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A. Barioli et al.
not be detected with the latter method. In turn,
the hemodynamic signicance of MBs depends
upon several factors, including the length of the
bridged segment, the thickness of the myocardium overlying the tunneled artery, the nature
and characteristics of the tissue surrounding the
vessel, the orientation between myocardial bers
and the coronary artery, the presence of a coronary stenosis proximal to the MB, and observer
experience [14].
Anatomy
The left anterior descending (LAD) artery is the
most common coronary artery affected by MBs,
although bridging can be found less frequently in
the other major epicardial coronary arteries.
Eventually, diagonal and marginal branches may
be involved in 18% and 40% of cases, respectively [1, 15].
LAD-MBs may signicantly vary in depth
(1–10 mm) and length of encasement (10–
30 mm) [16]. These characteristics, along with
the degree of systolic diameter reduction and secondary branches involvement, are key elements
for the evaluation of the hemodynamic signicance of MBs.Ferreira etal. proposed a classication of LAD-MBs into two subtypes, according
to the depth of embedment of the coronary artery:
a more common supercial bridge (75% of
cases), in which the myocardial bers cross the
artery transversely towards the apex of the heart
at an acute angle or perpendicularly; and a deep
variant (25% of cases), in which the LAD deviates towards the right ventricle and deepens into
the interventricular septum, where it is crossed
transversely, obliquely or helically by a muscle
bundle arising from the apex of the right ventricle
[17]. While the supercial variant rarely results
in systolic compression of the artery, the deep
variant is supposed to cause myocardial ischemia
due to the distortion and twisting of the bridged
segment induced by the overlying muscle bundle,
resulting in impaired coronary blood ow.
Pathophysiology
The physiology of MBs is substantially different
both from that of xed defects and from the
dynamic phenomenon of coronary vasospasm.
Therefore, in the last decades, numerous studies
have been carried out to understand the mechanism by which the presence of a MB can cause
myocardial ischemia.
It is known that myocardial perfusion occurs
mainly during the diastolic phase of the cardiac
cycle. How the presence of a MB should impair
diastolic coronary blood ow, since extravascular
compression of the tunneled artery occurs during
systole? It has been shown that the systolic narrowing of the bridged segment can extend into
the early diastolic phase, resulting in the socalled “spillover” phenomenon [18]. In general,
the more severe the systolic compression, the
more likely the luminal area will be compromised in the early and even mid-diastole, where a
persistent reduction of 34–51% in the bridged
segment has been observed [19]. This phenomenon is further exacerbated by an increased heart
rate, which causes a reduction of the diastolic
perfusion time and an increase in epicardial coronary vasoconstriction and contraction of the MB
[20, 21]. The resulting reduction in diastolic coronary blood ow may cause subendocardial ischemia downstream of severe arterial bridge
compression, as the shortened diastolic perfusion
time may exacerbate the normal time delay in
early diastolic subendocardial hyperemia compared to the subepicardial layers. More often,
MBs can trigger septal ischemia by the “branch
steal” mechanism, whereby increased ow velocity in the compressed artery results in depressurization of septal branches within the MB [22].
MBs are thought to be protective against the
formation of atherosclerotic plaques within the
bridged segment. As a matter of fact, it has been
postulated that the characteristics of the intima of
the tunneled segment, which contains a predominance of the contractile subtype of smooth muscle cells, the separation of the bridged segment
from epicardial perivascular adipose tissue and
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the absence of foam cells may play a role in this
anti-atherosclerotic effect [23–25]. On the other
hand, MBs are associated with up to 90%
increased atherogenesis at the vessel segment
proximal to the bridge [26]. This could be
explained by the fact that systolic compression of
the tunneled artery results in retrograde ow in
the segment proximal to MB entrance, causing
disturbance in systolic wall shear stress that has
been linked to coronary plaques formation at this
site [27, 28]. In addition, the altered hemodynamic pattern at the level of the MB has also been
associated with other potential complications,
including plaque vulnerability/thrombosis [27],
increase in vasospasticity [29], and intimal injury
possibly leading to dissection [30].
Clinical Presentation
Most MBs are clinically silent and usually represent an incidental nding on angiography, CCT,
or autopsy. Patients with MB may present with
stable symptomatic or silent myocardial ischemia, as well as with acute coronary syndromes.
