Cardiac Catheterization and Interventional Cardiology © 1991 S. Karger AG, Basel 0008-6312/91/0794-0245S2.75/0
Cardiology 1991:79:245-248
Percutaneous Transluminal Coronary Angioplasty of a Coronary Artery Stenosis at the Site of Myocardial Bridging Lawrence 1. Laifer, Bonnie H. Weiner Division of Cardiovascular Medicine. University of Massachussetts School of Medicine. Worcester. Mass., USA
Key Words. Myocardial bridging • Angioplasty • Myocardial Bridge Abstract. The incidence of myocardial bridging observed at angiography (0.5-16%) is far less than at pathologic study (> 50%). Myocardial bridging is felt to have a ‘protective effect’ on the coronary artery at the site of bridging, and significant atherosclerosis within the bridge is almost never seen at pathologic examination. To date, there have been no reports of significant atherosclerosis at the site of angiographically documented myocardial bridging. We report a unique case of an angioplasty of a left anterior descending artery stenosis within a myocardial bridge. This report also discusses the possible difference in the protective effect of myocardial bridging that is seen at angiography and myocardial bridging that is only appreciated pathologically but not angiographically.
Angiographically documented myocar dial bridging has been reported with a fre quency ranging from 0.5 to 16% [1-7]. Nu merous investigators have observed that the coronary artery at the site of a myocardial bridge is almost always free of atherosclero sis. It has been postulated that the myocar dial bridge exerts a ‘protective effect’ on the coronary artery at the site of bridging. We report an unusual case of a percutaneous transluminal coronary angioplasty (PTCA)
of a left anterior descending artery (LAD) stenosis occurring within a myocardial bridge. Case Report A 53-year-old hypertensive male underwent coro nary artery bypass grafting in December 1982 because of post-infarction angina. Three saphenous vein grafts were placed respectively to his LAD, left circumflex and right coronary arteries. Following surgery he did quite well and remained pain-free until March 1989 when he developed recurrent angina. A thallium exer cise treadmill test was performed and revealed mod-
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Introduction
Fig. 1. Diastolic image of the LAD (in the cranial posteroanterior projection) following successful PTCA. The tip of the pacemaker marks the LAD approximately 0.2 cm prior to the site of dilatation. The distal portion of the LAD graft is seen filling ret rograde and anastomoses with the LAD approxi mately 2 cm beyond the PTCA site. Fig. 2. Systolic image of the LAD following suc cessful PTCA. There is almost complete luminal oblit eration of the PTCA site during systole, which is con sistent with myocardial bridging.
Laifer/Weiner
crate defects in the posterobasal, inferoapical and sep tal segments, with complete redistribution in the sep tum and apex. The patient subsequently underwent cardiac catheterization which revealed an occluded graft to the LAD. and patent grafts to the left circum flex and right coronary arteries. The posterolateral branch had a 70% distal stenosis. The native LAD demonstrated a 40% stenosis proximallv. The midLAD had a long sublotally occluded segment prior to the graft insertion site. There was retrograde filling of the graft and faint opacification of the distal LAD. The native left circumflex artery was totally occluded proximally. Left ventriculography showed mild apical hypokincsis with overall preserved ventricular func tion. An attempt was made to manage the patient medically, but because of continued frequent angina he underwent PTCA of his native LAD at its subto tal^ occluded mid-segment. Several inflations at this site were performed with a 2.5-mm balloon. Repeal angiography following dilatation revealed myocardial bridging at the site of the successful coronary dilata tion (bridging was not appreciated prior to his PTCA since the LAD was sublotally occluded at the proxi mal end of the myocardial bridge segment). As shown in figure I. in diastole there is no appreciable residual stenosis. Figure 2 is a systolic image and reveals almost complete obliteration of the lumen of the LAD at the sile of dilatation. Review of the patient's 1982 cardiac catheterization (prior to his coronary artery bypass surgery) demonstrated myocardial bridging of the LAD at the same site, but with less marked sys tolic compression of the vessel. 1'hcre was no angio graphic evidence of atherosclerosis at this site or in its proximity. The very proximal LAD exhibited a 40% stenosis which was unchanged betweent the two stud ies. The patient became angina-free following his an gioplasty and did well until August 1989 when he began to experience nocturnal chest burning similar to his prior angina. A thallium exercise treadmill was performed, and revealed moderate defects in the dis tal anterior, distal anterolateral, posterobasal and api cal segments. Three-hour-delavcd images showed no change in the posterobasal segment, but almost com plete redistribution in the distal anterolateral, distal anterior and apical regions. These findings were felt to be consistent with restenosis of the LAD, but the patient declined repeat cardiac catheterization since his angina had improved on an intensified medical regimen.
