Letter to the Editor Myocardial bridging causing transmural ischemia Successful coronary artery bypass surgery Caio B. Vianna ⁎ , Maria M. Gonzalez, Fabio B. Jatene, Marcus N. Gama, Sergio Timerman, Luiz A. Cesar Heart Institute (InCor), University of São Paulo Medical School, Brazil Received 4 April 2006; received in revised form 28 July 2006; accepted 29 July 2006 Available online 23 October 2006 Abstract Myocardial bridging is a common and usually benign inborn coronary anomaly. We report on a 51-year-old man who presented with recent angina on minimum physical effort. Cineangiography showed myocardial bridging of the mid-left anterior descending artery (LAD), and intracoronary ultrasonography excluded atherosclerotic disease. Gated single-photon emission computed tomography (SPECT), with exercise stress, showed an extensive anterior perfusion defect, and remarkable ST-segment elevation (up to 10 mm) in recovery. Vasospasm of the LAD was the main hypothesis. Additional oral drugs did not bring about improvement, as indicated on a new SPECT; disabling angina persisted. Surgical revascularization of the LAD by left internal mammary artery graft was performed. Two years later, SPECT and exercise tests returned to normal. The patient remains asymptomatic. © 2006 Elsevier Ireland Ltd. All rights reserved. Keywords: Myocardial bridging; Ischemia; Coronary vasospasm; Coronary artery bypass; Intravascular ultrasound 1. Case report We report the case of a 43-year-old man who presented with angina on effort (class-II, Cardiovascular Canadian Society). A cineangiography showed myocardial bridging in the mid- segment of the left anterior descending artery (LAD). The patient was medicated with atenolol and simvastatin, and the angina was alleviated considerably. Eight years later, at age 51, the angina suddenly worsened, to class-III, and the patient was transferred to this University Hospital. The patient never smoked and had no family history of heart disease. He did have hypertension and hypercholester- olemia. The physical examination was unremarkable. An electrocardiogram recorded sinus bradycardia, slow progres- sion of the R-wave from V 1 to V 3 , and a flat inverted T-wave in I, aVL, V 5 , and V 6 leads. Transthoracic echocardiogram was normal. Gated single-photon emission computed-tomography (SPECT) imaging of myocardial perfusion (Tc-99 m sestamibi tracer) with an exercise stress test was performed. All me- dication was withdrawn 7 days before testing. Treadmill tes- ting (Bruce-protocol) had a maximal duration of 8:50 min (Fig. 1). At peak exercise, ST-segment elevation was recorded in V 1 , V 2 , and V 3 leads, maximum of 3 mm in V 3 . A few seconds into the recovery phase, a remarkable ST-segment elevation was observed in all precordial leads, maximum of 10 mm in V 3 . These ischemic changes persisted for at least 10 min during recovery (Fig. 1). The patient experienced discrete chest pain. SPECT imaging showed reversible anterior, septal, and apical perfusion defects. At rest, only a small area of perfusion abnormality was noted in the apex. A new cineangiography confirmed myocardial bridging in the mid-LAD (Fig. 2). The bridge caused strong systolic compression (“milking effect”)(Fig. 2B). Left ventriculography showed discrete apical hypokinesia. Simultaneous intravascular ultrasonography showed the “half moon” sign surrounding the tunneled segment, during all cardiac cycle, and mild thickening of the intima was seen in all segments of the LAD (Fig. 3). International Journal of Cardiology 115 (2007) e49 – e51 www.elsevier.com/locate/ijcard ⁎ Corresponding author. Av. Doutor Enéas Carvalho Aguiar 44, 05403.900, São Paulo, Brazil. Tel.: +55 1130695387; fax: +55 1130695348. E-mail address: caio.vianna@incor.usp.br (C.B. Vianna). 0167-5273/$ - see front matter © 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2006.07.159