Update on Myocardial Bridging        Stefan Möhlenkamp, Waldemar Hort, Junbo Ge and Raimund Erbel                         ...
Mini-Review: Current Perspective                                   Update on Myocardial Bridging             Stefan Möhlen...
Möhlenkamp et al             Update on Myocardial Bridging                 2617                                           ...
2618       Circulation        November 12, 2002                                                                           ...
Möhlenkamp et al        Update on Myocardial Bridging                 2619                                                ...
2620       Circulation          November 12, 2002Figure 6. ICD-images of the myocardial bridge showing retro-grade flow dur...
Möhlenkamp et al             Update on Myocardial Bridging                          2621have thus far been treated with co...
2622           Circulation            November 12, 2002      Endokards, der Koronararterien und des Myokards. Berlin, Germ...
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Update on myocardial bridging circulation 2002

  1. 1. Update on Myocardial Bridging Stefan Möhlenkamp, Waldemar Hort, Junbo Ge and Raimund Erbel Circulation 2002, 106:2616-2622 doi: 10.1161/01.CIR.0000038420.14867.7A Circulation is published by the American Heart Association. 7272 Greenville Avenue, Dallas, TX 72514Copyright © 2002 American Heart Association. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539 The online version of this article, along with updated information and services, is located on the World Wide Web at: http://circ.ahajournals.org/content/106/20/2616Subscriptions: Information about subscribing to Circulation is online athttp://circ.ahajournals.org//subscriptions/Permissions: Permissions & Rights Desk, Lippincott Williams & Wilkins, a division of WoltersKluwer Health, 351 West Camden Street, Baltimore, MD 21202-2436. Phone: 410-528-4050. Fax:410-528-8550. E-mail:journalpermissions@lww.comReprints: Information about reprints can be found online athttp://www.lww.com/reprints Downloaded from http://circ.ahajournals.org/ by guest on July 13, 2011
  2. 2. Mini-Review: Current Perspective Update on Myocardial Bridging Stefan Möhlenkamp, MD; Waldemar Hort, MD; Junbo Ge, MD; Raimund Erbel, MDM uscle overlying the intramyocardial segment of an epicardial coronary artery, first mentioned by Reyman1in 1737, is termed a myocardial bridge, and the artery Comparative Anatomy An epicardial course of coronary arteries is not obligatory in mammals. In rodents and lagomorpha, the major vessels arecoursing within the myocardium is called a tunneled artery embedded in myocardium beneath the epicardial surface(Figure 1). It is characterized by systolic compression of the (Type I).5,29 Animals with a predominantly epicardial coursetunneled segment, which remains clinically silent in the vast of coronary arteries (Type II) include small ruminants,majority of cases. An in-depth analysis of autopsy samples carnivores, and primates.29,37 Whereas the major coronarywas first presented by Geiringer et al2 in 1951, but clinical arteries in the gorilla form an epicardial network, they tend tointerest and systematic research was triggered by an observed take a mural course in the chimpanzee.36 In goats and sheep,association of myocardial bridging with myocardial bridges are more frequent than in humans.8 They can also beischemia.2–5 observed in canines, felines, and seals.37 In some mammals New imaging techniques have led to improved identifica- they are missing or extremely rare, such as in horses and pigstion and functional quantitation of myocardial bridging in (Type III).29 Myocardial bridges are congenital in origin38 – 40vivo, which is crucial for establishing a link between systolic and likely reflect an evolutionary remnant in the genetic code.compression and the clinical presentation, and hence forcommencing appropriate therapy. In the present article, we Morphologysummarize clinically relevant aspects of myocardial bridging Myocardial bridges are most commonly localized in the middle segment of the left anterior descending coronarywith an emphasis on morphological and hemodynamic alter- artery (LAD).29 In the presence of two parallel LADations and their representation in imaging techniques. branches, one frequently takes an intramural course.2 Diago- nal and marginal branches may be involved in 18% and 40% Prevalence of cases, respectively.8,36 Angiographically, myocardialThe prevalence varies substantially among studies with a bridges are almost exclusively spotted in the LAD. They aremuch higher rate at autopsy versus angiography (Table).2,4 –28 located at a depth of 1 to 10 