Schwarz E R, Klues H G, vom Dahl J, Klein I, Krebs W, Hanrath P
Medical Clinic I, University Hospital, Rheinisch Westfälische Technische Hochschule (RWTH) Aachen, Germany.
Eur Heart J. 1997 Mar;18(3):434-42. doi: 10.1093/oxfordjournals.eurheartj.a015263.
Combined quantitative coronary angiography and intracoronary Doppler flow velocity measurements were performed to study the underlying haemodynamic mechanisms leading to myocardial ischaemia in patients with myocardial bridging in the absence of coronary artery disease.
In 42 symptomatic patients with myocardial bridging of the left anterior descending coronary artery, quantitative coronary angiography was used to measure absolute and relative vessel diameters during systole and diastole. In 14 patients, serial frame-by-frame diameter quantification during a complete cardiac cycle was performed. Intracoronary blood flow velocities were determined using a 0.014 inch Doppler flow guide wire proximal, within, and distal to myocardial bridges, and coronary flow reserve was calculated. Quantitative coronary angiography revealed a maximal systolic lumen diameter reduction of 71 +/- 16% with a persistent diameter reduction of 35 +/- 13% during mid-diastole. Flow velocities revealed increased average diastolic peak flow velocities within myocardial bridges of 38.6 +/- 19 cm.s-1 vs 22.4 +/- 7.7 cm.s-1 proximal and 18.6 +/- 4.6 cm.s-1 distal (P < 0.001), which increased during rapid pacing (64.7 +/- 25 cm.s-1, P < 0.001 vs baseline). Coronary flow reserve distal to myocardial bridges was 2.3 +/- 0.9 (vs 2.9 +/- 0.9 proximal, P < 0.05). There was a characteristic Doppler flow profile within myocardial bridges with an early diastolic overshoot, which was further augmented during rapid pacing.
Myocardial bridging is characterized by a delay in diastolic lumen gain and a concomitant increase in diastolic intracoronary Doppler flow velocities, which are enhanced by rapid pacing. In combination with a reduced coronary flow reserve and anginal symptoms these findings support the concept of a haemodynamically significant obstruction to coronary flow due to myocardial bridging in a selected subset of patients.
采用冠状动脉定量血管造影术和冠状动脉内多普勒血流速度测量相结合的方法，研究在无冠状动脉疾病的心肌桥患者中导致心肌缺血的潜在血流动力学机制。
对42例有症状的左前降支冠状动脉心肌桥患者，采用冠状动脉定量血管造影术测量收缩期和舒张期的绝对和相对血管直径。对14例患者在完整心动周期内进行逐帧连续直径量化。使用0.014英寸多普勒血流导丝测定心肌桥近端、心肌桥内和心肌桥远端的冠状动脉血流速度，并计算冠状动脉血流储备。冠状动脉定量血管造影显示，收缩期最大管腔直径减少71±16%，舒张中期持续直径减少35±13%。血流速度显示，心肌桥内舒张期平均峰值流速增加，为38.6±19cm/s，而近端为22.4±7.7cm/s，远端为18.6±4.6cm/s（P<0.001），在快速起搏时增加（64.7±25cm/s，与基线相比P<0.001）。心肌桥远端的冠状动脉血流储备为2.3±0.9（近端为2.9±0.9，P<0.05）。心肌桥内有特征性的多普勒血流频谱，舒张早期有过冲，在快速起搏时进一步增强。
心肌桥的特征是舒张期管腔增大延迟，同时冠状动脉内舒张期多普勒血流速度增加，快速起搏可增强这种增加。结合冠状动脉血流储备降低和心绞痛症状，这些发现支持了在部分患者中，心肌桥对冠状动脉血流存在血流动力学显著梗阻的概念。
