Majalah Kardiologi Indonesia (Mar 2014)

Symptomatic Myocardial Bridging Treated by Coronary Stenting

  • Johan Winata,
  • Eben Reppi,
  • Bambang Budiono,
  • Reggy L Lefrandt

DOI
https://doi.org/10.30701/ijc.v34i3.345
Journal volume & issue
Vol. 34, no. 3

Abstract

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Background : Myocardial bridging is a congenital coronary anomaly with mostly benign course throughout life. However, several pathological clinical manifestations may accompany myocardial bridging, such as arrhythmia, angina, depressed left ventricular function, myocardial stunning, myocardial infarction, and sudden death. Symptomatic management with anti anginal agents should be adequate in most cases. Stenting, surgical resection of the bridge (myotomy), and coronary bypass surgery are only reserved for the rare patient with severe symptoms. Case Report : A 44 year old man was admitted to the hospital because of the recurrent episodes of palpitations, syncope and chest pain. ECG showed sinus rhythm with bigeminy ventricular extra systoles. Echocardiography showed no regional wall motion abnormalities with normal ejection fraction. Coronary angiography showed myocardial bridging in mid LAD with no associated atherosclerotic coronary disease. Recurrent episodes of angina and non-sustained VT were detected during observation in ICCU, despite anti-arrhytmic drug treatment and Kalium correction. Decision was made to perform PCI to cover bridging segment using drug eluting stent (DES). Post stent angiography showed no subsequent milking effect of systole with improvement in the occurrence of arrhythmia. Holter monitoring which was done 1 week after PCI showed no ventricular extrasystole found. Clinical evaluation and treadmill test at 3 months after the procedure demonstrated good clinical condition and the patient remained free of symptoms. Conclusion : A successful coronary stenting to mid LAD due to myocardial bridging with persistent symptoms despite medial therapy. A thorough follow up should be done to identify the possibility of luminal narrowing caused by intimal proliferation or stent fracture due to external compression.

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