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246
Discussion The first angiographic description of myocardial bridging is credited to Portsman and Iwig [8] who in 1960 published a report describing the systolic narrowing of the LAD in a 19-year-old patient. While there is gen eral agreement that systolic compression of coronary arteries seen during coronary angi ography is a reflection of myocardial bridg ing, there are no controlled studies with ana tomic verification. The incidence of myocar dial bridging varies considerably between angiographic and pathologic studies. Angio graphic series report myocardial bridging with a frequency ranging from 0.5 to 16%, with the majority reporting less than a 2% frequency [ 1,2. 6, 7]. In contrast, myocardial bridging in autopsy series is reported with a frequency ranging from 5.4 to 85.7% [9-14], with most series reporting bridging with a frequency greater than 50%. Channer et al. [7] have suggested that the lower frequency of bridging appreciated angiographically may reflect the higher pressure filling of the coronary arteries with contrast. The pressure generated by the myocardial bridge neces sary to cause systolic compression during coronary artery dye injection may need to be greater than under normal physiologic con ditions. Many anatomically documented bridges, therefore, may not be apparent an giographically. With the exception of one autopsy study [11], there has been general agreement that it is unusual for atherosclerosis to involve the segment of coronary artery within the myo cardial bridge. In an autopsy study of myo cardial bridging by Geiringer [12], only 3 of 23 bridging segments were found to contain significant atherosclerosis. There are no an giographic reports of myocardial bridging
247
with lesions at the site of the bridge. In a recent study of 1,102 consecutive angio grams [7], myocardial bridging was never associated with demonstrable lesion forma tion at the bridge site. The mechanism by which myocardial bridging exerts this pro tective effect is not known, but it has been postulated that the myocardial bridge, by compressing the involved arterial segment during systole, minimizes the potential en dothelial trauma of the systolic wave [4], This would similarly protect the vessel distal to the bridge and would also explain the decreased incidence of atherosclerosis distal to a myocardial bridge [13,15], The current report is unique in two re spects. First, it appears to be the first angio graphic report of myocardial bridging in which a coronary artery stenosis is located within the bridge segment. We emphasize the fact that this is the first angiographic report because there are two apparent dis crepancies between autopsy and angio graphic studies of myocardial bridging which are quite interesting. First, as men tioned earlier, the incidence of bridging found at autopsy is far greater than the inci dence of bridging visualized angiographi cally [1-7, 9-14], Second, while most au topsy studies report a low incidence of lesion formation at the site of the bridging, angio graphic studies have not reported the occur rence of any angiographically demonstrable coronary disease within the segment of the myocardial bridge. While speculative, it is interesting to postulate that these two find ings (the incidence of bridging and the de gree to which atherosclerosis is found at the site of the bridge) are related. Perhaps only myocardial bridging of a sufficient degree to cause systolic compression of the artery dur ing high pressure injection is of adequate
Downloaded by: Univ. of California Santa Barbara 128.111.121.42 - 3/14/2018 12:13:10 PM
PTCA of an LAD Stenosis within a Myocardial Bridge
Laifer/Weiner
248
References 1 Noble J, Bourassa M. Petitclerc R. ct al: Myocar dial bridging and the milking effect of the left anterior descending coronary artery: Normal vari ant or obstruction. Am J Cardiol 1976;37:993— 999. 2 Ishimori T, Raizner A. Chahine R, et al: Myocar dial bridges in man: Clinical correlations and an giographic accentuation with nitroglycerin. Cathet Cardiovasc Diagn 1977:3:59-65. 3 Rossi L, Dander B, Nidasio G, et al: Myocardial bridges and ischemic heart disease. Eur Heart J 1980:1:239-245. 4 Angelini P, Trivellato M, Donis J, et al: Myocar dial bridges: A review. Prog Cardiovasc Dis 1983; 26:75-88.