Other reported clinical presentations are coronary spasm, myocardial stunning, transient ventricular dysfunction, stress cardiomyopathy,
syncope, exercise-induced dysrhythmias like
supraventricular tachycardia, atrioventricular
conduction block, and life-threatening ventricular arrhythmias possibly leading to sudden death
[1–5, 10, 31, 32]. Previously silent MBs may
become symptomatic over time.
Pathophysiological factors that may reveal or
exacerbate symptoms are age, heart rate, left ventricular hypertrophy, and coronary atherosclerosis [33].
Diagnosis
Morphological Assessment
CCT is a prime important, non-invasive tool in
the diagnosis of MBs, being reported superior to
coronary angiography in terms of detection rates
[1]. CCT provides three-dimensional images
with high spatial and contrast resolution, allowing identication of morphological features of
MBs, including the length and the degree of
encasement of the bridged artery, as well as the
length and thickness of the MB over the tunneled
segment [34, 35] (Fig. 4.1). The technique also
allows the classication of the vessel intramyocardial course in supercial or deep. Recently,
the use of new post-processing algorithms for the
derivation of functional information from the
anatomic assessment provided by CCT, such as
transluminal attenuation gradient and CCT-based
fractional ow reserve (FFR), has brought
encouraging, albeit initial, results [36–39].
as a systolic compression, or milking, of the tunneled artery, that reverses during diastole. A systolic narrowing is dened as a ≥50% systolic
diameter stenosis not present or less evident during diastole, and can be enhanced by intracoronary administration of nitroglycerine [40, 41]. To
note, the severity of systolic compression at angiography does not always correlate with the functional relevance of MBs [42]. In addition to
coronary milking, a MB can be suspected when a
characteristic “step-down” and “step-up” morphology, also known as the “U” sign, of the intramural course of the LAD is observed [40].
Several angiographic views, including the lateral
projection, are usually obtained to better visualize and characterize the vessel course (Fig.4.2)
(Videos 4.1 and 4.2).
thickness, and location of the MB, IVUS assessment can be an adjunctive valuable tool to
increase the detection rate of this coronary
anomaly. Imaging with IVUS may display the
reduced vessel area within the MB segment, the
loss of the circular morphology of the artery
under the compression of the bridge, as well as
the characteristic, hypoechogenic “half-moon”
sign over the bridged segment [43] (Fig. 4.3)
(Video 4.3). Although the etiology of this last
phenomenon is still a matter of debate, it appears
to be highly specic as it can only be found in
the bridged segment and not in adjacent reference segments or other coronary arteries [26].
Lastly, IVUS examination can provide useful
With coronary angiography, the MB appears
Given its ability to characterize the length,
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Fig. 4.1 Volume rendering 3D image showing myocardial bridging of the LAD. The intramyocardial course
involves the middle third of the vessel and shows overly-
information on the presence, severity, and distribution of subangiographic atherosclerosis [43],
in order to guide treatment (e.g. appropriate stent
selection and placement). Other intravascular
imaging techniques, such as optical coherence
tomography (OCT), may theoretically improve
the characterization of the vessel wall within the
bridged segment, but existing evidence is still
scarce [44, 45].
Functional Assessment
An appropriate diagnostic workup of MBs should
include the hemodynamic assessment of the
bridged coronary artery. As previously mentioned, physiology of MBs is rather different to
that of xed lesions. Because the dynamic stenoses in the context of MBs are dependent on extravascular compression and intramyocardial
tension, their functional assessment should not
ing myocardial tissue. Therefore, the MB can be addressed
as deep. LAD left anterior descending artery. MB myocardial bridge
be limited to resting conditions and thus should
include chronotropic and inotropic stimulation.
Also, during systole, the vascular compression
causes distal pressure overshooting due to milking of blood against a highly restrictive circulation. This translates into higher intracoronary
over aortic pressures distal to the MB, or, in other
words, in negative pressure systolic gradients
across the MB [46] (Fig. 4.4). Distal pressure
overshooting and systolic pressure gradient
inversion may lead to an underestimation of the
functional impact of the MB when assessed with
conventional FFR, this being an average of systolic and diastolic gradients. In view of these considerations, the use of diastolic-FFR during
dobutamine challenge or after intracoronary adenosine administration has been shown to be a better alternative approach to test MB functional
signicance [42]. However, the acquisition of
diastolic rather than mean FFR is complex and
more vulnerable to measurement errors, and
ab
cd
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Fig. 4.2 Angiographic appearance of a LAD-MB in a
patient with hypertrophic cardiomyopathy, both in diastole (a and c) and systole (b and d). The lateral projection
therefore is not routinely performed in most cardiac laboratories [47].
