Update on myocardial bridging circulation 2002

Stefan Möhlenkamp, Waldemar Hort, Junbo Ge and Raimund ErbelUpdate on Myocardial Bridging

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Update on Myocardial BridgingStefan Möhlenkamp, MD; Waldemar Hort, MD; Junbo Ge, MD; Raimund Erbel, MD

Muscle overlying the intramyocardial segment of anepicardial coronary artery, first mentioned by Reyman1

in 1737, is termed a myocardial bridge, and the arterycoursing within the myocardium is called a tunneled artery(Figure 1). It is characterized by systolic compression of thetunneled segment, which remains clinically silent in the vastmajority of cases. An in-depth analysis of autopsy sampleswas first presented by Geiringer et al2 in 1951, but clinicalinterest and systematic research was triggered by an observedassociation of myocardial bridging with myocardialischemia.2–5

New imaging techniques have led to improved identifica-tion and functional quantitation of myocardial bridging invivo, which is crucial for establishing a link between systoliccompression and the clinical presentation, and hence forcommencing appropriate therapy. In the present article, wesummarize clinically relevant aspects of myocardial bridgingwith an emphasis on morphological and hemodynamic alter-ations and their representation in imaging techniques.

PrevalenceThe prevalence varies substantially among studies with amuch higher rate at autopsy versus angiography (Table).2,4–28

Variation at autopsy may in part be attributable to the caretaken at preparation and the selection of hearts. Pola´cek, whoincluded myocardial loops, reports the highest rate withbridges or loops in 86% of cases.29 On average, myocardialbridges are present in about one third of adults.

The rate of angiographic bridging is�5%, attributable tothin bridges causing little compression. In subjects withangiographically normal coronary arteries, the use of provo-cation tests may enhance systolic myocardial compressionand thereby reveal myocardial bridges in�40% of cases.26,30

A high prevalence has also been reported in heart trans-plant recipients23 and in patients with hypertrophic obstruc-tive cardiomyopathy (HOCM).31 In the latter, more rigorouscontraction may unmask otherwise undetectable bridges.Myocardial bridging may be found at multiple sites inHOCM,32 but also in patients without.33 De novo, previouslynonexistent myocardial bridging has been suggested for bothtransplanted hearts34 and HOCM,35 but conclusive proof islacking.36

Comparative AnatomyAn epicardial course of coronary arteries is not obligatory inmammals. In rodents and lagomorpha, the major vessels areembedded in myocardium beneath the epicardial surface(Type I).5,29 Animals with a predominantly epicardial courseof coronary arteries (Type II) include small ruminants,carnivores, and primates.29,37 Whereas the major coronaryarteries in the gorilla form an epicardial network, they tend totake a mural course in the chimpanzee.36 In goats and sheep,bridges are more frequent than in humans.8 They can also beobserved in canines, felines, and seals.37 In some mammalsthey are missing or extremely rare, such as in horses and pigs(Type III).29 Myocardial bridges are congenital in origin38–40

and likely reflect an evolutionary remnant in the genetic code.

MorphologyMyocardial bridges are most commonly localized in themiddle segment of the left anterior descending coronaryartery (LAD).29 In the presence of two parallel LADbranches, one frequently takes an intramural course.2 Diago-nal and marginal branches may be involved in 18% and 40%of cases, respectively.8,36 Angiographically, myocardialbridges are almost exclusively spotted in the LAD. They arelocated at a depth of 1 to 10 mm10,41 with a typical length of�10 to 30 mm.5 Deformation is predominantly eccentric,5 asconfirmed by intravascular ultrasound (IVUS)–based stud-ies.42 Occasionally, the arteries may take a very deep coursethrough the septum approaching the right ventricular suben-docardium36 (Figure 2).

