Letter to the Editor Transient myocardial bridging of the left anterior descending coronary artery in acute inferior myocardial infarction Harun Kilic ⁎ , Ramazan Akdemir, Asuman Bicer, Mehmet Dogan Diskapi Yildirim Beyazit Training and Education Hospital, Cardiology Department, Ankara, Turkey Received 10 August 2007; received in revised form 11 August 2007; accepted 18 August 2007 Available online 24 October 2007 Abstract We observed transient myocardial bridging of left anterior descending coronary artery (LAD) in 18.75% (12 of the total 64) of the patients during acute inferior myocardial infarction (MI). Myocardial bridging occurred only in the acute phase of inferior MI and not in the chronic phase. In the acute phase of inferior MI, compensatory hypercontraction of the anterior wall is assumed to occur in response to the decrease in the movement of the infarct-related walls. In the chronic phase, disappearance of the myocardial bridging observed due to the resolution of compensatory anterior wall hypercontraction, as a result of the reperfusion of infarct-related coronary artery. Most of the myocardial bridges seen in autopsy series are not seen angiographically. Variation at angiography may in part be attributable to small and thin bridges causing little compression. Adrenergic stimulation or afterload reduction by nitroglycerin facilitates diagnosis of myocardial bridging by increasing coronary compression. Both of these conditions are almost always present in acute MI. We concluded that transient myocardial bridging of LAD can be observed in some patients with acute inferior MI during acute stage. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Myocardial bridging; Acute inferior myocardial infarction; Percutaneous coronary intervention Muscle fibers overlying the intramyocardial segment of an epicardial coronary artery are termed myocardial bridging. The presence of myocardial bridging is indicated angiographically by narrowing of the coronary arteries during systole and normalization during diastole [1]. In pathological series, the prevalence of myocardial bridging has varied from 5% to 86% [2–5] and in angiographic series, the prevalence has been shown as between 0.5% and 33% [6–12]. Variation at angiography may in part be attributable to small and thin bridges causing little compression. Myocardial bridging is almost always confined to the left anterior descending coronary artery (LAD). Myocardial bridging was generally thought of as a harmless anatomical variant of the coronary arteries [13]. But myocardial bridging may be associated with myocardial ischemia and infarction [6–12]. Stent implantation, myotomy, coronary artery bypass surgery are the treatment options for myocardial bridging [14–16]. We observed marked myocardial bridging of the LAD in patients with acute inferior myocardial infarction (MI) only in the acute phase of MI. Of 86 patients admitted to the hospital within 12 h of onset of their acute inferior MI between January 2005 and April 2007, 64 underwent primary percutaneous coronary intervention (PCI). Of these 64 (49 men, 15 women, mean age 58+14 years) patients, 48 had infarct-related lesion (IRL) in the right coronary artery (RCA) and 16 had IRL in the left circumflex coronary artery (CX). Of these 64 patients 32 had single coronary artery disease. Coronary angiography was performed. Images were obtained with a Siemens cardiovascular imaging system. The lesion responsible for the inferior MI, the severity of stenosis, location of stenosis, and dominance of the coronary artery were evaluated. Dominance; reference to the vessel, either the right coronary or the left circumflex artery, that supplies the posterior part of the heart; in codominance both arteries provide circulation to the posterior heart. Myocardial bridging was considered present if coronary artery narrowing of N 50% was observed during systole. Patients were considered International Journal of Cardiology 131 (2009) e112 – e114 www.elsevier.com/locate/ijcard ⁎ Corresponding author. Oyak 10. Kisim 10/16 06530 Cayyolu/Ankara, Turkey. Tel./fax: +90 3122414830. E-mail address: doctorharun@gmail.com (H. Kilic). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.08.010