More recently, the introduction of a lesionspecic, non-hyperemic diastolic index, the
instantaneous wave-free ratio (iFR®, Volcano
corporation, San Diego, Ca, USA), has shed
new light on functional assessment of MBs.
This index measures the translesional pressure
enhances the step-down (top arrow) and step-up (bottom
arrow) of the bridged LAD (c and d). LAD left anterior
descending artery. MB myocardial bridge
gradient in a specic phase of the cardiac diastole (the wave-free period), in which coronary
ow is maximal and microcirculatory resistances are low and stable. As such, it might not
be hampered by systolic pressure overshooting
and negative systolic pressure gradient caused
by extravascular compression of the tunneled
artery. Moreover, iFR allows anatomic mapping
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A. Barioli et al.
Fig. 4.3 IVUS imaging of a LAD-MB during diastole (a)
and systole (b). An hypoechogenic “half-moon” image
surrounding the bridge is present during the entire cardiac
Fig. 4.4 Intracoronary
pressure tracings at
baseline and during
inotropic challenge in
MB.Pressure
overshooting during
dobutamine challenge
occurs because of
systolic milking of blood
distal to the MB, causing
higher intracoronary
(Pd– blue tracing) over
aortic (Pa– red tracing)
pressures. MB
myocardial bridge
of the vessel by guidewire pullback (iFR Scout),
providing information on the ischemic contribution of the MB [48]. iFR has been shown to have
greater correlation to patients’ symptoms or
presence of myocardial ischemia than FFR.In a
series of 20 patients with angina, no signicant
coronary artery disease (CAD), silent ischemia
conrmed by non-invasive stress test, and angiographic or CCT evidence of MB, iFR at rest
was abnormal in 65% of cases (with a clear
step-up across the MB at iFR pullback), whereas
FFR at rest was negative in all patients. In addi-
cycle (arrows). IVUS: intravascular ultrasound. LAD: left
anterior descending artery. MB: myocardial bridge
tion, after inotropic stimulus by intravenous
dobutamine infusion, iFR dropped in all cases,
while conventional FFR did not signicantly
change. The discrepancy between FFR and iFR
correlated with the reduction or negativization
of the systolic pressure gradient both at rest and
after dobutamine challenge, further supporting
the hypothesis that systolic pressure gradient
inversion observed in signicant MBs can
invariably affect FFR measurements [49]. A
typical clinical example of LAD-MB functional
evaluation is shown in Fig.4.5.
eg
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a
b
c
d
f
h
Fig. 4.5 Morphological and functional assessment of a
patient with LAD-MB. (a and b) Diastolic and systolic
angiographic appearance of the MB at resting conditions
and (c and d) after dobutamine administration (20μ/kg/
min). Hemodynamic assessment shows near-cutoff values
for both FFR (e) and iFR (f) in basal conditions. FFR values increase during dobutamine infusion (g). Conversely,
iFR measurements become more positive after dobutamine challenge (h). Red and yellow tracings indicate
proximal (Pa) and distal (Pd) pressures, respectively. LAD
left anterior descending artery, MB myocardial bridge,
FFR fractional ow reserve, iFR instantaneous wave-free
ratio
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The use of Doppler-tipped guidewires to
assess intracoronary ow velocity and coronary
ow reserve is by far a less diffuse tool to evaluate MB functional signicance. The analysis of
ow velocity in vessels with MB revealed a systolic ow reversal proximal to the bridged segment and a characteristic “spike and dome”
pattern or “ngertip phenomenon”, due to abrupt
early diastolic ow acceleration, rapid middiastolic ow deceleration and mid to late diastolic plateau [26, 50]. An impaired coronary
ow reserve has been observed when measured
distal to the MB [19].
Among functional non-invasive imaging tests,
stress echocardiography, stress cardiac magnetic
resonance, single-photon emission-computed
tomography and positron emission tomography
are the most widely used [51]. As already mentioned, transluminal attenuation gradient and
CCT-derived FFR are emerging as new postprocessing techniques to derive functional information from CCT [36–39].