mm10,41 with a typical length ofVariation at autopsy may in part be attributable to the care 10 to 30 mm.5 Deformation is predominantly eccentric,5 astaken at preparation and the selection of hearts. Polacek, who ´ˇ confirmed by intravascular ultrasound (IVUS)– based stud-included myocardial loops, reports the highest rate with ies.42 Occasionally, the arteries may take a very deep coursebridges or loops in 86% of cases.29 On average, myocardial through the septum approaching the right ventricular suben-bridges are present in about one third of adults. docardium36 (Figure 2). The rate of angiographic bridging is 5%, attributable to Ferreira et al12 distinguished between two types of bridg-thin bridges causing little compression. In subjects with ing: (1) superficial bridges (75% of cases) crossing the arteryangiographically normal coronary arteries, the use of provo- perpendicularly or at an acute angle toward the apex, and (2)cation tests may enhance systolic myocardial compression muscle bundles arising from the right ventricular apicaland thereby reveal myocardial bridges in 40% of cases.26,30 trabeculae (25% of cases) that cross the LAD transversely, A high prevalence has also been reported in heart trans- obliquely, or helically before terminating in the interventric-plant recipients23 and in patients with hypertrophic obstruc- ular septum. Arterial segments may also be located in a deeptive cardiomyopathy (HOCM).31 In the latter, more rigorous interventricular gorge. Such “incomplete” bridges may ap-contraction may unmask otherwise undetectable bridges. pear during adulthood in concomitant disease,2 in which aMyocardial bridging may be found at multiple sites in segment is compressed during systole although its surface isHOCM,32 but also in patients without.33 De novo, previously not fully covered by myocardial fibers, but by a thin layer ofnonexistent myocardial bridging has been suggested for both connective tissue, nerves, and fatty tissue.36transplanted hearts34 and HOCM,35 but conclusive proof is Myocardial loops derive from atrial myocardium, surroundlacking.36 the vessel three quarters of the circumference, and return to From the Clinic of Cardiology (S.M., R.E.), University Clinic Essen, Germany; Institute of Pathology (W.H.), Heinrich Heine University Düsseldorf,Germany; and Department of Cardiology (J.G.), Zhongshan Hospital, Fudan University, China. Correspondence to Professor Raimund Erbel, MD, FACC, FESC, Clinic of Cardiology, University Clinic Essen, Hufelandstrasse 55, 45122 Essen,Germany. E-mail erbel@med.uni-essen.de (Circulation. 2002;106:2616-2622.) © 2002 American Heart Association, Inc. Circulation is available at http://www.circulationaha.org DOI: 10.1161/01.CIR.0000038420.14867.7A 2616 Downloaded from http://circ.ahajournals.org/ by guest on July 13, 2011
  3. 3. Möhlenkamp et al Update on Myocardial Bridging 2617 Presence and Absence of Atherosclerosis in Relation to Myocardial Bridging Coronary atherosclerosis in association with myocardial bridging has primarily been studied in the LAD. The segment proximal to the bridge frequently shows athero- sclerotic plaque formation, although the tunneled segment is typically spared5,8 (Figures 3 and 4). This is supported by studies on a cellular and ultrastructural level43,44: In contrast to proximal and distal segments, foam cells and modified smooth muscle cells were missing in patients’ tunneled segments.43 Extramural, epicardial segments inFigure 1. Typical systolic compression (arrows) of the mid LADat two sites in series. Diastolic lumen dimensions are normal. cholesterol-fed rabbits developed intimal atherosclerosisThe coronary tree shows no angiographic signs of coronary with accumulation of ApoB and proliferating cell nuclearatherosclerosis. antigens (PCNA) in smooth muscle cells of the intima.44 These changes were not seen in any arterial wall compo-atrial myocardium.8 They are usually thinner compared with nent in tunneled segments.44 Furthermore, endothelial cellLAD bridges (0.1 to 0.3 mm) and have a width of 10 to permeability was increased both in atherosclerotic and15 mm (range 2 to 30 mm). Occasionally, a bridge may nonatherosclerotic portions of epicardial segments in high-involve a coronary vein.14 However, myocardial loops and cholesterol rabbits but not in tunneled segments or invenous bridges appear to have no clinical relevance. normal control arteries.44 Prevalence of Myocardial Bridging at Autopsy and Angiography Sample With Author (Reference No.) Size, n Bridges, % Comment Autopsy Geiringer2 100 23 LAD Edwards et al6 276 5 All coronaries, 87% in the LAD Polacek7 ´ˇ 70 86 Including RCA loops, LAD: 60% 8 Giampalmo et al 560 7 All