vessels in 15 patients with AS before and after TAVI and in 12 control patients. Coronary flow reserve, systolic and diastolic velocity time integrals, and the energies of forward (aorta-originating) and backward (microcirculatory-originating) coronary waves were determined. Coronary flow reserve was 2.8±0.2 (mean±SEM) in control and 1.8±0.1 in AS (P&lt;0.005) and was not restored by TAVI. Compared with control, the resting backward expansion wave was 45% higher in AS. The peak of the systolic forward compression wave was delayed in AS, consistent with a delayed peak aortic pressure, which was partially restored after TAVI. The energy of forward waves doubled after TAVI, whereas the backward expansion wave increased by &gt;30%. The increase in forward compression wave with TAVI was related to an increase in systolic velocity time integral. AS or TAVI did not alter diastolic velocity time integral. CONCLUSIONS—Reduced coronary forward wave energy and systolic velocity time integral imply a compromised systolic flow velocity with AS that is restored after TAVI, suggesting an acute relief of excess compression in systole that likely benefits subendocardial perfusion. Vasodilation is observed to be a major determinant of backward waves.</description><identifier>ISSN: 1941-7640</identifier><identifier>EISSN: 1941-7632</identifier><identifier>DOI: 10.1161/CIRCINTERVENTIONS.114.002356</identifier><identifier>PMID: 27001805</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Aged ; Aged, 80 and over ; Aortic Valve - physiopathology ; Aortic Valve Stenosis - diagnosis ; Aortic Valve Stenosis - physiopathology ; Aortic Valve Stenosis - therapy ; Blood Flow Velocity ; Cardiac Catheterization - instrumentation ; Case-Control Studies ; Coronary Angiography ; Coronary Circulation ; Coronary Vessels - diagnostic imaging ; Coronary Vessels - physiopathology ; Female ; Heart Valve Prosthesis Implantation - instrumentation ; Heart Valve Prosthesis Implantation - methods ; Hemodynamics ; Humans ; Male ; Middle Aged ; Pulsatile Flow ; Recovery of Function ; Systole ; Time Factors ; Treatment Outcome ; Vasodilation</subject><ispartof>Circulation. Cardiovascular interventions, 2016-04, Vol.9 (4), p.e002356-e002356</ispartof><rights>2016 American Heart Association, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4887-79cf4e5c2b80ad07cf8a2c6871ef25d7cd8a795710796364cdc338bc5b3969153</citedby><cites>FETCH-LOGICAL-c4887-79cf4e5c2b80ad07cf8a2c6871ef25d7cd8a795710796364cdc338bc5b3969153</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27001805$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rolandi, M Cristina</creatorcontrib><creatorcontrib>Wiegerinck, Esther M.A</creatorcontrib><creatorcontrib>Casadonte, Lorena</creatorcontrib><creatorcontrib>Yong, Ze-Yie</creatorcontrib><creatorcontrib>Koch, Karel T</creatorcontrib><creatorcontrib>Vis, Marije</creatorcontrib><creatorcontrib>Piek, Jan J</creatorcontrib><creatorcontrib>Baan, Jan</creatorcontrib><creatorcontrib>Spaan, Jos A.E</creatorcontrib><creatorcontrib>Siebes, Maria</creatorcontrib><title>Transcatheter Replacement of Stenotic Aortic Valve Normalizes Cardiac–Coronary Interaction by Restoration of Systolic Coronary Flow Dynamics as Assessed by Wave Intensity Analysis</title><title>Circulation. Cardiovascular interventions</title><addtitle>Circ Cardiovasc Interv</addtitle><description>BACKGROUND—Aortic valve stenosis (AS) can cause angina despite unobstructed coronary arteries, which may be related to increased compression of the intramural microcirculation, especially at the subendocardium. We assessed coronary wave intensity and phasic flow velocity patterns to unravel changes in cardiac–coronary interaction because of transcatheter aortic valve implantation (TAVI). METHODS AND RESULTS—Intracoronary pressure and flow velocity were measured at rest and maximal hyperemia in undiseased vessels in 15 patients with AS before and after TAVI and in 12 control patients. Coronary flow reserve, systolic and diastolic velocity time integrals, and the energies of forward (aorta-originating) and backward (microcirculatory-originating) coronary waves were determined. Coronary flow reserve was 2.8±0.2 (mean±SEM) in control and 1.8±0.1 in AS (P&lt;0.005) and was not restored by TAVI. Compared with control, the resting backward expansion wave was 45% higher in AS. The peak of the systolic