Treatment
Medical Therapy
The treatment of MBs should be reserved only
for patients with symptoms and/or objective
signs of ischemia, and should focus on relieving
potential triggers and hemodynamic disturbances
that aggravate the MB, such as hypertension/
hypertrophy, increased heart rate, reduced diastolic coronary lling period, and inappropriate
compression of the artery. Although evidence is
limited, symptomatic patients seem to respond
well to pharmacological treatment with betablockers or non-dihydropyridine calciumchannel blockers (CCB), which are therefore
considered as rst-line therapy [52–54]. By
reducing heart rate and myocardial contractility,
beta-blockers have been shown to restore baseline pressure tracings in patients with signicant
overshooting induced by inotropic challenge,
providing evidence of treatment efcacy [42, 49,
52]. Given the similar hemodynamic effect of
beta-blockers and the additional benet in reduc-
ing concomitant vasospasm, CCB can be used as
an alternative to beta-blockers when they are not
tolerated or contraindicated [54]. Pure vasodilators, such as nitrates, are contraindicated in
patients with functional signicant MBs, as they
may exacerbate symptoms by augmentation of
the systolic narrowing and increase in vessel wall
compliance [41]. Ivabradine, which acts by slowing the heart rate and thereby prolonging the diastolic period, may be considered as a second-line
therapy for patients who cannot tolerate betablockers or CCB, or in combination with lower
doses of these drugs [10]. Patients with concomitant atherosclerotic disease may benet from
aggressive risk factor modication and treatment
with antiplatelet and statin therapy.
Percutaneous Coronary Intervention
No randomized studies between optimal medical
treatment and medical therapy plus percutaneous
coronary intervention (PCI) in patients with MB
have been reported so far. Nevertheless, percutaneous stent implantation may be considered in
selected patients refractory to maximal medical
therapy. Although some initial experiences had
shown an improvement in hemodynamic abnormalities and symptoms [50, 55], further studies
have raised concerns by reporting higher rates of
target lesion revascularization after PCI of the
bridged segments [56]. In addition, stent implantation in MBs has been associated with higher
rates of complications, including coronary perforation [57], stent fracture [58, 59], in-stent restenosis [56], and stent thrombosis [60]. An elegant
study using IVUS reported increased rates of late
events after stenting of the LAD when the stent
extended unintentionally into the MB, compared
to patients who underwent stent implantation
only in the epicardial obstructive lesion [61].
Given these unfavorable outcomes, revascularization using drug-eluting stents should be considered only for severely symptomatic patients
who are refractory to optimal medical therapy
and who are not amenable for surgery.
Bioresorbable scaffolds, when implanted in MBs,
have recently been shown to be superior to
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everolimus- eluting stents in terms of angiographic late loss and tissue proliferation, suggesting a potential benet of vascular restoration in
this setting [62].
Surgery
Surgical options for MBs include supra-arterial
myotomy (i.e. surgical unroong of the bridged
LAD) and coronary artery bypass grafting
(CABG). Isolated supra-arterial myotomy can be
performed in the absence of severe atherosclerotic disease, and involves dissection of the myocardial bers overlying the bridged segment with
complete exposure of the coronary artery [63–
65]. This procedure is not without risk, and may
result in wall perforation, ventricular aneurism
formation, and post-operative bleeding [64]. In
this regard, intraoperative high-frequency epicardial echocardiography may help to identify the
course of the vessel thereby reducing the risk of
complications [66]. CABG has been shown to be
superior to myotomy in cases of extensive
(>25mm) or deep (>5mm) MBs, and might be a
better option for patients with signicant atherosclerotic disease proximal to the MB [67, 68].
However, graft failure rates have been reported to
be high due to potential competitive ow [69].
Surgical treatment should be considered for
patients with persistent symptoms despite optimal medical therapy and with proven inducible
ischemia, especially for those who have experienced myocardial infarction, life-threatening
arrhythmias, and resuscitated cardiac arrest. A
recent meta-analysis of 18 studies comparing different therapeutic strategies for patients with MB
showed that, among invasively treated patients,
surgery was superior to percutaneous treatment
in terms of symptoms relief and major cardiovascular events related to target vessel revascularization [70].
References
1. Möhlenkamp S, Hort W, Ge J, Erbel R. Update on
myocardial bridging. Circulation. 2002;106:2616–22.
2. Migliore F, Maffei E, Perazzolo Marra M, Bilato C,
Napodano M, Corbetti F, Zorzi A, Andres AL, Sarais
C, Cacciavillani L, Favaretto E, Martini C, Seitun
S, Cademartiri F, Corrado D, Iliceto S, Tarantini
G.LAD coronary artery myocardial bridging and apical ballooning syndrome. JACC Cardiovasc Imaging.