coronaries, 95% LAD only Lee and Wu9 108 58 LAD Penther et al10 187 18 LAD Risse and Weiler11 1056 26 All coronaries, 88% in the LAD Ferreira et al12 90 56 All coronaries Baptista and DiDio13 82 54 All coronaries, 35% in the LAD Ortale et al14 37 56 LAD (7% coronary veins with bridges) Kosinski and Grzybiak15 100 41 All coronaries Angiography Noble et al4 5250 0.5 All patients Binet et al16 700 0.7 Unspecified series of patients Ishimori et al17 313 1.6 All patients, systolic compression 50% 18 Greenspan et al 1600 0.9 All patients, exclusion of associated disease Rossi et al19 1146 4.5 All patients Voß et al20 848 2.5 All patients Kramer et al21 658 12 Patients with otherwise normal angiograms 5 Angelini et al 1100 4.5 All patients Garcia et al22 936 4.9 All patients Wymore et al23 64 33 Heart transplantation patients Somanath et al24 1500 1.1 All patients 25 Gallet et al 1920 1.0 LAD only (13 of 19 patients with an isolated bridge) Diefenbach et al26 1780 3.5 All patients Among those: 62 40 Patients with normal coronaries, use of provocation tests Juilliere et al27 ` 7467 0.8 All patients 28 Harikrishnan et al 3200 0.6 All patients Downloaded from http://circ.ahajournals.org/ by guest on July 13, 2011
  4. 4. 2618 Circulation November 12, 2002 Mechanisms for Ischemia Neither nonsignificant stenosis proximal to the bridge nor systolic compression of the tunneled segment alone can sufficiently explain severe ischemia and associated symp- toms. Experimental LCX occlusion, initially during systole only and then during continuing occlusion extending increas- ingly into diastole, resulted in distinct shortening of inflow time with significant reduction of epicardial flow, subendo- cardial flow, and distal coronary pressure.50,51 After releasing the occlusion, diastolic flow increased in correspondence with an increasing duration of vessel occlusion, despite a decrease in mean flow.51 This increased diastolic/systolic flow ratio was later verified in patients.42 Consistent with clinical findings,42,48 the increase in diastolic flow could not fully compensate for the decrease in mean flow resulting in reduced coronary flow reserve, which could not be explained by impaired vasodilatory capacity of resistance vessel.51 When arterial occlusion was limited to systole, phasic coronary blood flow and distal coronary pressure was ob- served to resume with considerable delay contributing to reduced myocardial oxygen consumption and increased cor- onary sinus lactate concentration.52 This delayed diastolic relaxation was later identified in humans as an important mechanism contributing to ischemia with frame-by-frame analysis of IVUS images.53,54 With the use of simultaneous proximal and distal pressure recordings, Ge et al47 identified the highest intravascular pressure just proximal to the bridge and a pressure gradient across the bridge. A distinct negative pressure in late diastole was preceded by a pressure peak beneath the bridge.42,47Figure 2. Myocardial bridge of the LAD in consecutive 1 cm Klues et al42 observed the highest systolic pressure within thethick left ventricular slices with the use of post mortem coronary tunneled segment but found no pressure gradient acrossangiography. (1) The tunneled segment runs in the interventricu-lar sulcus, giving off a large septal branch, (2) dives into the the bridge. All their patients had significant tortuosity of theseptal myocardium approaching the right ventricular chamber, tunneled segment at the entry and exit sites. The central(3) passes along the right ventricular endocardium, and (4) pressure chamber was interpreted as a result of heterogeneousreturns to the interventricular sulcus. Reprinted from Figure 3.8 compression of the tunneled segment with higher proximalof reference 36 with permission from Springer-Verlag GmbH &Co. Copyright 2000 Springer-Verlag GmbH & Co. and distal forces compared with the central portion, poten- tially contributing to reduced coronary flow reserve.42 Mechanisms for Atherosclerosis in the The likelihood of ischemia also increases with the intramyo- Segment Proximal to the Bridge cardial depth of the tunneled segment: In 22 of 39 hearts,Hemodynamic forces may explain atherosclerotic plaqueformation at the entrance to the tunneled segment. There, theendothelium is flat, polygonal, and polymorph, indicating lowshear, whereas in the tunneled segment, the endothelium hasa helical, spindle-shaped orientation along the course of thesegment as a sign of laminar flow and high shear.43– 45 Lowshear stress may induce the release of endothelial vasoactiveagents such as endothelial nitric oxide synthase (eNOS),endothelin-1 (ET-1), and angiotensin-converting enzyme(ACE).46 