M. Agirbasli et al., STENT PROCEDURE COMPLICATED BY THROMBUS FORMATION DISTAL TO THE LESION WITHIN A MUSCLE BRIDGE, Catheterization and cardiovascular diagnosis, 43(1), 1998, pp. 73-76
We report here a case of a patient who underwent percutaneous interven
tion to the left anterior descending artery, complicated by thrombus f
ormation within the myocardial bridge distal to the lesion, There was
complete angiographic resolution of thrombus and restoration of the no
rmal antegrade blood flow after infusion of glycoprotein IIb/IIIa anta
gonist (abciximab). Our observation may suggest that the presence of m
yocardial bridging distal to coronary lesions should be considered ser
iously in preprocedural evaluation of the lesions as a potential risk
factor for intracoronary thrombus formation. The main coronary arterie
s and the proximal segments of their major branches lie free on the ep
icardial surface of the heart. However, in some instances these vessel
s may penetrate into the muscle being surrounded by the myocardium, wi
th the overlying muscle referred to as a ''bridge''. Myocardial bridgi
ng appears to be a congenital anomaly, due to failure of exteriorizati
on of the primitive coronary intratrabecular arterial network. It occu
rs in 5-86% of patients in autopsy studies [1-3], and it is observed a
s systolic coronary artery narrowing in 0.5-12% of patients undergoing
coronary arteriography [3]. Although the gross anatomist had long rec
ognized that the epicardial coronary artery might on occasion course d
irectly through a segment of cardiac muscle, the physiological signifi
cance of this phenomenon was considered benign [4]. This is partly bec
ause traditional teaching concerning coronary blood flow delivery to t
he left ventricular myocardium emphasized the primacy of the diastolic
phase of the cardiac cycle. However, myocardial bridging is not alway
s a benign finding, with recent reports suggesting an association with
myocardial ischemia, infarction, vasospasm, cardiac arrhythmias, and
sudden death [3,5]. (C) 1998 Wiley-Liss, Inc.