5 Hashimoto A. Takekoshi N. Murakami E: Clini cal significance of myocardial briging of the coro nary artery. Jpn Heart J 1984:25:913-922. 6 Binet J, Guiraudon G, Langois J. et al: Angine de poitrine et ponts musculaires sur l'artère interven triculaire antérieure: A propos de trois cas opérés. Arch Mal Cœur 1987;71:251-258. 7 Channer K. Bukis E, Hartnell G. et al: Myocardial bridging of the coronary arteries. Clin Radiol 1989:40:355-359. 8 Portsmann W. IwigJ: Die intramurale Koronarie im Angiogramm. Fortschr Rontgcnstr 1960:92: 129-132. 9 Polacek P. Kravlove H: Relation of myocardial bridges and loops on the coronary arteries to cor onary occlusions. Am Heart J 1961:61:44-52. 10 Zapecowski Z: Pattern of coronary arteries in man as the morphological ground for the analysis of the place and extent of the infarctions of the wall of the left ventricle (in Polish). Buletvn Vojskowj Akademii Medycznej 1965:2:1. 11 Edwards J, Burnsides C, Swarm R: Arteriosclero sis in the intramural and extramural portions of coronary arteries in the human heart. Circulation 1956;13:235-241. 12 Geiringer E: The mural coronary artery. Am Heart J 1951:41:359-368. 13 Lee S, Wu T: The role of the mural coronary artery in prevention of coronary atherosclerosis. Arch Pathol 1972:93:32-35. 14 Ishii T, Hosoda Y, Osaka T, et al: The significance of myocardial bridge upon atherosclerosis in the left anterior descending coronary artery. J Pathol 1986:148:279-291. 15 Stolte M, Weis P. Prestele H: Die koronare Muskelbriicke des Ramus descendens anterior. Vir chows Arch [A] 1977:375:23-36.
Received: November 11, 1990 Accepted: February 15, 1991 Lawrence 1. Laifer Division of Cardiovascular Medicine University of Massachussetts School of Medicine 55 Lake Avenue North Worcester, MA 01655 (USA)
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hemodynamic significance to afford the ‘protective’ effect from the development of atherosclerosis. Any bridging noted at angi ography is significant (for its potential pro tective effect), while myocardial bridging de termined at autopsy is ‘unselectcd’ and may therefore not have the same hemodynamic significance (i.e. an anatomic but not physio logically significant bridge). Therefore, only myocardial bridging that can be visualized angiographically would be sufficient to af ford protection from atherosclerosis. This is also the first report of an angio plasty of a coronary artery stenosis at the site of a myocardial bridge. One might think a priori that a PTCA in this situation would be deleteriously affected by the systolic com pression of the myocardial bridge, especially had a significant dissection been created during dilatation. While it would be unrea sonable to generalize from a single case, in this individual report the angioplasty was successfully accomplished, and no dissection was noted. It cannot be determined whether his (presumed) restenosis is related in any way to the overlying myocardial bridge.
Cardiology 1991:79:245-248
Percutaneous Transluminal Coronary Angioplasty of a Coronary Artery Stenosis at the Site of Myocardial Bridging Lawrence 1. Laifer, Bonnie H. Weiner Division of Cardiovascular Medicine. University of Massachussetts School of Medicine. Worcester. Mass., USA
Key Words. Myocardial bridging • Angioplasty • Myocardial Bridge Abstract. The incidence of myocardial bridging observed at angiography (0.5-16%) is far less than at pathologic study (> 50%). Myocardial bridging is felt to have a ‘protective effect’ on the coronary artery at the site of bridging, and significant atherosclerosis within the bridge is almost never seen at pathologic examination. To date, there have been no reports of significant atherosclerosis at the site of angiographically documented myocardial bridging. We report a unique case of an angioplasty of a left anterior descending artery stenosis within a myocardial bridge. This report also discusses the possible difference in the protective effect of myocardial bridging that is seen at angiography and myocardial bridging that is only appreciated pathologically but not angiographically.
Angiographically documented myocar dial bridging has been reported with a fre quency ranging from 0.5 to 16% [1-7]. Nu merous investigators have observed that the coronary artery at the site of a myocardial bridge is almost always free of atherosclero sis. It has been postulated that the myocar dial bridge exerts a ‘protective effect’ on the coronary artery at the site of bridging. We report an unusual case of a percutaneous transluminal coronary angioplasty (PTCA)
of a left anterior descending artery (LAD) stenosis occurring within a myocardial bridge. Case Report A 53-year-old hypertensive male underwent coro nary artery bypass grafting in December 1982 because of post-infarction angina. Three saphenous vein grafts were placed respectively to his LAD, left circumflex and right coronary arteries. Following surgery he did quite well and remained pain-free until March 1989 when he developed recurrent angina. A thallium exer cise treadmill test was performed and revealed mod-
Downloaded by: Univ. of California Santa Barbara 128.111.121.42 - 3/14/2018 12:13:10 PM
Introduction
Fig. 1. Diastolic image of the LAD (in the cranial posteroanterior projection) following successful PTCA. The tip of the pacemaker marks the LAD approximately 0.2 cm prior to the site of dilatation. The distal portion of the LAD graft is seen filling ret rograde and anastomoses with the LAD approxi mately 2 cm beyond the PTCA site. Fig. 2. Systolic image of the LAD following suc cessful PTCA. There is almost complete luminal oblit eration of the PTCA site during systole, which is con sistent with myocardial bridging.
