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Myocardial Bridge as a Cause of Exertional Chest Pain

Tuesday, March 2, 2021

Velasquez C, Garza T, McTaggart L, DeAnda A, Gal L. Myocardial Bridge as a Cause of Exertional Chest Pain. March 2021. doi:10.25373/ctsnet.14120288

The authors present an interesting cases of a myocardial bridging as a cause of exertional chest pain. This is the case is of a 42-year-old woman with a past medical history of HTN and PAHTN who has been worked up by cardiology for chest pain with minimal exertion. The CXR didn’t show any acute abnormalities, and the EKG showed sinus rhythm with some indeterminate ST segment changes in the anterior leads. A normal EF of 60% was seen on the echocardiogram as well as a flattening ventricular septum consisting of right ventricular pressure overload. Due to her history of PAH, a right heart cath was performed, evidencing a severe pulmonary hypertension with baseline pulmonary artery pressures of 88/36. Finally, and as part of her workup, a left heart cath was performed, and there was evidence of codominance as well as an LAD and the mid-portion had a segment that was compressing during systole, concerning for myocardial bridging. This phenomenon can be clearly seen in the video.

Intramyocardial tunneling of a coronary artery can mimic myocardial ischemia, where the LAD is positioned intramuscular, different to the normal epicardial positioning of the coronary arteries. It is more frequent in females, and it is a benign finding. However, when symptomatic, myocardial bridging produces a decrease in the blood flow to the myocardium, when the vessel gets compressed during systole.

Generally, patients with angina received a regular workup, including an echocardiogram. They are then started on medical management. However, if it doesn’t work, additional imaging is required to prove the presence of a myocardial bridge and these patients are referred for a surgical consultation.

After a median sternotomy, the heart was arrested. The distal LAD was identified distally and was dissected out of the myocardium. Using self-retaining retractors, the authors were able to trace the intramyocardial LAD back to the first diagonal where the LAD was in its normal epicardial anatomic position. After dissection, and to prevent scarring over the LAD again and promote patency, myocardial edges were imbricated with a 4-0 running prolene. Finally, the authors reanimated the heart and came off bypass without any issues.

Postoperatively, the patient was taken to the surgical ICU. She was extubated and taken off pressors and inotropes by postoperative day two. She required CPAP at night and supplemental oxygen secondary to her pulmonary artery hypertension, and aggressive diuresis was started. The patient was discharged on postoperative day six without any additional complications.


  1. Boyd JH, Pargaonkar VS, Scoville DH, Rogers IS, Kimura T, Tanaka S, et al. Surgical unroofing of hemodynamically significant left anterior descending myocardial bridges. Ann Thorac Surg. 2017;103(5):1443-1450.
  2. Mok S, Majdalany D, Pettersson GB. Extensive unroofing of myocardial bridge: A case report and literature review. SAGE Open Med Case Rep. 2019;7:2050313X18823380. eCollection 2019.


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Thank you. A fantastic presentation and a great clinical case. It would have been really interesting and potentially very clinically relevant to have preoperative FFR +/- OCT to confirm that, although angiographically impressive, the 'bridge' was truly causing myocardial ischemia rather than being an incidental finding. i am 95% sure that you are correct but i personally would also have requested FFR. thank you for a great case ! bw, dt
We have performed ~150 myocardial bridge unroofings in the past 5 years. We have found dFFR (diastolic FFR) under dobutamine stress to be more reliable in determining hemodynamic significance (and presumably the cause of symptoms) than the standard FFR with adenosine. This is based on the dynamic nature of myocardial bridge physiology and the impact being greater at higher heart rates.
Thank you. Surely moderate to severe PAH also contributed to her symptoms, I assume. About physiology, all the coronary branches end up becoming intramuscular, the most sensitive part finally being the subendocardial layer? I would have loved to see other evidence for anterior wall ischemia. Interesting case, thank you, PH
Thank you for an excellent and interesting video. Did the patient have a long term follow up? It would be interesting to know whether her angina resolved, also it would be good to see case series of these patients and whether their angina resolves in the long term. The concern one might have is formation of scaring leading to the same symptoms, also although the LAD has been deroofed, there is still muscle that surrounds the LAD that might lead to the same phenomenon. In summary, long term follow up would be really helpful and it might be useful to see a post-op angiogram. Best wishes.
Thank you for this presentation! Could you, please, make it clear: 1) if the patient had pulmonary fibrosis or pulmonary tromboembolic events resulted in CTEPH, or any other diagnosed causes for pulmonary hypertension of high degree, and if pulmonary angiography was performed during right heart catheterization, or the patient underwent CT-angiography of PA; 2) did she show the increase in exercise tolerance and regress of chest pain on exertion during the follow-up; 3) if there was a techical possibility to perform iFR/diastolic FFR at the moment of CAG; 4) if any functional tests (stress-ECG/Echo) were made pre- and postoperatively, or elective CAG performed post-op; 5) how many coronary angiographies are performed annualy at your center and what is the quantity of patients with intramiocardial middle segment of LAD per year; 6) what is the percentage of patients with hemodinamically significant miocardial bridges (hence, requiring surgical unroofing/revascularization) at your center? Thank you very much for your attention and response.

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