AIMS: 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. METHODS AND RESULTS: 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. CONCLUSION: 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.
AIMS: 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. METHODS AND RESULTS: 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. CONCLUSION: 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.