Ferreira et al12 distinguished between two types of bridg-ing: (1) superficial bridges (75% of cases) crossing the arteryperpendicularly or at an acute angle toward the apex, and (2)muscle bundles arising from the right ventricular apicaltrabeculae (25% of cases) that cross the LAD transversely,obliquely, or helically before terminating in the interventric-ular septum. Arterial segments may also be located in a deepinterventricular gorge. Such “incomplete” bridges may ap-pear during adulthood in concomitant disease,2 in which asegment is compressed during systole although its surface isnot fully covered by myocardial fibers, but by a thin layer ofconnective tissue, nerves, and fatty tissue.36

Myocardial loops derive from atrial myocardium, surroundthe 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 [email protected]

(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

Mini-Review: Current Perspective



atrial myocardium.8 They are usually thinner compared withLAD bridges (0.1 to 0.3 mm) and have a width of 10 to15 mm (range 2 to 30 mm). Occasionally, a bridge mayinvolve a coronary vein.14 However, myocardial loops andvenous bridges appear to have no clinical relevance.

Presence and Absence of Atherosclerosis inRelation to Myocardial Bridging

Coronary atherosclerosis in association with myocardialbridging has primarily been studied in the LAD. Thesegment proximal to the bridge frequently shows athero-sclerotic plaque formation, although the tunneled segmentis typically spared5,8 (Figures 3 and 4). This is supportedby studies on a cellular and ultrastructural level43,44: Incontrast to proximal and distal segments, foam cells andmodified smooth muscle cells were missing in patients’tunneled segments.43 Extramural, epicardial segments incholesterol-fed rabbits developed intimal atherosclerosiswith accumulation of ApoB and proliferating cell nuclearantigens (PCNA) in smooth muscle cells of the intima.44

These changes were not seen in any arterial wall compo-nent in tunneled segments.44 Furthermore, endothelial cellpermeability was increased both in atherosclerotic andnonatherosclerotic portions of epicardial segments in high-cholesterol rabbits but not in tunneled segments or innormal control arteries.44

Figure 1. Typical systolic compression (arrows) of the mid LADat two sites in series. Diastolic lumen dimensions are normal.The coronary tree shows no angiographic signs of coronaryatherosclerosis.

Prevalence of Myocardial Bridging at Autopsy and Angiography

Author (Reference No.)SampleSize, n

WithBridges, % Comment

Autopsy

Geiringer2 100 23 LAD

Edwards et al6 276 5 All coronaries, 87% in the LAD

Polacek7 70 86 Including RCA loops, LAD: 60%

Giampalmo et al8 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%

Greenspan et al18 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

Angelini et al5 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

Gallet et al25 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

Harikrishnan et al28 3200 0.6 All patients

Möhlenkamp et al Update on Myocardial Bridging 2617



Mechanisms for Atherosclerosis in theSegment Proximal to the Bridge

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.45

Thus, 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 fissuringwith subsequent thrombus formation in the proximal seg-ment,47,48 which is supported by autopsy and clinicalobservations.11,41,49

Mechanisms for IschemiaNeither nonsignificant stenosis proximal to the bridge norsystolic compression of the tunneled segment alone cansufficiently explain severe ischemia and associated symp-toms. Experimental LCX occlusion, initially during systoleonly and then during continuing occlusion extending increas-ingly into diastole, resulted in distinct shortening of inflowtime with significant reduction of epicardial flow, subendo-cardial flow, and distal coronary pressure.50,51 After releasingthe occlusion, diastolic flow increased in correspondencewith an increasing duration of vessel occlusion, despite adecrease in mean flow.51 This increased diastolic/systolicflow ratio was later verified in patients.42 Consistent withclinical findings,42,48 the increase in diastolic flow could notfully compensate for the decrease in mean flow resulting inreduced coronary flow reserve, which could not be explainedby impaired vasodilatory capacity of resistance vessel.51

When arterial occlusion was limited to systole, phasiccoronary blood flow and distal coronary pressure was ob-served to resume with considerable delay contributing toreduced myocardial oxygen consumption and increased cor-onary sinus lactate concentration.52 This delayed diastolicrelaxation was later identified in humans as an importantmechanism contributing to ischemia with frame-by-frameanalysis of IVUS images.53,54