Their levels were significantly higher in proximaland distal segments compared with the tunneled segment.45Thus, low shear stress may contribute to atheroscleroticplaque formation proximal to the bridge, whereas high shearstress may have a protective role within the tunneled seg-ment.46 In addition, an increase in local wall tension andstretch may induce endothelial injury and plaque fissuring Figure 3. Histologic cross section showing (a) a tunneled seg-with subsequent thrombus formation in the proximal seg- ment and (b) an epicardial branch of the LAD. The epicardialment,47,48 which is supported by autopsy and clinical segment shows intima thickening as a sign of early atheroscle-observations.11,41,49 rosis but the tunneled segment does not. Downloaded from http://circ.ahajournals.org/ by guest on July 13, 2011
  5. 5. Möhlenkamp et al Update on Myocardial Bridging 2619 Figure 5. IVUS-images of the myocardial bridge during diastole (left) and systole (right). A “half-moon”–like area surrounding the tunneled segment is present during the entire cardiac cycle. Reprinted from reference 42 with permission from Elsevier Science. ity and the length or depth of the tunneled segment or the degree of systolic compression.12,20,60 Resting ECGs are frequently normal; stress testing may induce nonspecific signs of ischemia, conduction distur- bances, or arrhythmias.5,20 Children with HOCM and myo- cardial bridges may have an increased QTc dispersion and a higher rate of monomorphic ventricular tachycardia on Holter ECG compared with subjects without myocardial bridges.39 Perfusion defects may be seen on myocardial scintigraphy61 but are not obligatory even in deep bridges with significant systolic compression or after vasoactive stimulation.18,20 Coronary Angiography The current gold standard for diagnosing myocardial bridges is coronary angiography with the typical “milking effect” and a “step down–step up” phenomenon induced by systolic compres- sion of the tunneled segment (Figure 1). However, these signsFigure 4. Pathological specimen showing an opened coronary artery provide little information on the functional impact at the myo-with a thin myocardial bridge (arrows) and adjacent proximal and dis-tal epicardial segments. The proximal segment shows fatty lesions, cardial level. In the presence of a proximal stenosis, myocardialwhereas the tunneled segment is spared from atherosclerosis. bridging may only be identifiable after PTCA when higher intravascular pressures and reversed hypokinesis unmask myo-myocardial fibrosis and contraction band necrosis were detect- cardial bridging.62 In patients with thin bridges, the milkingable in myocardium distal to the bridge.55 Among these subjects, effect may be missed and new imaging techniques and provo-13 died suddenly and 6 during heavy exercise. These 13 cation tests may be required to detect a bridge.53,54,63,64tunneled segments were significantly deeper in the myocardiumthan the ones from the victims who did not die suddenly.55 New Imaging Techniques An increase in sympathetic drive during stress or exercise With the use of IVUS, intracoronary Doppler ultrasoundlikely facilitates ischemia, because tachycardia leads to an (ICD), and intracoronary pressure devices, morphologicalincrease of the systolic-diastolic time ratio at the expense of and functional features of myocardial bridging can be visu-diastolic flow. Increased contractility during stress further alized and quantified.42,48,53,65 The “half-moon phenome-aggravates systolic (and diastolic) compression.4 Endothelial non”42 is a characteristic IVUS observation, but its physiol-dysfunction and coronary artery spasm may also contribute to ogy and anatomy are not fully understood (Figure 5). It seemsconstriction of the tunneled segment. specific for the existence of myocardial bridging inasmuch as it is only found in tunneled segments but not in proximal or Clinical Presentation distal segments or in other arteries. In the presence of aAngina, myocardial ischemia, myocardial infarction, left half-moon phenomenon on IVUS, milking can be provokedventricular dysfunction, myocardial stunning, paroxysmal by intracoronary provocation tests, even if the bridge wasAV blockade, as well as exercise-induced ventricular angiographically undetectable.26,42,66 IVUS-based frame-by-tachycardia and sudden cardiac death are accused sequelae of frame analysis of lumen area during the entire cardiac cyclemyocardial bridging.4,19,36,56 –59 However, considering the can also be used to quantify the delay in relaxation afterprevalence of myocardial bridging, these complications are systolic compression.53 Further, IVUS pullback studies sup-rare. Patients may present with atypical or angina-like chest ported the absence of atherosclerosis within tunneled seg-pain with no consistent association between symptom sever- ments, although 90% of patients showed plaque formation Downloaded from http://circ.ahajournals.org/ by guest on July 13, 2011
