Bothe Wolfgang, Ennis Daniel B, Carlhäll Carl Johan, Nguyen Tom C, Timek Tomasz A, Lai David T, Itoh Akinobu, Ingels Neil B, Miller D Craig
Department of Cardiothoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, California 94305-5247, USA.
J Heart Valve Dis. 2009 Nov;18(6):586-96; discussion 597.
Diastolic mitral valve (MV) opening characteristics during ischemic mitral regurgitation (IMR) are poorly characterized. The diastolic MV opening dynamics were quantified along the entire valvular coaptation line in an ovine model of acute IMR.
Ten radiopaque markers were sutured in pairs on the anterior (A1-E1) and corresponding posterior (A2-E2) leaflet edges from the anterior (A1/A2) to the posterior (E1/E2) commissure in 11 adult sheep. Immediately after surgery, 4-D marker coordinates were obtained before and during occlusion of the proximal left circumflex coronary artery. Distances between marker pairs were calculated throughout the cardiac cycle every 16.7 ms. Leaflet opening was defined as the time after end-systole (ES) when the first derivative of the distance between marker pairs was greater than a threshold value of 3 cm/s. Valve opening velocity was defined as the maximum slope of marker pair tracings.
Hemodynamics were consistent with acute ischemia, as reflected by increased MR grade (0.5 +/- 0.3 versus 2.3 +/- 0.7, p < 0.05), decreased contractility (dP/dt(max): 1,948 +/- 598 versus 1,119 +/- 293 mmHg/s, p < 0.05), and slower left ventricular relaxation rate (dP/dt(min): -1,079 +/- 188 versus -538 +/- 147 mmHg/s, p < 0.05). During ischemia, valve opening occurred earlier (A1/A2: 112 +/- 28 versus 83 +/- 43 ms, B1/B2: 105 +/- 32 versus 68 +/- 35 ms, C1/C2: 126 +/- 25 versus 74 +/- 37 ms, D1/D2: 114 +/- 28 versus 71 +/- 34 ms, E1/E2: 125 +/- 29 versus 105 +/- 33 ms; all p < 0.05) and was slower (A1/A2: 16.8 +/- 9.6 versus 14.2 +/- 9.4 cm/s, B1/B2: 40.4 +/- 9.9 versus 32.2 +/- 10.0 cm/s, C1/C2: 59.0 +/- 14.9 versus 50.4 +/- 18.1 cm/s, D1/D2: 34.4 +/- 10.4 versus 25.5 +/- 10.9 cm/s; all p < 0.05), except at the posterior edge (E1/E2: 13.3 +/- 8.7 versus 10.6 +/- 7.2 cm/s). The sequence of regional mitral leaflet separation along the line of coaptation did not change with ischemia.
Acute posterolateral left ventricular ischemia causes earlier leaflet opening, probably due to a MR-related elevation in left-atrial pressure; reduces leaflet opening velocity, potentially reflecting an impaired left ventricular relaxation rate; and does not perturb the homogeneous temporal pattern of regional valve opening along the line of coaptation. Future studies will confirm whether these findings are apparent in patients with chronic IMR, and may help to refine the current strategies used to treat IMR.
缺血性二尖瓣反流(IMR)期间二尖瓣(MV)舒张期开放特征尚不明确。在急性IMR羊模型中,沿整个瓣膜贴合线对舒张期MV开放动力学进行量化分析。
在11只成年绵羊中,从前(A1/A2)至后(E1/E2)瓣环,在前叶(A1 - E1)和相应后叶(A2 - E2)边缘成对缝合10个不透X线的标记物。手术后立即在左回旋支冠状动脉近端闭塞前和闭塞期间获取4D标记物坐标。在整个心动周期中,每隔16.7毫秒计算标记物对之间的距离。瓣叶开放定义为收缩末期(ES)后,标记物对之间距离的一阶导数大于3 cm/s阈值的时间。瓣叶开放速度定义为标记物对轨迹的最大斜率。
血流动力学与急性缺血相符,表现为二尖瓣反流分级增加(0.5±0.3对2.3±0.7,p<0.05)、收缩力降低(dP/dt(max):1948±598对1119±293 mmHg/s,p<0.05)以及左心室舒张速率减慢(dP/dt(min): - 1079±188对 - 538±147 mmHg/s,p<0.05)。缺血期间,瓣叶开放更早(A1/A2:112±28对83±43毫秒,B1/B2:105±32对68±35毫秒,C1/C2:126±25对74±37毫秒,D1/D2:114±28对71±34毫秒,E1/E2:125±29对105±33毫秒;均p<0.05)且更慢(A1/A2:16.8±9.6对14.2±9.4 cm/s,B1/B2:40.4±9.9对32.2±10.0 cm/s,C1/C2:59.0±14.9对50.4±18.1 cm/s,D1/D2:34.4±10.4对25.5±10.9 cm/s;均p<0.05),后叶边缘(E1/E2:13.3±8.7对10.6±7.2 cm/s)除外。沿贴合线区域二尖瓣叶分离顺序未因缺血而改变。
急性左心室后外侧缺血导致瓣叶更早开放,可能是由于二尖瓣反流相关的左心房压力升高;降低瓣叶开放速度,可能反映左心室舒张速率受损;且不扰乱沿贴合线区域瓣膜开放的均匀时间模式。未来研究将证实这些发现是否在慢性IMR患者中也很明显,并可能有助于完善当前用于治疗IMR的策略。