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Functional characteristics of myocardial bridging. A combined angiographic and intracoronary Doppler flow study
E R Schwarz1, H G Klues, J vom Dahl
1Medical Clinic I, University Hospital, Rheinisch Westfälische Technische Hochschule (RWTH) Aachen, Germany.
Insights
Myocardial bridging causes delayed diastolic blood flow and increased velocities within the coronary artery. This obstruction can lead to angina, indicating a significant hemodynamic issue in some patients.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- Myocardial bridging, a congenital anomaly, can cause myocardial ischemia.
- The hemodynamic mechanisms underlying ischemia in myocardial bridging require further elucidation.
Purpose of the Study:
- To investigate the hemodynamic mechanisms of myocardial ischemia in patients with myocardial bridging.
- To assess coronary flow dynamics and reserve in the presence of myocardial bridging.
Main Methods:
- Combined quantitative coronary angiography and intracoronary Doppler flow velocity measurements.
- Serial frame-by-frame diameter quantification during the cardiac cycle.
- Measurement of blood flow velocities proximal, within, and distal to myocardial bridges.
Main Results:
- Significant systolic lumen reduction (71%) and persistent diastolic reduction (35%) in myocardial bridges.
- Increased diastolic peak flow velocities within bridges (38.6 cm/s) compared to proximal (22.4 cm/s) and distal (18.6 cm/s) segments.
- Reduced coronary flow reserve distal to bridges (2.3) versus proximal (2.9), with flow augmentation during rapid pacing.
Conclusions:
- Myocardial bridging causes delayed diastolic lumen gain and increased diastolic flow velocities.
- These hemodynamic changes, along with reduced coronary flow reserve, support a significant coronary obstruction in symptomatic patients.
- Findings suggest myocardial bridging can be a hemodynamically significant cause of angina in a 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.
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