Laifer/Weiner
crate defects in the posterobasal, inferoapical and sep tal segments, with complete redistribution in the sep tum and apex. The patient subsequently underwent cardiac catheterization which revealed an occluded graft to the LAD. and patent grafts to the left circum flex and right coronary arteries. The posterolateral branch had a 70% distal stenosis. The native LAD demonstrated a 40% stenosis proximallv. The midLAD had a long sublotally occluded segment prior to the graft insertion site. There was retrograde filling of the graft and faint opacification of the distal LAD. The native left circumflex artery was totally occluded proximally. Left ventriculography showed mild apical hypokincsis with overall preserved ventricular func tion. An attempt was made to manage the patient medically, but because of continued frequent angina he underwent PTCA of his native LAD at its subto tal^ occluded mid-segment. Several inflations at this site were performed with a 2.5-mm balloon. Repeal angiography following dilatation revealed myocardial bridging at the site of the successful coronary dilata tion (bridging was not appreciated prior to his PTCA since the LAD was sublotally occluded at the proxi mal end of the myocardial bridge segment). As shown in figure I. in diastole there is no appreciable residual stenosis. Figure 2 is a systolic image and reveals almost complete obliteration of the lumen of the LAD at the sile of dilatation. Review of the patient's 1982 cardiac catheterization (prior to his coronary artery bypass surgery) demonstrated myocardial bridging of the LAD at the same site, but with less marked sys tolic compression of the vessel. 1'hcre was no angio graphic evidence of atherosclerosis at this site or in its proximity. The very proximal LAD exhibited a 40% stenosis which was unchanged betweent the two stud ies. The patient became angina-free following his an gioplasty and did well until August 1989 when he began to experience nocturnal chest burning similar to his prior angina. A thallium exercise treadmill was performed, and revealed moderate defects in the dis tal anterior, distal anterolateral, posterobasal and api cal segments. Three-hour-delavcd images showed no change in the posterobasal segment, but almost com plete redistribution in the distal anterolateral, distal anterior and apical regions. These findings were felt to be consistent with restenosis of the LAD, but the patient declined repeat cardiac catheterization since his angina had improved on an intensified medical regimen.
Downloaded by: Univ. of California Santa Barbara 128.111.121.42 - 3/14/2018 12:13:10 PM
246
Discussion The first angiographic description of myocardial bridging is credited to Portsman and Iwig [8] who in 1960 published a report describing the systolic narrowing of the LAD in a 19-year-old patient. While there is gen eral agreement that systolic compression of coronary arteries seen during coronary angi ography is a reflection of myocardial bridg ing, there are no controlled studies with ana tomic verification. The incidence of myocar dial bridging varies considerably between angiographic and pathologic studies. Angio graphic series report myocardial bridging with a frequency ranging from 0.5 to 16%, with the majority reporting less than a 2% frequency [ 1,2. 6, 7]. In contrast, myocardial bridging in autopsy series is reported with a frequency ranging from 5.4 to 85.7% [9-14], with most series reporting bridging with a frequency greater than 50%. Channer et al. [7] have suggested that the lower frequency of bridging appreciated angiographically may reflect the higher pressure filling of the coronary arteries with contrast. The pressure generated by the myocardial bridge neces sary to cause systolic compression during coronary artery dye injection may need to be greater than under normal physiologic con ditions. Many anatomically documented bridges, therefore, may not be apparent an giographically. With the exception of one autopsy study [11], there has been general agreement that it is unusual for atherosclerosis to involve the segment of coronary artery within the myo cardial bridge. In an autopsy study of myo cardial bridging by Geiringer [12], only 3 of 23 bridging segments were found to contain significant atherosclerosis. There are no an giographic reports of myocardial bridging
247