6:32–41.
3. Migliore F, Zorzi A, Marra MP, Basso C, Corbetti
F, De Lazzari M, Tarantini G, Buja P, Lacognata C,
Thiene G, Corrado D, Iliceto S. Myocardial edema
underlies dynamic T-wave inversion (Wellens' ECG
pattern) in patients with reversible left ventricular
dysfunction. Heart Rhythm. 2011;8:1629–34.
4. Feld H, Guadanino V, Hollander G, Greengart A,
Lichstein E, Shani J. Exercise-induced ventricular
tachycardia in association with a myocardial bridge.
Chest. 1991;99:1295–6.
5. Desseigne P, Tabib A, Loire R.Pont myocardique Sur
l'interventriculaire antérieure et mort subite. A propos
de 19 cas autopsiés [myocardial bridging on the left
anterior descending coronary artery and sudden death.
Apropos of 19 cases with autopsy]. Arch Mal Coeur
Vaiss. 1991;84:511–6.
6. Rossi L, Dander B, Nidasio GP, Arbustini E, Paris
B, Vassanelli C, Buonanno C, Poppi A.Myocardial
bridges and ischemic heart disease. Eur Heart J.
1980;1:239–45.
7. Hostiuc S, Negoi I, Rusu MC, Hostiuc M.Myocardial
bridging: a meta-analysis of prevalence. J Forensic
Sci. 2018;63:1176–85.
8. La Grutta L, Runza G, Lo Re G, Galia M, Alaimo V,
Grassedonio E, Bartolotta TV, Malagò R, Tedeschi C,
Cademartiri F, De Maria M, Cardinale AE, Lagalla
R, Midiri M.Prevalence of myocardial bridging and
correlation with coronary atherosclerosis studied
with 64-slice CT coronary angiography. Radiol Med.
2009;114:1024–36.
9. Hwang JH, Ko SM, Roh HG, Song MG, Shin JK,
Chee HK, Kim JS. Myocardial bridging of the left
anterior descending coronary artery: depiction rate
and morphologic features by dual-source CT coronary angiography. Korean J Radiol. 2010;11:514–21.
10. Tarantini G, Migliore F, Cademartiri F, Fraccaro C,
Iliceto S.Left anterior descending artery myocardial
bridging: a clinical approach. J Am Coll Cardiol.
2016;68:2887–99.
11. Tsujita K, Maehara A, Mintz GS, Doi H, Kubo
T, Castellanos C, Liu J, Yang J, Oviedo C,
Franklin- Bond T, Dasgupta N, Biro S, Dani L,
Dangas GD, Mehran R, Kirtane AJ, Lansky AJ,
Kreps EM, Collins MB, Stone GW, Moses JW, Leon
MB. Comparison of angiographic and intravascular ultrasonic detection of myocardial bridging of
the left anterior descending coronary artery. Am J
Cardiol. 2008;102:1608–13.
12. Sorajja P, Ommen SR, Nishimura RA, Gersh BJ,
Tajik AJ, Holmes DR. Myocardial bridging in adult
patients with hypertrophic cardiomyopathy. J Am
Coll Cardiol. 2003;42:889–94.
13. Wymore P, Yedlicka JW, Garcia-Medina V, Olivari
MT, Hunter DW, Castañeda-Zúñiga WR, Amplatz
K.The incidence of myocardial bridges in heart transplants. Cardiovasc Intervent Radiol. 1989;12:202–6.
54
https://t.me/medicina_free
A. Barioli et al.
14. Alegria JR, Herrmann J, Holmes DR Jr, Lerman
A, Rihal CS. Myocardial bridging. Eur Heart J.
2005;26:1159–68.
15. Polacek P, Kralove H.Relation of myocardial bridges
and loops on the coronary arteries to coronary occlusions. Am Heart J. 1961;61:44–52.
16. Angelini P, Trivellato M, Donis J, Leachman
RD. Myocardial bridges: a review. Prog Cardiovasc
Dis. 1983;26:75–88.
17. Ferreira AG Jr, Trotter SE, König B Jr, Décourt
LV, Fox K, Olsen EG. Myocardial bridges: morphological and functional aspects. Br Heart J.
1991;66:364–7.
18. Sivananthan M. Coronary anatomy. In: Vasan RS,
Sawyer DB, editors. Encyclopedia of Cardiovascular
Research and Medicine. Amsterdam: Elsevier; 2018.