  6. 6. 2620 Circulation November 12, 2002Figure 6. ICD-images of the myocardial bridge showing retro-grade flow during systole (double arrows) in the proximal seg- Figure 7. Noninvasive electron beam CT coronary angiographyment of the bridge after nitroglycerin provocation. A typical “fin- depicting a brief tunneled segment in mid LAD in a patient with nogertip” phenomenon can be visualized in diastole (single arrow). coronary calcification and angiographically normal coronary arteries.Scale in cm · s 1. Reprinted from reference 42 with permissionfrom Elsevier Science. been explored: (1) negative inotropic and/or negative chro-proximal to the bridge. When deep tunneled segments 42 notropic agents, ie, -blockers69,70 and calcium antagonists71;approach the right ventricular subendocardium, the trabecu- (2) surgical myotomy and/or CABG16,30; and (3) stenting oflated right chamber myocardium and the right ventricular the tunneled segment.48,72–74cavity may be visible on IVUS. Medication is considered first-line therapy. Intracoronary In ICD studies, pullback of the Doppler-flow wire frequently administration of a short-acting -blocker attenuated vascularreveals a characteristic flow pattern, the “fingertip phenome- compression and early diastolic blood velocity.70 The systol-non”42 or “spike-and-dome pattern.”65 This flow pattern had ic/diastolic flow ratio was normalized and anginal symptomspreviously been described in experimental studies51 and consists were alleviated.70 Volume loading may also reduce compres-of a sharp acceleration of flow in early diastole followed by sion of the tunneled segment, whereas administration ofimmediate marked deceleration and a mid-diastolic pressure nitroglyceride may aggravate compression and ischemia.75plateau. It can frequently be observed within and just proximal to In subjects refractory to medication, surgical myotomy,the tunneled segment (Figure 6),42,48,65 and can be explained by first reported by Binet et al in 1975,3 abolishes clinicalan increased pressure gradient in early diastole as a result of symptoms76 –78 and is associated with reversal of local myo-reduced distal coronary resistance and delayed relaxation of the cardial ischemia and an increase in coronary flow.79 Recently,myocardial fibers with continuing lumen compression and the minimally invasive myotomy was successfully performed.80ensuing lumen gain. However, surgery should be limited to patients with severe Particularly in deep myocardial bridges, rapid diastolic angina and evidence for clinically relevant ischemia. Inforward flow may be preceded by end-systolic flow inversion bridges that take a deep subendocardial course, the rightas a result of a local increase in pressure above aortic driving ventricle may accidentally be opened during surgery,30,81 andpressures (Figure 6).47,48 These changes result in an increased a case of aneurysm at the site of myocardial cleavage hasdiastolic/systolic flow ratio of almost 3.0, compared with been reported.82 Thus, the risk associated with surgery shouldvalues of 1.8 and 1.3 in normal controls and significant carefully be weighed against the usually uneventful long-termcoronary artery stenosis, respectively.42,67 As in experimental course even in patients with substantial systolic compression.studies,51 coronary flow reserves are frequently reduced to In 1995, Stables et al72 first reported coronary stenting as anvalues below 3.0, which can be regarded as the lower limit of interventional approach to severe myocardial bridging refractorythe norm in otherwise healthy individuals.42,48,68 to medication. Normalization of the pathological coronary flow Myocardial bridging can also be visualized with the use of profile, the reduced coronary flow reserve, and symptoms afternovel noninvasive imaging techniques such as electron beam stent deployment promised successful use of stents in thesetomography (EBT, Figure 7) and, potentially, multislice CT patients.48 In 11 patients with signs of ischemia but absence of(MSCT), magnetic resonance tomography (MRT), or trans- other cardiac disorders, all patients had good angiographicthoracic Doppler echocardiography. Whether these tools have outcome with a marked improvement in the angina score after 6a sensitivity and specificity high enough to advocate its use months and after 2 years of follow-up.74 However, at 7 weeks,for clinical or research purposes remains to be shown. 