Ischemia in three left ventricular regions: Insights into the pathogenesis of acute ischemic mitral regurgitation

Background: Acute posterolateral left ventricular ischemia in sheep results in ischemic mitral regurgitation, but the effects of ischemia in other left ventricular regions on ischemic mitral regurgitation is unknown. Methods: Six adult sheep had radiopaque markers placed on the left ventricle, mitra...

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Veröffentlicht in:The Journal of thoracic and cardiovascular surgery 2003-03, Vol.125 (3), p.559-569
Hauptverfasser: Timek, Tomasz A., Lai, David T., Tibayan, Frederick, Liang, David, Daughters, George T., Dagum, Paul, Zasio, Mary K., Lo, Sidney, Hastie, Trevor, Ingels, Neil B., Miller, D.Craig
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container_issue 3
container_start_page 559
container_title The Journal of thoracic and cardiovascular surgery
container_volume 125
creator Timek, Tomasz A.
Lai, David T.
Tibayan, Frederick
Liang, David
Daughters, George T.
Dagum, Paul
Zasio, Mary K.
Lo, Sidney
Hastie, Trevor
Ingels, Neil B.
Miller, D.Craig
description Background: Acute posterolateral left ventricular ischemia in sheep results in ischemic mitral regurgitation, but the effects of ischemia in other left ventricular regions on ischemic mitral regurgitation is unknown. Methods: Six adult sheep had radiopaque markers placed on the left ventricle, mitral annulus, and anterior and posterior mitral leaflets at the valve center and near the anterior and posterior commissures. After 6 to 8 days, animals were studied with biplane videofluoroscopy and transesophageal echocardiography before and during sequential balloon occlusion of the left anterior descending, distal left circumflex, and proximal left circumflex coronary arteries. Time of valve closure was defined as the time when the distance between leaflet edge markers reached its minimum plateau, and systolic leaflet edge separation distance was calculated on the basis of left ventricular ejection. Results: Only proximal left circumflex coronary artery occlusion resulted in ischemic mitral regurgitation, which was central and holosystolic. Delayed valve closure (anterior commissure, 58 ± 29 vs 92 ± 24 ms; valve center, 52 ± 26 vs 92 ± 23 ms; posterior commissure, 60 ± 30 vs 94 ± 14 ms; all P
doi_str_mv 10.1067/mtc.2003.43
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Methods: Six adult sheep had radiopaque markers placed on the left ventricle, mitral annulus, and anterior and posterior mitral leaflets at the valve center and near the anterior and posterior commissures. After 6 to 8 days, animals were studied with biplane videofluoroscopy and transesophageal echocardiography before and during sequential balloon occlusion of the left anterior descending, distal left circumflex, and proximal left circumflex coronary arteries. Time of valve closure was defined as the time when the distance between leaflet edge markers reached its minimum plateau, and systolic leaflet edge separation distance was calculated on the basis of left ventricular ejection. Results: Only proximal left circumflex coronary artery occlusion resulted in ischemic mitral regurgitation, which was central and holosystolic. Delayed valve closure (anterior commissure, 58 ± 29 vs 92 ± 24 ms; valve center, 52 ± 26 vs 92 ± 23 ms; posterior commissure, 60 ± 30 vs 94 ± 14 ms; all P &lt;.05) and increased leaflet edge separation distance during ejection (mean increase, 2.2 ± 1.5 mm, 2.1 ± 1.9 mm, and 2.1 ± 1.5 mm at the anterior commissure, valve center, and posterior commissure, respectively; P &lt;.05 for all) was seen during proximal left circumflex coronary artery occlusion but not during left anterior descending or distal left circumflex coronary artery occlusion. Ischemic mitral regurgitation was associated with a 19% ± 10% increase in mitral annular area, and displacement of both papillary muscle tips away from the septal annulus at end systole. Conclusions: Acute ischemic mitral regurgitation in sheep