19. Schwarz ER, Klues HG, vom Dahl J, Klein I, Krebs
W, Hanrath P.Functional characteristics of myocardial
bridging. A combined angiographic and intracoronary
Doppler ow study. Eur Heart J. 1997;18:434–42.
20. Bourassa MG, Butnaru A, Lespérance J, Tardif
JC. Symptomatic myocardial bridges: overview of
ischemic mechanisms and current diagnostic and treatment strategies. J Am Coll Cardiol. 2003;41:351–9.
21. Gould KL, Johnson NP.Imaging coronary blood ow
in AS: let the data talk, again. J Am Coll Cardiol.
2016;67:1423–6.
22. Lin S, Tremmel JA, Yamada R, Rogers IS, Yong CM,
Turcott R, McConnell MV, Dash R, Schnittger I.A
novel stress echocardiography pattern for myocardial
bridge with invasive structural and hemodynamic correlation. J Am Heart Assoc. 2013;2:e000097.
23. Risse M, Weiler G. Die koronare Muskelbrücke und
ihre Beziehungen zu lokaler Koronarsklerose, regionaler Myokardischämie und Koronarspasmus. Eine
morphometrische Studie [coronary muscle bridge and
its relations to local coronary sclerosis, regional myocardial ischemia and coronary spasm. A morphometric study]. Z Kardiol. 1985;74:700–5.
24. Verhagen SN, Rutten A, Meijs MF, Isgum I, Cramer
MJ, van der Graaf Y, Visseren FL. Relationship
between myocardial bridges and reduced coronary
atherosclerosis in patients with angina pectoris. Int J
Cardiol. 2013;167:883–8.
25. Ishii T, Asuwa N, Masuda S, Ishikawa Y.The effects
of a myocardial bridge on coronary atherosclerosis
and ischaemia. J Pathol. 1998;185:4–9.
26. Ge J, Jeremias A, Rupp A, Abels M, Baumgart D, Liu
F, Haude M, Görge G, von Birgelen C, Sack S, Erbel
R. New signs characteristic of myocardial bridging demonstrated by intracoronary ultrasound and
Doppler. Eur Heart J. 1999;20:1707–16.
27. Ishikawa Y, Akasaka Y, Suzuki K, Fujiwara M,
Ogawa T, Yamazaki K, Niino H, Tanaka M, Ogata
K, Morinaga S, Ebihara Y, Kawahara Y, Sugiura H,
Takimoto T, Komatsu A, Shinagawa T, Taki K, Satoh
H, Yamada K, Yanagida-Iida M, Shimokawa R,
Shimada K, Nishimura C, Ito K, Ishii T. Anatomic
properties of myocardial bridge predisposing to myocardial infarction. Circulation. 2009;120:376–83.
28. Uusitalo V, Saraste A, Pietilä M, Kajander S, Bax
JJ, Knuuti J. The functional effects of intramural
course of coronary arteries and its relation to coronary atherosclerosis. JACC Cardiovasc Imaging.
2015;8:697–704.
29. Kim JW, Park CG, Suh SY, Choi CU, Kim EJ, Rha
SW, Seo HS, Oh DJ.Comparison of frequency of coronary spasm in Korean patients with versus without
myocardial bridging. Am J Cardiol. 2007;100:1083–6.
30. Wu S, Liu W, Zhou Y. Spontaneous coronary artery
dissection in the presence of myocardial bridge causing myocardial infarction: an insight into mechanism.
Int J Cardiol. 2016;206:77–8.
31. den Dulk K, Brugada P, Braat S, Heddle B, Wellens
HJ. Myocardial bridging as a cause of paroxysmal atrioventricular block. J Am Coll Cardiol.
1983;1:965–9.
32. Ural E, Bildirici U, Celikyurt U, Kilic T, Sahin T, Acar
E, Kahraman G, Ural D.Long-term prognosis of noninterventionally followed patients with isolated myocardial bridge and severe systolic compression of the
left anterior descending coronary artery. Clin Cardiol.
2009;32:454–7.
33. Corban MT, Hung OY, Eshtehardi P, Rasoul-Arzrumly
E, McDaniel M, Mekonnen G, Timmins LH, Lutz J,
Guyton RA, Samady H. Myocardial bridging: contemporary understanding of pathophysiology with
implications for diagnostic and therapeutic strategies.
J Am Coll Cardiol. 2014;63:2346–55.
