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Disturbed intracoronary hemodynamics in myocardial bridging: early normalization by intracoronary stent placement
H G Klues1, E R Schwarz, J vom Dahl
1Medical Clinic I, University Hospital, Rheinisch Westfälische Technische Hochschule, Aachen, Germany.
Insights
Myocardial bridging causes significant coronary artery narrowing and abnormal blood flow, leading to ischemia. Stenting these bridges resolves these hemodynamic issues and improves symptoms.
Area of Science:
- Cardiovascular Medicine
- Interventional Cardiology
- Physiology
Background:
- Myocardial bridging is a congenital anomaly where a segment of a coronary artery tunneled within the heart muscle.
- This condition can lead to angina and myocardial ischemia due to altered coronary hemodynamics.
Purpose of the Study:
- To investigate the hemodynamic mechanisms underlying myocardial ischemia in patients with myocardial bridging.
- To evaluate the impact of intracoronary stent placement on these hemodynamic abnormalities and clinical symptoms.
Main Methods:
- Quantitative coronary angiography to measure vessel diameters in bridged segments.
- Doppler flow wire and pressure microtransducer for assessing coronary flow velocities, flow reserve, and pressures.
- Hemodynamic measurements before and after stent implantation in symptomatic patients.
Main Results:
- Significant systolic (80.6%) and diastolic (35.3%) diameter reduction in bridged segments.
- Increased diastolic flow velocities and peak systolic pressure within the bridged segment.
- Reduced coronary flow reserve distal to the bridge (2.5), which improved to 3.8 post-stenting.
- Stent placement eliminated lumen compression, flow abnormalities, and improved symptoms.
Conclusions:
- Myocardial bridging causes complex hemodynamic alterations, including phasic compression and reduced flow reserve, explaining ischemia and symptoms.
- Intracoronary stent placement effectively resolves these hemodynamic abnormalities.
- Stenting offers a potential treatment for symptomatic patients with myocardial bridges, particularly those refractory to other therapies.
Background:
The purpose of this study was to evaluate the hemodynamic mechanisms leading to myocardial ischemia in patients with myocardial bridging. Myocardial bridging is known to induce angina and even severe myocardial ischemia.
Methods And Results:
In 12 symptomatic patients with myocardial bridges, quantitative coronary angiography was performed to obtain systolic/diastolic vessel diameters within the bridged segments. Coronary flow velocities, flow reserve, and pressures were determined with a 0.014-in Doppler and a 0.014-in pressure microtransducer. In 3 symptomatic patients, coronary stents were implanted and hemodynamic measurements were repeated immediately and after 7 weeks. An in vitro validation of the pressure measurements was performed. Angiography revealed a systolic diameter reduction of 80.6+/-9.2% and a persistent diastolic reduction of 35.3+/-11% within the bridged segment. Diastolic flow velocities (cm/s) were increased (31.5+/-14.3 within versus 17.3+/-5.7 proximal and 15.2+/-6.3 distal, P<.001). Coronary flow reserve distal to the bridge was 2.5+/-0.5. There was an increased peak systolic pressure within the bridged segment (171+/-48 versus 113+/-10 mm Hg proximal, P<.001). Stent placement abolished the phasic lumen compression, the diastolic flow abnormalities, the intracoronary peak systolic pressure, and clinical symptoms. Coronary flow reserve improved to 3.8+/-0.3.
Conclusions:
Coronary hemodynamics in myocardial bridges are characterized by a phasic systolic vessel compression with a localized peak pressure, persistent diastolic diameter reduction, increased blood flow velocities, retrograde flow, and a reduced flow reserve. These alterations may explain the occurrence of symptoms and ischemia in these patients. Intracoronary stent placement abolished all hemodynamic abnormalities and may improve clinical symptoms in otherwise unsuccessfully treated patients with myocardial bridges.