With the use of simultaneous proximal and distal pressurerecordings, Ge et al47 identified the highest intravascularpressure just proximal to the bridge and a pressure gradientacross the bridge. A distinct negative pressure in late diastolewas preceded by a pressure peak beneath the bridge.42,47

Klues et al42 observed the highest systolic pressure within thetunneled segment but found no pressure gradient acrossthe bridge. All their patients had significant tortuosity of thetunneled segment at the entry and exit sites. The centralpressure chamber was interpreted as a result of heterogeneouscompression of the tunneled segment with higher proximaland distal forces compared with the central portion, poten-tially contributing to reduced coronary flow reserve.42

The likelihood of ischemia also increases with the intramyo-cardial depth of the tunneled segment: In 22 of 39 hearts,

Figure 3. Histologic cross section showing (a) a tunneled seg-ment and (b) an epicardial branch of the LAD. The epicardialsegment shows intima thickening as a sign of early atheroscle-rosis but the tunneled segment does not.

Figure 2. Myocardial bridge of the LAD in consecutive 1 cmthick left ventricular slices with the use of post mortem coronaryangiography. (1) The tunneled segment runs in the interventricu-lar sulcus, giving off a large septal branch, (2) dives into theseptal myocardium approaching the right ventricular chamber,(3) passes along the right ventricular endocardium, and (4)returns to the interventricular sulcus. Reprinted from Figure 3.8of reference 36 with permission from Springer-Verlag GmbH &Co. Copyright 2000 Springer-Verlag GmbH & Co.

2618 Circulation November 12, 2002



myocardial fibrosis and contraction band necrosis were detect-able in myocardium distal to the bridge.55 Among these subjects,13 died suddenly and 6 during heavy exercise. These 13tunneled segments were significantly deeper in the myocardiumthan the ones from the victims who did not die suddenly.55

An increase in sympathetic drive during stress or exerciselikely facilitates ischemia, because tachycardia leads to anincrease of the systolic-diastolic time ratio at the expense ofdiastolic flow. Increased contractility during stress furtheraggravates systolic (and diastolic) compression.4 Endothelialdysfunction and coronary artery spasm may also contribute toconstriction of the tunneled segment.

Clinical PresentationAngina, myocardial ischemia, myocardial infarction, leftventricular dysfunction, myocardial stunning, paroxysmalAV blockade, as well as exercise-induced ventriculartachycardia and sudden cardiac death are accused sequelae ofmyocardial bridging.4,19,36,56–59 However, considering theprevalence of myocardial bridging, these complications arerare. Patients may present with atypical or angina-like chestpain with no consistent association between symptom sever-

ity and the length or depth of the tunneled segment or thedegree of systolic compression.12,20,60

Resting ECGs are frequently normal; stress testing mayinduce 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 ahigher rate of monomorphic ventricular tachycardia on HolterECG compared with subjects without myocardial bridges.39

Perfusion defects may be seen on myocardial scintigraphy61

but are not obligatory even in deep bridges with significantsystolic compression or after vasoactive stimulation.18,20

Coronary AngiographyThe current gold standard for diagnosing myocardial bridges iscoronary 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 signsprovide little information on the functional impact at the myo-cardial level. In the presence of a proximal stenosis, myocardialbridging may only be identifiable after PTCA when higherintravascular pressures and reversed hypokinesis unmask myo-cardial bridging.62 In patients with thin bridges, the milkingeffect may be missed and new imaging techniques and provo-cation tests may be required to detect a bridge.53,54,63,64