occurred only after proximal left circumflex coronary artery occlusion along with delayed valve closure in early systole and increased leaflet edge separation throughout ejection in all 3 leaflet coaptation sites. The degree of left ventricular systolic dysfunction induced did not correlate with ischemic mitral regurgitation, but both altered valvular and subvalvular 3-dimensional geometry were necessary to produce ischemic mitral regurgitation during acute left ventricular ischemia. J Thorac Cardiovasc Surg 2003;125:559-69</description><identifier>ISSN: 0022-5223</identifier><identifier>EISSN: 1097-685X</identifier><identifier>DOI: 10.1067/mtc.2003.43</identifier><identifier>PMID: 12658198</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Acute Disease ; Animals ; Balloon Occlusion ; Cardiac Catheterization ; Disease Models, Animal ; Echocardiography, Transesophageal ; Fluoroscopy ; Hemodynamics ; Mitral Valve Insufficiency - etiology ; Myocardial Ischemia - complications ; Myocardial Ischemia - diagnosis ; Myocardial Ischemia - physiopathology ; Papillary Muscles - physiopathology ; Severity of Illness Index ; Sheep ; Stroke Volume ; Systole ; Time Factors ; Ventricular Dysfunction, Left - complications ; Ventricular Dysfunction, Left - diagnosis ; Ventricular Dysfunction, Left - physiopathology</subject><ispartof>The Journal of thoracic and cardiovascular surgery, 2003-03, Vol.125 (3), p.559-569</ispartof><rights>2003 American Association for Thoracic Surgery</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c400t-2cf099912bbbb53de90c06c9fa66870910e318a62608b6344ba30efaafb2c52b3</citedby><cites>FETCH-LOGICAL-c400t-2cf099912bbbb53de90c06c9fa66870910e318a62608b6344ba30efaafb2c52b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S002252230273290X$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12658198$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Timek, Tomasz A.</creatorcontrib><creatorcontrib>Lai, David T.</creatorcontrib><creatorcontrib>Tibayan, Frederick</creatorcontrib><creatorcontrib>Liang, David</creatorcontrib><creatorcontrib>Daughters, George T.</creatorcontrib><creatorcontrib>Dagum, Paul</creatorcontrib><creatorcontrib>Zasio, Mary K.</creatorcontrib><creatorcontrib>Lo, Sidney</creatorcontrib><creatorcontrib>Hastie, Trevor</creatorcontrib><creatorcontrib>Ingels, Neil B.</creatorcontrib><creatorcontrib>Miller, D.Craig</creatorcontrib><title>Ischemia in three left ventricular regions: Insights into the pathogenesis of acute ischemic mitral regurgitation</title><title>The Journal of thoracic and cardiovascular surgery</title><addtitle>J Thorac Cardiovasc Surg</addtitle><description>Background: Acute posterolateral left ventricular ischemia in sheep results in ischemic mitral regurgitation, but the effects of ischemia in other left ventricular regions on ischemic mitral regurgitation is unknown. Methods: Six adult sheep had radiopaque markers placed on the left ventricle, mitral annulus, and anterior and posterior mitral leaflets at the valve center and near the anterior and posterior commissures. After 6 to 8 days, animals were studied with biplane videofluoroscopy and transesophageal echocardiography before and during sequential balloon occlusion of the left anterior descending, distal left circumflex, and proximal left circumflex coronary arteries. Time of valve closure was defined as the time when the distance between leaflet edge markers reached its minimum plateau, and systolic leaflet edge separation distance was calculated on the basis of left ventricular ejection. Results: Only proximal left circumflex coronary artery occlusion resulted in ischemic mitral regurgitation, which was central and holosystolic. Delayed valve closure (anterior commissure, 58 ± 29 vs 92 ± 24 ms; valve center, 52 ± 26 vs 92 ± 23 ms; posterior commissure, 60 ± 30 vs 94 ± 14 ms; all P &lt;.05) and increased leaflet edge separation distance during ejection (mean increase, 2.2 ± 1.5 mm, 2.1 ± 1.9 mm, and 2.1 ± 1.5 mm at the anterior commissure, valve center, and posterior