forward compression wave was delayed in AS, consistent with a delayed peak aortic pressure, which was partially restored after TAVI. The energy of forward waves doubled after TAVI, whereas the backward expansion wave increased by &gt;30%. The increase in forward compression wave with TAVI was related to an increase in systolic velocity time integral. AS or TAVI did not alter diastolic velocity time integral. CONCLUSIONS—Reduced coronary forward wave energy and systolic velocity time integral imply a compromised systolic flow velocity with AS that is restored after TAVI, suggesting an acute relief of excess compression in systole that likely benefits subendocardial perfusion. 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Cardiovascular interventions</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rolandi, M Cristina</au><au>Wiegerinck, Esther M.A</au><au>Casadonte, Lorena</au><au>Yong, Ze-Yie</au><au>Koch, Karel T</au><au>Vis, Marije</au><au>Piek, Jan J</au><au>Baan, Jan</au><au>Spaan, Jos A.E</au><au>Siebes, Maria</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transcatheter Replacement of Stenotic Aortic Valve Normalizes Cardiac–Coronary Interaction by Restoration of Systolic Coronary Flow Dynamics as Assessed by Wave Intensity Analysis</atitle><jtitle>Circulation. Cardiovascular interventions</jtitle><addtitle>Circ Cardiovasc Interv</addtitle><date>2016-04</date><risdate>2016</risdate><volume>9</volume><issue>4</issue><spage>e002356</spage><epage>e002356</epage><pages>e002356-e002356</pages><issn>1941-7640</issn><eissn>1941-7632</eissn><abstract>BACKGROUND—Aortic valve stenosis (AS) can cause angina despite unobstructed coronary arteries, which may be related to increased compression of the intramural microcirculation, especially at the subendocardium. We assessed coronary wave intensity and phasic flow velocity patterns to unravel changes in cardiac–coronary interaction because of transcatheter aortic valve implantation (TAVI). METHODS AND RESULTS—Intracoronary pressure and flow velocity were measured at rest and maximal hyperemia in undiseased vessels in 15 patients with AS before and after TAVI and in 12 control patients. Coronary flow reserve, systolic and diastolic velocity time integrals, and the energies of forward (aorta-originating) and backward (microcirculatory-originating) coronary waves were determined. Coronary flow reserve was 2.8±0.2 (mean±SEM) in control and 1.8±0.1 in AS (P&lt;0.005) and was not restored by TAVI. Compared with control, the resting backward expansion wave was 45% higher in AS. The peak of the systolic forward compression wave was delayed in AS, consistent with a delayed peak aortic pressure, which was partially restored after TAVI. The energy of forward waves doubled after TAVI, whereas the backward expansion wave increased by &gt;30%. The increase in forward compression wave with TAVI was related to an increase in systolic velocity time integral. AS or TAVI did not alter diastolic velocity time integral. CONCLUSIONS—Reduced coronary forward wave energy and systolic velocity time integral imply a compromised systolic flow velocity with AS that is restored after TAVI, suggesting an acute relief of excess compression in systole that likely benefits subendocardial perfusion. Vasodilation is observed to be a major determinant of backward waves.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>27001805</pmid><doi>10.1161/CIRCINTERVENTIONS.114.002356</doi><oa>free_for_read</oa></addata></record>
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subjects Aged
Aged, 80 and over
Aortic Valve - physiopathology
Aortic Valve Stenosis - diagnosis
Aortic Valve Stenosis - physiopathology
Aortic Valve Stenosis - therapy
Blood Flow Velocity
Cardiac Catheterization - instrumentation
Case-Control Studies
Coronary Angiography
Coronary Circulation
Coronary Vessels - diagnostic imaging
Coronary Vessels - physiopathology
Female
Heart Valve Prosthesis Implantation - instrumentation
Heart Valve Prosthesis Implantation - methods
Hemodynamics
Humans
Male
Middle Aged
Pulsatile Flow
Recovery of Function
Systole
Time Factors
Treatment Outcome
Vasodilation
title Transcatheter Replacement of Stenotic Aortic Valve Normalizes Cardiac–Coronary Interaction by Restoration of Systolic Coronary Flow Dynamics as Assessed by Wave Intensity Analysis
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