New Imaging TechniquesWith the use of IVUS, intracoronary Doppler ultrasound(ICD), and intracoronary pressure devices, morphologicaland functional features of myocardial bridging can be visu-alized and quantified.42,48,53,65 The “half-moon phenome-non” 42 is a characteristic IVUS observation, but its physiol-ogy and anatomy are not fully understood (Figure 5). It seemsspecific for the existence of myocardial bridging inasmuch asit is only found in tunneled segments but not in proximal ordistal segments or in other arteries. In the presence of ahalf-moon phenomenon on IVUS, milking can be provokedby intracoronary provocation tests, even if the bridge wasangiographically undetectable.26,42,66 IVUS-based frame-by-frame analysis of lumen area during the entire cardiac cyclecan also be used to quantify the delay in relaxation aftersystolic compression.53 Further, IVUS pullback studies sup-ported the absence of atherosclerosis within tunneled seg-ments, although �90% of patients showed plaque formation

Figure 4. Pathological specimen showing an opened coronary arterywith a thin myocardial bridge (arrows) and adjacent proximal and dis-tal epicardial segments. The proximal segment shows fatty lesions,whereas the tunneled segment is spared from atherosclerosis.

Figure 5. IVUS-images of the myocardial bridge during diastole(left) and systole (right). A “half-moon”–like area surrounding thetunneled segment is present during the entire cardiac cycle.Reprinted from reference 42 with permission from Elsevier Science.




proximal to the bridge.42 When deep tunneled segmentsapproach the right ventricular subendocardium, the trabecu-lated right chamber myocardium and the right ventricularcavity may be visible on IVUS.

In ICD studies, pullback of the Doppler-flow wire frequentlyreveals a characteristic flow pattern, the “fingertip phenome-non”42 or “spike-and-dome pattern.”65 This flow pattern hadpreviously been described in experimental studies51 and consistsof a sharp acceleration of flow in early diastole followed byimmediate marked deceleration and a mid-diastolic pressureplateau. It can frequently be observed within and just proximal tothe tunneled segment (Figure 6),42,48,65 and can be explained byan increased pressure gradient in early diastole as a result ofreduced distal coronary resistance and delayed relaxation of themyocardial fibers with continuing lumen compression and theensuing lumen gain.

Particularly in deep myocardial bridges, rapid diastolicforward flow may be preceded by end-systolic flow inversionas a result of a local increase in pressure above aortic drivingpressures (Figure 6).47,48 These changes result in an increaseddiastolic/systolic flow ratio of almost 3.0, compared withvalues of 1.8 and 1.3 in normal controls and significantcoronary artery stenosis, respectively.42,67 As in experimentalstudies,51 coronary flow reserves are frequently reduced tovalues below 3.0, which can be regarded as the lower limit ofthe norm in otherwise healthy individuals.42,48,68

Myocardial bridging can also be visualized with the use ofnovel noninvasive imaging techniques such as electron beamtomography (EBT, Figure 7) and, potentially, multislice CT(MSCT), magnetic resonance tomography (MRT), or trans-thoracic Doppler echocardiography. Whether these tools havea sensitivity and specificity high enough to advocate its usefor clinical or research purposes remains to be shown.

TherapyIn symptomatic patients, therapy may be initiated to improvequality of life, although hard evidence for a favorable effecton morbidity and mortality is missing. On the basis of theabove mechanisms for ischemia, 3 treatment strategies have

been explored: (1) negative inotropic and/or negative chro-notropic agents, ie, �-blockers69,70 and calcium antagonists71;(2) surgical myotomy and/or CABG16,30; and (3) stenting ofthe tunneled segment.48,72–74

Medication is considered first-line therapy. Intracoronaryadministration of a short-acting �-blocker attenuated vascularcompression and early diastolic blood velocity.70 The systol-ic/diastolic flow ratio was normalized and anginal symptomswere alleviated.70 Volume loading may also reduce compres-sion of the tunneled segment, whereas administration ofnitroglyceride may aggravate compression and ischemia.75

In subjects refractory to medication, surgical myotomy,first reported by Binet et al in 1975,3 abolishes clinicalsymptoms76–78 and is associated with reversal of local myo-cardial ischemia and an increase in coronary flow.79 Recently,minimally invasive myotomy was successfully performed.80

However, surgery should be limited to patients with severeangina and evidence for clinically relevant ischemia. Inbridges that take a deep subendocardial course, the rightventricle may accidentally be opened during surgery,30,81 anda case of aneurysm at the site of myocardial cleavage hasbeen reported.82 Thus, the risk associated with surgery shouldcarefully be weighed against the usually uneventful long-termcourse even in patients with substantial systolic compression.