46% of patients required revascularization as a result of in-stent restenosis.74 To our knowledge, a total of 25 patients to date Therapy have been reported to have received coronary stents for myo-In symptomatic patients, therapy may be initiated to improve cardial bridging. In 50% of these cases, restenosis or majorquality of life, although hard evidence for a favorable effect periprocedural complications were reported, including perfora-on morbidity and mortality is missing. On the basis of the tion of the artery.83,84 Despite a favorable long-term outcome inabove mechanisms for ischemia, 3 treatment strategies have the above patients, too few subjects refractory to medication Downloaded from http://circ.ahajournals.org/ by guest on July 13, 2011
  7. 7. Möhlenkamp et al Update on Myocardial Bridging 2621have thus far been treated with coronary stents and the rate of 9. Lee SS, Wu TL. The role of the mural coronary artery in prevention ofrestenosis has been too high to generally recommend this coronary atherosclerosis. Arch Pathol. 1972;93:32–35. 10. Penther P, Blanc JJ, Boschat J, et al. L’artère interventriculaire antérieureapproach in symptomatic patients. intramurale: étude anatomique. Arch Mal Coeur. 1977;70:1075–1079. 11. Risse M, Weiler G. Die koronare Muskelbrücke und ihre Beziehung zu Prognosis lokaler Koronarsklerose, regionaler Myokardischämie und Koronarspasmus.Long-term prognosis in patients with isolated myocardial bridg- Eine morphometrische Studie. Z Kardiol. 1985;74:700–705.ing is generally good. Five-year survival in 81 subjects aged 46 12. Ferreira AG Jr, Trotter SE, König B, et al. Myocardial bridges: morpho-years was 97.5%, with neither of the 2 deaths related to the logical and functional aspects. Br Heart J. 1991;66:364 –367. 13. Baptisda CAC, DiDio LJA. The relationship between the directions ofmyocardial bridge.21 In another group of 61 patients aged 50 myocardial bridges and the branches of the coronary arteries in the humanyears with bridging of the LAD, 11-year survival was 98%, heart. Surg Radiol Anat. 1992;14:137–140.again with no deaths attributable to myocardial bridging.27 In 14. Ortale JR, Gabriel EA, Lost C, et al. The anatomy of the coronary sinus and its tributaries. Surg Radiol Anat. 2001;23:15–21.these studies, none of the patients with otherwise normal 15. Kosinski A, Grzybiak M. Myocardial bridges in the human heart: mor-coronary arteries sustained a myocardial infarction during phological aspects. Folia Morphologica. 2001;60:65– 68.follow-up. Among 21 patients monitored for 3.4 years,28 two 16. Binet JP, Guiraudon G, Langlois J, et al. Angine de poitrine et pontspatients with coexistent CAD experienced a myocardial infarc- musculaires sur l’artère interventriculaire anterieure: a propos trois cas opérés. Arch Mal Cœur. 1978;71:251–258.tion and underwent CABG. All other patients, including 7 with 17. Ishimori T. Myocardial bridges: a new horizon in the evaluation ofHOCM and 8 with normal coronaries remained event-free.28 In ischemic heart disease. Cath Cardiovasc Diagn. 1980;6:355–357.a recent 43-month follow-up study, one of the 35 patients died, 18. Greenspan M, Iskandrian AS, Catherwood E, et al. Myocardial bridging of the LAD: evaluation using exercise thallium-201 myocardial scintig-20% of patients continued to have CCS class I-II angina, and raphy. Cathet Cardiovasc Diagn. 1980;6:173–180.63% of subjects required medication at the end of follow-up.85 In 19. Rossi L, Dander B, Nidasio GP, et al. Myocardial bridges and ischemicchildren with HOCM, myocardial bridging was suggested to be heart disease. 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Arch Inst Cardiol Méx. 1983;53:413–420.enhanced our understanding of the pathophysiological mech- 23. Wymore P, Yedlicka JW, Garcia-Medina V, et al. The incidence ofanisms involved in these complications. Myocardial bridging myocardial bridges in heart transplants. Cardiovasc Intervent Radiol.must be considered especially in patients at low risk for 1989;12:202–206. 24. Somanath HS, Reddy KN, Gupta SK, et al. Myocardial bridge: an angio-coronary atherosclerosis but with angina-like chest pain or graphic curiosity? Indian Heart J. 1989;41:296 –300.established myocardial ischemia. However, the low rate of 25. Gallet B, Adams C, Saudemont JP, et al. Pont myocardique de l’artèreclinical manifestation and the large variability of morpholog- interventriculaire anterieure et infarctus du myocarde. Le spasme coronarie a-t-il un rôle? Arch Mal Cœur. 1991;84:517–523.ical, functional, and clinical presentations precludes sound 26. Diefenbach C, Erbel R, Treese N, et al. 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