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Author Spotlight: Enhancing Coronary Artery Revascularization
Published on: September 15, 2023
Going under the bridge: unmasking ischaemia and endothelial dysfunction of myocardial bridging: a case report
Sukhdeep Bhogal1, Ron Waksman1, Hayder Hashim1
1Section of Interventional Cardiology, MedStar Washington Hospital Center, 110 Irving St. NW, Suite 4B1, Washington, DC 20010, USA.
Insights
Physiological assessment of myocardial bridging is crucial for symptomatic patients. Hyperemic testing can reveal ischemia missed by non-invasive methods, guiding appropriate treatment.
Area of Science:
- Cardiology
- Physiology
Background:
- Myocardial bridging can cause ischemia, but non-invasive assessments may underestimate its severity.
- Symptomatic patients require thorough physiological evaluation to guide interventions.
Observation:
- A 74-year-old male with exertional chest pain and shortness of breath had myocardial bridging.
- Coronary angiography revealed myocardial bridging with normal resting flow but abnormal hyperemic flow and spastic response.
Findings:
- Hyperemic assessment revealed significant ischemia in myocardial bridging, missed by resting measurements.
- Endothelial dysfunction and spastic response to hyperemia contributed to the patient's symptoms.
Implications:
- Thorough physiological workup, including hyperemic testing, is vital for symptomatic myocardial bridging.
- Accurate assessment of ischemia and endothelial function improves patient management and prevents unnecessary procedures.
Background:
Physiological assessment of myocardial bridging prevents unnecessary interventions. Non-invasive workup or visual coronary artery compression may underestimate the underlying ischaemia associated with myocardial bridging in symptomatic patients.
Case Summary:
A 74-year-old male presented to the outpatient clinic with chest pain and shortness of breath on exertion. He underwent coronary artery calcium scan showing an elevated calcium score of 404. On follow-up, he endorsed progressive worsening of symptoms with chest pain and decreased exercise tolerance. He was then referred for coronary angiography that revealed mid-left anterior descending myocardial bridging with initial normal resting full-cycle ratio of 0.92. Further workup after ruling out coronary microvascular disease demonstrated abnormal hyperaemic full-cycle ratio of 0.80 with a diffuse rise across the myocardial bridging segment on pullback. Our patient also had increased spastic response to hyperaemia on angiography, supporting the presence of underlying endothelial dysfunction and ischaemia, likely contributing to his exertional symptomology. The patient was started on beta-blocker therapy with improvement in symptoms and resolution of chest pain on follow-up.
Conclusion:
Our case highlights the importance of thorough workup of myocardial bridging in symptomatic patients to better understand the underlying physiology and endothelial function after ruling out microvascular disease and consideration of hyperaemic testing if symptoms are suggestive of ischaemia.
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