In 1995, Stables et al72 first reported coronary stenting as aninterventional approach to severe myocardial bridging refractoryto medication. Normalization of the pathological coronary flowprofile, the reduced coronary flow reserve, and symptoms afterstent deployment promised successful use of stents in thesepatients.48 In 11 patients with signs of ischemia but absence ofother cardiac disorders, all patients had good angiographicoutcome with a marked improvement in the angina score after 6months and after 2 years of follow-up.74 However, at 7 weeks,46% of patients required revascularization as a result of in-stentrestenosis.74 To our knowledge, a total of 25 patients to datehave been reported to have received coronary stents for myo-cardial bridging. In 50% of these cases, restenosis or majorperiprocedural complications were reported, including perfora-tion of the artery.83,84 Despite a favorable long-term outcome inthe above patients, too few subjects refractory to medication

Figure 6. ICD-images of the myocardial bridge showing retro-grade flow during systole (double arrows) in the proximal seg-ment of the bridge after nitroglycerin provocation. A typical “fin-gertip” phenomenon can be visualized in diastole (single arrow).Scale in cm · s�1. Reprinted from reference 42 with permissionfrom Elsevier Science.

Figure 7. Noninvasive electron beam CT coronary angiographydepicting a brief tunneled segment in mid LAD in a patient with nocoronary calcification and angiographically normal coronary arteries.




have thus far been treated with coronary stents and the rate ofrestenosis has been too high to generally recommend thisapproach in symptomatic patients.

PrognosisLong-term prognosis in patients with isolated myocardial bridg-ing is generally good. Five-year survival in 81 subjects aged 46years was 97.5%, with neither of the 2 deaths related to themyocardial bridge.21 In another group of 61 patients aged 50years with bridging of the LAD, 11-year survival was 98%,again with no deaths attributable to myocardial bridging.27 Inthese studies, none of the patients with otherwise normalcoronary arteries sustained a myocardial infarction duringfollow-up. Among 21 patients monitored for 3.4 years,28 twopatients with coexistent CAD experienced a myocardial infarc-tion and underwent CABG. All other patients, including 7 withHOCM and 8 with normal coronaries remained event-free.28 Ina recent 43-month follow-up study, one of the 35 patients died,20% of patients continued to have CCS class I-II angina, and63% of subjects required medication at the end of follow-up.85 Inchildren with HOCM, myocardial bridging was suggested to bea highly significant independent predictor for 5-year mortali-ty,38,39 but these findings were disputed by others.40

Clinical RelevanceMyocardial bridging can occasionally generate clinicallyimportant complications, despite usually being a benigncondition. A considerable number of studies and reports haveenhanced our understanding of the pathophysiological mech-anisms involved in these complications. Myocardial bridgingmust be considered especially in patients at low risk forcoronary atherosclerosis but with angina-like chest pain orestablished myocardial ischemia. However, the low rate ofclinical manifestation and the large variability of morpholog-ical, functional, and clinical presentations precludes soundrecommendations for diagnosis and therapy on the basis ofcurrently available reports, which are mostly on a limitednumber of patients. We agree with others86 that large multi-center clinical databases are required to identify criteria thatjustify the link between clinical signs or symptoms and themyocardial bridge as the primary culprit and which movebeyond the current empirical approach to the clinical man-agement of this frequent coronary anomaly.

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KEY WORDS: myocardial bridging � anatomy � tunneled artery � arteries




Update on myocardial bridging circulation 2002

Health & Medicine

Transcript of Update on myocardial bridging circulation 2002