34. Konen E, Goitein O, Sternik L, Eshet Y, Shemesh J,
Di Segni E.The prevalence and anatomical patterns of
intramuscular coronary arteries: a coronary computed
tomography angiographic study. J Am Coll Cardiol.
2007;49:587–93.
35. Forsdahl SH, Rogers IS, Schnittger I, Tanaka S,
Kimura T, Pargaonkar VS, Chan FP, Fleischmann D,
Tremmel JA, Becker HC.Myocardial bridges on coronary computed tomography angiography- correlation
with intravascular ultrasound and fractional ow
reserve. Circ J. 2017;81:1894–900.
36. Stuijfzand WJ, Danad I, Raijmakers PG, Marcu
CB, Heymans MW, van Kuijk CC, van Rossum AC,
Nieman K, Min JK, Leipsic J, van Royen N, Knaapen
P.Additional value of transluminal attenuation gradient in CT angiography to predict hemodynamic significance of coronary artery stenosis. JACC Cardiovasc
Imaging. 2014;7:374–86.
37. Yoon YE, Choi JH, Kim JH, Park KW, Doh JH, Kim
YJ, Koo BK, Min JK, Erglis A, Gwon HC, Choe YH,
Choi DJ, Kim HS, Oh BH, Park YB. Noninvasive
diagnosis of ischemia-causing coronary stenosis
using CT angiography: diagnostic value of transluminal attenuation gradient and fractional ow reserve
computed from coronary CT angiography compared
to invasively measured fractional ow reserve. JACC
Cardiovasc Imaging. 2012;5:1088–96.
38. Zhou F, Wang YN, Schoepf UJ, Tesche C, Tang CX,
Zhou CS, Xu L, Hou Y, Zheng MW, Yan J, Lu MJ,
Lu GM, Zhang DM, Zhang B, Zhang JY, Zhang
LJ. Diagnostic performance of machine learning
4 Myocardial Bridge(s)
https://t.me/medicina_free
55
based CT-FFR in detecting ischemia in myocardial
bridging and concomitant proximal atherosclerotic
disease. Can J Cardiol. 2019;35:1523–33.
39. Koo HJ, Yang DH, Kim YH, Kang JW, Kang SJ,
Kweon J, Kim HJ, Lim TH. CT-based myocardial ischemia evaluation: quantitative angiography,
transluminal attenuation gradient, myocardial perfusion, and CT-derived fractional ow reserve. Int J
Cardiovasc Imaging. 2016;32(Suppl 1):1–19.
40. Juilliére Y, Berder V, Suty-Selton C, Buffet P, Danchin
N, Cherrier F.Isolated myocardial bridges with angiographic milking of the left anterior descending coronary artery: a long-term follow-up study. Am Heart J.
1995;129:663–5.
41. Hongo Y, Tada H, Ito K, Yasumura Y, Miyatake K,
Yamagishi M. Augmentation of vessel squeezing at
coronary-myocardial bridge by nitroglycerin: study
by quantitative coronary angiography and intravascular ultrasound. Am Heart J. 1999;138:345–50.
42. Escaned J, Cortés J, Flores A, Goicolea J, Alfonso
F, Hernández R, Fernández-Ortiz A, Sabaté M,
Bañuelos C, Macaya C.Importance of diastolic fractional ow reserve and dobutamine challenge in physiologic assessment of myocardial bridging. J Am Coll
Cardiol. 2003;42:226–33.
43. Ge J, Erbel R, Rupprecht HJ, Koch L, Kearney P,
Görge G, Haude M, Meyer J.Comparison of intravascular ultrasound and angiography in the assessment of
myocardial bridging. Circulation. 1994;89:1725–32.
44. Cao HM, Jiang JF, Deng B, Xu JH, Xu WJ.Evaluation
of myocardial bridges with optical coherence tomography. J Int Med Res. 2010;38:681–5.
45. Bose D, Philipp S.Images in clinical medicine. Highresolution imaging of myocardial bridging. N Engl J
Med. 2008;358:392.
46. Hakeem A, Cilingiroglu M, Leesar MA.
Hemodynamic and intravascular ultrasound assessment of myocardial bridging: fractional ow reserve
paradox with dobutamine versus adenosine. Catheter
Cardiovasc Interv. 2010;75:229–36.
47. Abe M, Tomiyama H, Yoshida H, Doba N.Diastolic
fractional ow reserve to assess the functional severity of moderate coronary artery stenoses: comparison
with fractional ow reserve and coronary ow velocity reserve. Circulation. 2000;102:2365–70.
