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, 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 <.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 <.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.
Timek
Tomasz A
TA
Department of Cardiovascular and Thoracic Surgery, Division of Cardiovascular Medicine, Stanford University School of Medicine, Calif 94305, USA.
Lai
David T
DT
Tibayan
Frederick
F
Liang
David
D
Daughters
George T
GT
Dagum
Paul
P
Zasio
Mary K
MK
Lo
Sidney
S
Hastie
Trevor
T
Ingels
Neil B
NB
Miller
D Craig
DC
D000208:Acute Disease; D000818:Animals; D021721:Balloon Occlusion; D006328:Cardiac Catheterization; D004195:Disease Models, Animal; D017548:Echocardiography, Transesophageal; D005471:Fluoroscopy; D006439:Hemodynamics; D008944:Mitral Valve Insufficiency / Q000209:etiology*; D017202:Myocardial Ischemia / Q000150:complications* / Q000175:diagnosis / Q000503:physiopathology; D010210:Papillary Muscles / Q000503:physiopathology; D012720:Severity of Illness Index; D012756:Sheep; D013318:Stroke Volume; D013599:Systole; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000150:complications* / Q000175:diagnosis / Q000503:physiopathology