with lesions at the site of the bridge. In a recent study of 1,102 consecutive angio grams [7], myocardial bridging was never associated with demonstrable lesion forma tion at the bridge site. The mechanism by which myocardial bridging exerts this pro tective effect is not known, but it has been postulated that the myocardial bridge, by compressing the involved arterial segment during systole, minimizes the potential en dothelial trauma of the systolic wave [4], This would similarly protect the vessel distal to the bridge and would also explain the decreased incidence of atherosclerosis distal to a myocardial bridge [13,15], The current report is unique in two re spects. First, it appears to be the first angio graphic report of myocardial bridging in which a coronary artery stenosis is located within the bridge segment. We emphasize the fact that this is the first angiographic report because there are two apparent dis crepancies between autopsy and angio graphic studies of myocardial bridging which are quite interesting. First, as men tioned earlier, the incidence of bridging found at autopsy is far greater than the inci dence of bridging visualized angiographi cally [1-7, 9-14], Second, while most au topsy studies report a low incidence of lesion formation at the site of the bridging, angio graphic studies have not reported the occur rence of any angiographically demonstrable coronary disease within the segment of the myocardial bridge. While speculative, it is interesting to postulate that these two find ings (the incidence of bridging and the de gree to which atherosclerosis is found at the site of the bridge) are related. Perhaps only myocardial bridging of a sufficient degree to cause systolic compression of the artery dur ing high pressure injection is of adequate
Downloaded by: Univ. of California Santa Barbara 128.111.121.42 - 3/14/2018 12:13:10 PM
PTCA of an LAD Stenosis within a Myocardial Bridge
Laifer/Weiner
248
References 1 Noble J, Bourassa M. Petitclerc R. ct al: Myocar dial bridging and the milking effect of the left anterior descending coronary artery: Normal vari ant or obstruction. Am J Cardiol 1976;37:993— 999. 2 Ishimori T, Raizner A. Chahine R, et al: Myocar dial bridges in man: Clinical correlations and an giographic accentuation with nitroglycerin. Cathet Cardiovasc Diagn 1977:3:59-65. 3 Rossi L, Dander B, Nidasio G, et al: Myocardial bridges and ischemic heart disease. Eur Heart J 1980:1:239-245. 4 Angelini P, Trivellato M, Donis J, et al: Myocar dial bridges: A review. Prog Cardiovasc Dis 1983; 26:75-88.
5 Hashimoto A. Takekoshi N. Murakami E: Clini cal significance of myocardial briging of the coro nary artery. Jpn Heart J 1984:25:913-922. 6 Binet J, Guiraudon G, Langois J. et al: Angine de poitrine et ponts musculaires sur l'artère interven triculaire antérieure: A propos de trois cas opérés. Arch Mal Cœur 1987;71:251-258. 7 Channer K. Bukis E, Hartnell G. et al: Myocardial bridging of the coronary arteries. Clin Radiol 1989:40:355-359. 8 Portsmann W. IwigJ: Die intramurale Koronarie im Angiogramm. Fortschr Rontgcnstr 1960:92: 129-132. 9 Polacek P. Kravlove H: Relation of myocardial bridges and loops on the coronary arteries to cor onary occlusions. Am Heart J 1961:61:44-52. 10 Zapecowski Z: Pattern of coronary arteries in man as the morphological ground for the analysis of the place and extent of the infarctions of the wall of the left ventricle (in Polish). Buletvn Vojskowj Akademii Medycznej 1965:2:1. 11 Edwards J, Burnsides C, Swarm R: Arteriosclero sis in the intramural and extramural portions of coronary arteries in the human heart. Circulation 1956;13:235-241. 12 Geiringer E: The mural coronary artery. Am Heart J 1951:41:359-368. 13 Lee S, Wu T: The role of the mural coronary artery in prevention of coronary atherosclerosis. Arch Pathol 1972:93:32-35. 14 Ishii T, Hosoda Y, Osaka T, et al: The significance of myocardial bridge upon atherosclerosis in the left anterior descending coronary artery. J Pathol 1986:148:279-291. 15 Stolte M, Weis P. Prestele H: Die koronare Muskelbriicke des Ramus descendens anterior. Vir chows Arch [A] 1977:375:23-36.
Received: November 11, 1990 Accepted: February 15, 1991 Lawrence 1. Laifer Division of Cardiovascular Medicine University of Massachussetts School of Medicine 55 Lake Avenue North Worcester, MA 01655 (USA)
Downloaded by: Univ. of California Santa Barbara 128.111.121.42 - 3/14/2018 12:13:10 PM
hemodynamic significance to afford the ‘protective’ effect from the development of atherosclerosis. Any bridging noted at angi ography is significant (for its potential pro tective effect), while myocardial bridging de termined at autopsy is ‘unselectcd’ and may therefore not have the same hemodynamic significance (i.e. an anatomic but not physio logically significant bridge). Therefore, only myocardial bridging that can be visualized angiographically would be sufficient to af ford protection from atherosclerosis. This is also the first report of an angio plasty of a coronary artery stenosis at the site of a myocardial bridge. One might think a priori that a PTCA in this situation would be deleteriously affected by the systolic com pression of the myocardial bridge, especially had a significant dissection been created during dilatation. While it would be unrea sonable to generalize from a single case, in this individual report the angioplasty was successfully accomplished, and no dissection was noted. It cannot be determined whether his (presumed) restenosis is related in any way to the overlying myocardial bridge.