commissure, respectively; P &lt;.05 for all) was seen during proximal left circumflex coronary artery occlusion but not during left anterior descending or distal left circumflex coronary artery occlusion. Ischemic mitral regurgitation was associated with a 19% ± 10% increase in mitral annular area, and displacement of both papillary muscle tips away from the septal annulus at end systole. Conclusions: Acute ischemic mitral regurgitation in sheep occurred only after proximal left circumflex coronary artery occlusion along with delayed valve closure in early systole and increased leaflet edge separation throughout ejection in all 3 leaflet coaptation sites. The degree of left ventricular systolic dysfunction induced did not correlate with ischemic mitral regurgitation, but both altered valvular and subvalvular 3-dimensional geometry were necessary to produce ischemic mitral regurgitation during acute left ventricular ischemia. 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Methods: Six adult sheep had radiopaque markers placed on the left ventricle, mitral annulus, and anterior and posterior mitral leaflets at the valve center and near the anterior and posterior commissures. After 6 to 8 days, animals were studied with biplane videofluoroscopy and transesophageal echocardiography before and during sequential balloon occlusion of the left anterior descending, distal left circumflex, and proximal left circumflex coronary arteries. Time of valve closure was defined as the time when the distance between leaflet edge markers reached its minimum plateau, and systolic leaflet edge separation distance was calculated on the basis of left ventricular ejection. Results: Only proximal left circumflex coronary artery occlusion resulted in ischemic mitral regurgitation, which was central and holosystolic. Delayed valve closure (anterior commissure, 58 ± 29 vs 92 ± 24 ms; valve center, 52 ± 26 vs 92 ± 23 ms; posterior commissure, 60 ± 30 vs 94 ± 14 ms; all P &lt;.05) and increased leaflet edge separation distance during ejection (mean increase, 2.2 ± 1.5 mm, 2.1 ± 1.9 mm, and 2.1 ± 1.5 mm at the anterior commissure, valve center, and posterior commissure, respectively; P &lt;.05 for all) was seen during proximal left circumflex coronary artery occlusion but not during left anterior descending or distal left circumflex coronary artery occlusion. Ischemic mitral regurgitation was associated with a 19% ± 10% increase in mitral annular area, and displacement of both papillary muscle tips away from the septal annulus at end systole. Conclusions: Acute ischemic mitral regurgitation in sheep occurred only after proximal left circumflex coronary artery occlusion along with delayed valve closure in early systole and increased leaflet edge separation throughout ejection in all 3 leaflet coaptation sites. The degree of left ventricular systolic dysfunction induced did not correlate with ischemic mitral regurgitation, but both altered valvular and subvalvular 3-dimensional geometry were necessary to produce ischemic mitral regurgitation during acute left ventricular ischemia. J Thorac Cardiovasc Surg 2003;125:559-69</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>12658198</pmid><doi>10.1067/mtc.2003.43</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record>
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subjects Acute Disease
Animals
Balloon Occlusion
Cardiac Catheterization
Disease Models, Animal
Echocardiography, Transesophageal
Fluoroscopy
Hemodynamics
Mitral Valve Insufficiency - etiology
Myocardial Ischemia - complications
Myocardial Ischemia - diagnosis
Myocardial Ischemia - physiopathology
Papillary Muscles - physiopathology
Severity of Illness Index
Sheep
Stroke Volume
Systole
Time Factors
Ventricular Dysfunction, Left - complications
Ventricular Dysfunction, Left - diagnosis
Ventricular Dysfunction, Left - physiopathology
title Ischemia in three left ventricular regions: Insights into the pathogenesis of acute ischemic mitral regurgitation
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