48. Sen S, Asrress KN, Nijjer S, Petraco R, Malik IS,
Foale RA, Mikhail GW, Foin N, Broyd C, Hadjiloizou
N, Sethi A, Al-Bustami M, Hackett D, Khan MA,
Khawaja MZ, Baker CS, Bellamy M, Parker KH,
Hughes AD, Francis DP, Mayet J, Di Mario C,
Escaned J, Redwood S, Davies JE.Diagnostic classication of the instantaneous wave-free ratio is
equivalent to fractional ow reserve and is not
improved with adenosine administration. Results of
CLARIFY (Classication Accuracy of Pressure-Only
Ratios Against Indices Using Flow Study). J Am Coll
Cardiol. 2013;61:1409–20.
49. Tarantini G, Barioli A, Nai Fovino L, Fraccaro C,
Masiero G, Iliceto S, Napodano M. Unmasking
myocardial bridge-related ischemia by intracoro-
nary functional evaluation. Circ Cardiovasc Interv.
2018;11:e006247.
50. Klues HG, Schwarz ER, vom Dahl J, Reffelmann T,
Reul H, Potthast K, Schmitz C, Minartz J, Krebs W,
Hanrath P.Disturbed intracoronary hemodynamics in
myocardial bridging: early normalization by intracoronary stent placement. Circulation. 1997;96:2905–13.
51. Danad I, Szymonifka J, Twisk JWR, Norgaard BL,
Zarins CK, Knaapen P, Min JK. Diagnostic performance of cardiac imaging methods to diagnose
ischaemia-causing coronary artery disease when
directly compared with fractional ow reserve as
a reference standard: a meta-analysis. Eur Heart J.
2017;38:991–8.
52. Schwarz ER, Klues HG, vom Dahl J, Klein I, Krebs
W, Hanrath P. Functional, angiographic and intracoronary Doppler ow characteristics in symptomatic
patients with myocardial bridging: effect of shortterm intravenous beta-blocker medication. J Am Coll
Cardiol. 1996;27:1637–45.
53. Nair CK, Dang B, Heintz MH, Sketch MH.Myocardial
bridges: effect of propranolol on systolic compression. Can J Cardiol. 1986;2:218–21.
54. Alessandri N, Dei Giudici A, De Angelis S, Urciuoli
F, Garante MC, Di Matteo A. Efcacy of calcium
channel blockers in the treatment of the myocardial
bridging: a pilot study. Eur Rev Med Pharmacol Sci.
2012;16:829–34.
55. Prendergast BD, Kerr F, Starkey IR. Normalisation
of abnormal coronary fractional ow reserve associated with myocardial bridging using an intracoronary
stent. Heart. 2000;83:705–7.
56. Haager PK, Schwarz ER, vom Dahl J, Klues HG,
Reffelmann T, Hanrath P. Long term angiographic
and clinical follow up in patients with stent implantation for symptomatic myocardial bridging. Heart.
2000;84:403–8.
57. Ernst A, Bulum J, Šeparović Hanževački J, Lovrić
Benčić M, Strozzi M. Five-year angiographic and
clinical follow-up of patients with drug-eluting stent
implantation for symptomatic myocardial bridging in absence of coronary atherosclerotic disease. J
Invasive Cardiol. 2013;25:586–92.
58. Tandar A, Whisenant BK, Michaels AD.Stent fracture following stenting of a myocardial bridge:
report of two cases. Catheter Cardiovasc Interv.
2008;71:191–6.
59. Srinivasan M, Prasad A.Metal fatigue in myocardial
bridges: stent fracture limits the efcacy of drugeluting stents. J Invasive Cardiol. 2011;23:E150–2.
60. Agirbasli M, Hillegass WB Jr, Chapman GD, Brott
BC. Stent procedure complicated by thrombus formation distal to the lesion within a muscle bridge.
Catheter Cardiovasc Diagn. 1998;43:73–6.
61. Tsujita K, Maehara A, Mintz GS, Doi H, Kubo T,
Castellanos C, Liu J, Yang J, Oviedo C, FranklinBond T, Sugirtharaj DD, Dangas GD, Lansky AJ,
Stone GW, Moses JW, Leon MB, Mehran R.Impact of
myocardial bridge on clinical outcome after coronary
stent placement. Am J Cardiol. 2009;103:1344–8.
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