□ EDITORIAL □

Myocardial Bridge: Harmless or Harmful

Key words: myocardial , coronary spasm, myocar- diameter reduction by the myocardial bridge. Quantitative dial infarction, coronary flow reserve, vascular analysis of the Doppler flow profile shows a highly charac- dysfunction teristic pattern in approximately 90% of the patients with an abrupt early diastolic flow acceleration, which has been termed as the “finger-tip” phenomenon, a rapid mid-diastolic deceleration and mid-to-late diastolic plateau. The abrupt The and their major branches usually run early diastolic flow acceleration is due to the persistent dia- on the surface of the heart in the subepicardial tissue. stolic diameter reduction. This is followed by a rapid dia- Sometimes, a portion of the artery runs under a “bridge” of stolic lumen gain leading to a plateau during late diastole. superficial myocardial fibers for a short distance. This condi- This characteristic flow pattern has been well described by tion has been given various terms “myocardial bridge”, “intr Bourassa et al (2). It is not hard to believe that a myocardial amural coronary artery”, “mural coronary artery”, “coronary bridge may cause flow limitation leading to myocardial artery overbridging” and “myocardial loop” (1). The inci- ischemia in such patients with a rapid heart rate where the dence of myocardial bridge has been reported to vary between diastolic phase is relatively shortened or in cases with maxi- 15% and 85% in autopsy, and 0.5% to 2.5% in angiographic mal coronary arterial dilation in which flow velocity is maxi- series (2). The length varies widely from 4 to 40 mm, the mal and any minor resistance against flow could cause flow thickness also varies from 1 to 4 mm (2). This is found most reduction. In fact, coronary flow reserve defined as the ratio often at the mid portion of the left anterior descending coro- of mean flow velocity achieved at peak hyperemia to mean nary artery, and sometimes at the right coronary artery and resting flow velocity obtained after intracoronary injection of left circumflex artery. Myocardial bridges are recognized pri- papaverine was reduced from 3.0 in normal subjects to 2.0 or marily because of the “systolic narrowing” or “milking effe- 2.6 in those with a myocardial bridge (2). 201Tl single photon ct” as seen on coronary . Angelini et al (1) have emission computed tomography (SPECT) immediately fol- concluded that at least 5% of the general population is esti- lowing treadmill in patients with myocardial bridge showed mated to have angiographic systolic narrowing, and myocar- a reversible perfusion defect (7). Dobutamine stress echocar- dial bridges are not likely causes of myocardial ischemia. diography also showed wall motion abnormalities in these Since the first angiographic description of myocardial patients (8). On the other hand, intracoronary stent place- bridge in vivo by Porstmann and Iwig (3) in 1960, many ment to a myocardial bridge was successful to normalize ischemic events possibly caused by myocardial bridge have coronary fractional flow reserve (19) and to abolish clinical been reported, including many reports from Japan (4–6). symptoms (20). Accumulating evidence throughout the world has indicated However, how can we explain many cases with coronary that myocardial bridge may cause pectoris (7, 8), spasms (9, 10) or (10–14) in patients coronary spasms (9, 10), myocardial infarction (10–14), ven- with a myocardial bridge? In this issue of the Journal, Kurisu tricular septal perforation (15), life threatening cardiac et al (18) report a 28-year-old Japanese male with myocar- (6, 16) and sudden cardiac death (2). Many case dial infarction. This patient was admitted 2 hours after the reports from Japan contributed much to the understanding of onset of , and emergency coronary angiogram re- the pathophysiological role of myocardial bridge (4–6, 9, 17) vealed a massive thrombus at the proximal portion of the left including a case report by Kurisu et al (18) in this issue of anterior descending coronary artery. Follow-up coronary the Journal. angiogram obtained 8 days after onset demonstrated an obvi- As coronary narrowing takes place during systole and be- ous myocardial bridge with systolic compression. Intravascu- cause a major portion of the flow occurs during diastole, it is lar ultrasound revealed an atherosclerotic plaque in the intriguing to consider how myocardial bridge causes myocar- segment immediately proximal to the myocardial bridge. dial ischemia. Bourassa et al (2) have clearly answered this They concluded that coronary spasm was elicited at the myo- question. In a frame-by-frame analysis of cineangiograms, cardial bridge followed by thrombus formation and myocar- they demonstrated that the milking effect of the coronary dial infarction (18). artery had an extension of the obstruction into diastole, which averaged 136 ms or 26% of diastole. Early diastolic See also p 1157. diameter gain was delayed with a persistent mid-diastolic

Internal Medicine Vol. 43, No. 12 (December 2004) 1097 There are numerous case reports of myocardial infarction 4) Ishii T, Hosoda Y, Osaka T, et al. The significance of myocardial related to myocardial bridge (10–14). Intravascular ultra- bridge upon atherosclerosis in the left anterior descending coronary ar- sound study by Ge et al (21) revealed atherosclerotic plaques tery. J Pathol 148: 279–291, 1986. 5) Hashimoto A, Takekoshi N, Murakami E. Clinical significance of myo- in the segments proximal to the bridge in 12 (86%) of 14 pa- cardial squeezing of the coronary artery. Jpn Heart J 111: 913–922, tients. Their follow-up study in 1999 revealed atherosclerotic 1984. involvement of the proximal segment in 61 (88%) of the 69 6) Endo M, Lee YW, Hayashi H, Wada J. Angiographic evidence of myo- patients, and no plaques were found in the bridge or distal cardial squeezing accompanying tachyarrhythmia as a possible cause of segments(22). The present report in this issue of the Journal myocardial infarction. Chest 73: 431–433, 1978. 7) Huang WS, Chang HD, Yang SP, Tsao TP, Cheng CY, Cherng SC. (18) is consistent with these observations (21, 22). Abnormal 201 Tl myocardial single photon emission computed tomo- Teragawa et al (9) have suggested a link between myocar- graphy in energetic male patients with myocardial bridge. Nucl Med dial bridge and coronary spasm. They performed a spasm- Commun 23: 1123–1128, 2002. provocation test in 114 Japanese patients with chest pain by 8) Ho YL, Wu CC, Yen RF, Hung SR, Chen MF, Huang PJ. Comparison infusing acetylcholine into the left coronary artery. Patients of ischemic patterns in myocardial bridge and syndrome X: evaluation by dobutamine stress echocardiography and stress thallium-201 with myocardial bridge (MB) experienced coronary spasm SPECT. J Formos Med Assoc 100: 83–88, 2001. more frequently than patients without MB (MB+: 73%; 9) Teragawa H, Fukuda Y, Matsuda K, et al. Myocardial bridging in- MB–: 40%, p=0.0006). They considered vascular dysfunc- creases the risk of coronary spasm. Clin Cardiol 26: 377–383, 2003. tion at level of the endothelium and/or smooth muscle as a 10) Sakuma M, Kamishirado H, Inoue T, et al. Acute myocardial infarction possible cause of spasm at the myocardial bridge. Endo- associated with myocardial bridge and coronary artery vasospasm. Int J Clin Pract 56: 721–722, 2002. thelial dysfunction (23) and/or dysfunction of smooth muscle 11) Diaz-Widmann J, Cox SL, Roongsritong C. Unappreciable myocardial cells (24) is thought to be involved in the genesis of coronary bridge causing anterior myocardial infarction and postinfarction angina. spasm. Ishii et al (25) have demonstrated that endothelial South Med J 96: 400–402, 2003. cells and smooth muscle cells are preserved beneath the 12) Bauters C, Chmait A, Tricot O, Lamblin N, Van Belle E, Lablanche myocardial bridge, but not in the segment proximal and dis- JM. and myocardial bridging. Circulation 105: 130, 2002. tal to the myocardial bridge. 