Lyseggen Erik, Vartdal Trond, Remme Espen W, Helle-Valle Thomas, Pettersen Eirik, Opdahl Anders, Edvardsen Thor, Smiseth Otto A
Institute for Surgical Research and Department of Cardiology, University of Oslo, Rikshospitalet University Hospital, Oslo, Norway.
Am J Physiol Heart Circ Physiol. 2009 Mar;296(3):H645-54. doi: 10.1152/ajpheart.00313.2008. Epub 2009 Jan 2.
The present study introduces a new clinical method to define left ventricular (LV) end systole (ES) during tissue Doppler imaging (TDI). Preliminary experiments showed a sharp inflection point in strain traces (S(IP)) from ischemic borderzones, which coincided with onset of a postsystolic shortening wave (V(PS)) in the velocity trace. In a single-vessel disease model, we investigated whether S(IP) and V(PS) may serve as markers of global ES and their mechanism. In six anesthetized dogs we measured LV pressure and myocardial long-axis function by using TDI and sonomicrometry. Ischemia was induced by left anterior descending coronary artery occlusion. ES was defined by the minimum first derivative of LV pressure. TDI and sonomicrometry demonstrated a sharp S(IP) and V(PS) at ES in the ischemic borderzone (defined as moderately ischemic myocardium by pressure-dimension loop analysis). Time differences relative to ES ( +/- SD) were -0.1 +/- 2.3 (intraclass correlation coefficient R(IC) = 0.996) and 6.8 +/- 10.7 ms (R(IC) = 0.89) for S(IP) as shown by sonomicrometry and TDI, respectively. There was a strong inverse relationship between postsystolic shortening in the borderzone and simultaneous lengthening of nonischemic myocardium. In 30 patients with acute myocardial infarction, S(IP) and V(PS) evaluated by TDI were compared with ES defined by aortic valve closure. Time differences were -4 +/- 14 (R(IC) = 0.94) and -2 +/- 11 ms (R(IC) = 0.96), respectively. In the ischemic borderzone, S(IP) and V(PS) identified global ES with high accuracy. The force balance or "tug of war" between borderzone and nonischemic myocardium is a likely underlying mechanism for these markers. The method may be used as an "all in one heart beat" approach for TDI analysis in acute myocardial ischemia.
本研究介绍了一种在组织多普勒成像(TDI)期间定义左心室(LV)收缩末期(ES)的新临床方法。初步实验显示,缺血边缘区应变曲线(S(IP))存在一个尖锐的拐点,这与速度曲线中收缩后缩短波(V(PS))的起始点一致。在单支血管疾病模型中,我们研究了S(IP)和V(PS)是否可作为整体ES的标志物及其机制。在6只麻醉犬中,我们使用TDI和超声心动图测量左心室压力和心肌长轴功能。通过左前降支冠状动脉闭塞诱导缺血。ES由左心室压力的最小一阶导数定义。TDI和超声心动图显示,缺血边缘区(通过压力-维度环分析定义为中度缺血心肌)在ES时出现尖锐的S(IP)和V(PS)。超声心动图和TDI显示,相对于ES的时间差异(±标准差),S(IP)分别为-0.1±2.3(组内相关系数R(IC)=0.996)和6.8±10.7毫秒(R(IC)=0.89)。边缘区收缩后缩短与非缺血心肌同时延长之间存在强烈的负相关关系。在30例急性心肌梗死患者中,将TDI评估的S(IP)和V(PS)与主动脉瓣关闭定义的ES进行比较。时间差异分别为-4±14(R(IC)=0.94)和-2±11毫秒(R(IC)=0.96)。在缺血边缘区,S(IP)和V(PS)能高精度识别整体ES。边缘区与非缺血心肌之间的力平衡或“拔河”可能是这些标志物的潜在机制。该方法可作为急性心肌缺血时TDI分析的“一次心跳全搞定”方法。