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Clinical Images

A STEMI Where Stenting Was Deferred: Acute Plaque Rupture in Myocardial Bridge

Issa Kutkut, MD1,2;  Rohini Manaktala, DO1,2;  Nayef Abouzaki, MD2

July 2022
1557-2501
J INVASIVE CARDIOL 2022;34(7):E578-E579. doi: 10.25270/jic/22.00048

Keywords: STEMI, myocardial bridge, stenting

Kutkut STEMI Figure 1
Figure 1. (A) Initial electrocardiogram (ECG) shows sinus bradycardia with nonspecific ST/T wave changes. (B) Follow-up ECG shows transient anterior ST-segment elevation myocardial infarction.
Kutkut STEMI Figure 2
Figure 2. (A) Mid left anterior descending artery myocardial bridging during systole (arrowhead) and (B) during diastole.
Kutkut STEMI Figure 3
Figure 3. Angiography shows 50% left circumflex (LCX) coronary artery disease at the bifurcation of the second obtuse marginal (OM2), 50% ostial OM2 stenosis, and 50% proximal third obtuse marginal (OM3) stenosis. Instantaneous wave-free ratio (iFR) of the LCX/OM2 bifurcation was 0.99 and iFR of the OM3 was 0.99 (both hemodynamically insignificant).

A 63-year-old male with a history significant for 50 pack years of tobacco use and a cerebrovascular accident presented with unstable angina. His electrocardiogram (ECG) showed sinus bradycardia with nonspecific ST/T wave changes (Figure 1A). Coronary angiography demonstrated significant myocardial bridging of the mid left anterior descending artery (LAD) (Video 1 and Figure 2) and nonobstructive coronary artery disease (CAD) otherwise. His left circumflex (LCX) CAD was physiologically insignificant on assessment with instantaneous wave-free ratio (Figure 3). The following day, the patient developed transient anterior ST-segment elevation myocardial infarction with a troponin of 0.5 ng/mL (Figure 1B). He was brought back for coronary angiography with intracoronary imaging. His baseline angiogram was unchanged and optical coherence tomography (OCT) was performed in the LAD, which showed evidence of acute plaque rupture within the myocardial bridging segment (Video 2 and Figure 4). There was a concern for stenting the bridging segment due to reported higher rates of target-lesion revascularization and concerns of stent thrombosis, stent fracture, and coronary perforation. Therefore, cardiothoracic surgery was consulted for unroofing of the mid LAD or surgical bypass, which are generally considered safe and effective.1,2 The left internal mammary artery was found to be a poor conduit in the operating room due to size and flow limitation. Given that the patient already had a median sternotomy, surgical revascularization with saphenous vein grafting and surgical myotomy to relieve the systolic compression were performed. The latter would facilitate durable percutaneous revascularization options in the future.

Kutkut STEMI Figure 4
Figure 4. (A) Angiography shows mid left anterior descending artery myocardial bridging segment. (B) Longitudinal view of the vessel on optical coherence tomography (OCT) with markers for the corresponding OCT cross sections.  (C) Site of acute plaque rupture (asterisk) partially shadowed by wire artifact with adherent white thrombus. (D) Adherent white thrombus in the myocardial bridging segment. (E) Myocardial bridge; neointimal hyperplasia. (F) Intimal disruption extending from the more proximal plaque rupture with some adherent white thrombus. (G) Non-flow limiting intimal dissection distal to the myocardial bridge.

This case of acute plaque rupture within a myocardial bridging segment demonstrates the importance of performing hemodynamic assessment of intermediate-appearing coronary lesions, as well as utilizing intracoronary imaging to characterize coronary lesions and aid in selecting the appropriate treatment plan.

References

1. Lee MS, Chen CH. Myocardial bridging: an up-to-date review. J Invasive Cardiol. 2015;27(11):521-528.

2. Tarantini G, Migliore F, Cademartiri F, Fraccaro C, Iliceto S. Left anterior descending artery myocardial bridging: a clinical approach. J Am Coll Cardiol. 2016;68(25):2887-2899. doi:10.1016/j.jacc.2016.09.973.

Affiliations and Disclosures

From the 1Division of Cardiology, Virginia Commonwealth University Pauley Heart Center, Richmond, Virginia; and 2Division of Cardiology, Central Virginia Veterans Affairs Healthcare System, Richmond, Virginia.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

The authors report that patient consent was provided for publication of the images used herein.

Manuscript accepted March 17, 2022.

Address for correspondence: Nayef Abouzaki, MD, 1201 Broad Rock Blvd, Box 111J, Richmond, VA 23249. Email: nayef.abouzaki@gmail.com

 

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