13) Bestetti RB, Costa RS, Zucolotto S, Oliveira JSM. Fatal outcome asso- Summarizing these reports, it can be said that the myocar- ciated with autopsy proven myocardial bridging of the left anterior de- dial bridge is no longer harmless, and it can be harmful. scending coronary artery. Eur Heart J 10: 573–576, 1989. Mechanical compression which persists during early diastole 14) van Brussel BL, van Tellingen C, Ernst MP, Plokker HW. Myocardial can cause myocardial ischemia and chest pain. The proximal bridging: a cause of myocardial infarction? Int J Cardiol 6: 78–82, 1984. portion of the myocardial bridge can be a favorite site of 15) Tio RA, Ebels T. Ventricular septal rupture caused by myocardial atherosclerotic lesions. Furthermore, vascular dysfunction at bridging. Ann Thorac Surg 72: 1369–1370, 2001. the myocardial bridge may cause vasospasm which can lead 16) Feld H, Guadanino V, Hollander G, Greengart A, Lichstein E, Shani J. to lethal ischemic events, arrhythmias, myocardial infarction Exercise-induced ventricular in association with a myocar- and sudden cardiac death. dial bridge. Chest 99: 1295–1296, 1991. 17) Kodama K, Morioka N, Hara Y, Shigematsu Y, Hamada M, Hiwada K. Fortunately, patients with myocardial bridge and systolic at the site of myocardial bridge. Report of two compression of the left anterior descending coronary artery cases. Angiology 49: 659–663, 1998. have been described as having a good or an excellent long- 18) Kurisu S, Inoue I, Kawagoe T, et al. Acute myocardial infarction asso- term prognosis. In their state-of-the-art paper, Bourassa et al ciated with myocardial bridging in a young adult. Intern Med 43: 1157– (2) summarized the demographic and clinical characteristics 1161, 2004. 19) Kurtoglu N, Mutlu B, Soydinc S, et al. Normalization of coronary frac- of patients with symptomatic myocardial bridges, based on tional flow reserve with successful intracoronary stent placement to a several clinical observations. Among them, observation myocardial bridge. J Interven Cardiol 17: 33–36, 2004. based on only 69 cases was the greatest number of patients 20) Klues HG, Schwarz ER, vom Dahl J, et al. Disturbed intracoronary (22). We need a greater number of patients followed up for hemodynamics in myocardial bridging. Early normalization by a sufficient time in order to conclude that the myocardial intracoronary stent placement. Circulation 96: 2905–2913, 1997. 21) Ge J, Erbel R, Rupprecht HJ, et al. Comparison of intravascular ultra- bridge is harmless. sound and angiography in the assessment of myocardial bridging. Circulation 89: 1725–1732, 1994. Takahiro HAYASHI,MDand Kinji ISHIKAWA,MD 22) Ge J, Jeremias A, Rupp A, et al. New signs characteristic of myocardial Department of Cardiology, Kinki University School of Medicine, bridging demonstrated by intracoronary ultrasound and Doppler. Eur Osaka 589-8511 Heart J 20: 1707–1716, 1999. 23) Kugiyama K, Yasue H, Okumura K, et al. Nitric oxide activity is defi- References cient in spasm arteries of patients with coronary spastic angina. Circulation 94: 266–272, 1996. 1) Angelini P, Trivellato M, Donis J, Leachman RD. Myocardial bridges: 24) Egashira K, Inou T, Yamada A, Hirooka Y, Takeshita A. Preserved en- a review. Prog Cardiovasc Dis 24: 75–88, 1983. dothelium-dependent vasodilation at the vasospastic site in patients 2) Bourassa MG, Butnaru A, Lespérance J, Tardif JC. Symptomatic myo- with variant angina. J Clin Invest 89: 1047–1052, 1992. cardial bridges: overview of ischemic mechanisms and current diagnos- 25) Ishii T, Asuwa N, Masuda S, Ishikawa Y, Kiguchi H, Shimada K. tic and treatment strategies. J Am Coll Cardiol 41: 351–359, 2003. Atherosclerosis suppression in the left anterior descending coronary ar- 3) Porstmann W, Iwig J. Die intramurale Koronarie im Angiogramm. tery by the presence of a myocardial bridge: an ultrastructural study. Fortschr Roentgenstr 92: 129–132, 1960. (in German). Mod Pathol 4: 424–431, 1991.

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