JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
25, 2016
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VOL. 68, NO.
ª 2016 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION ISSN 0735-1097/$36.00
PUBLISHED BY ELSEVIER http://dx.doi.org/10.1016/j.jacc.2016.09.973
THE PRESENT AND FUTURE
REVIEW TOPIC OF THE WEEK
Left Anterior Descending Artery
Myocardial Bridging
A Clinical Approach
Giuseppe Tarantini, MD, PHD,a Federico Migliore, MD, PHD,a Filippo Cademartiri, MD, PHD,b,c
Chiara Fraccaro, MD, PHD,a Sabino Iliceto, MDa
ABSTRACT
A myocardial bridge (MB) is the term for the muscle overlying the intramyocardial segment of the epicardial coronary
artery (referred to as a tunneled artery). Although MBs can be found in any epicardial artery, most of them involve the
left anterior descending artery. These congenital coronary anomalies have long been recognized anatomically, and are
traditionally considered a benign condition; however, the association between myocardial ischemia and MBs has
increased their clinical relevance. This review summarizes the prevalence, pathophysiology, and diagnostic findings,
including morphological, functional assessment, and treatment of patients with MB involving the left anterior
descending artery, suggesting a pragmatic clinical approach to this entity. (J Am Coll Cardiol 2016;68:2887–99)
© 2016 by the American College of Cardiology Foundation.
T
overlying
he coronary arteries may dip into the
myocardium for varying lengths, and then
reappear on the heart surface. The muscle
the intramyocardial segment of the
EPIDEMIOLOGY
The true prevalence of MB is not fully known and
varies widely according to the methods used to detect
epicardial coronary artery is termed a myocardial such an anatomic variant. Accordingly, an accurate
bridge (MB), and the artery running within the specific prevalence of LAD-MB is difficult to derive.
myocardium is referred to as a tunneled artery. Numerous necropsy series have been performed, with
Although MBs can be found in any epicardial artery, reported MB rates of 5% to 86% (4,5). On average,
most (70% to 98%) involve the left anterior MBs are present in one-fourth of adults. Pathological
descending artery (LAD) (1). These congenital coro- series including thin MBs, or even myocardial strands
nary anomalies have long been recognized anatom- with little hemodynamic consequences, reported
ically, and were traditionally considered a benign higher rates of MBs compared with coronary angiog-
condition (2); however, the association between raphy, which typically detects systolic compression
myocardial ischemia and MBs has heightened their (milking effect). Accordingly, the angiographic
clinical relevance (3). This review summarizes the detection rate of MBs varies from 0.5% to 12% (6) in
prevalence, pathophysiology, diagnostic findings, resting conditions to 40% with provocative tests
and treatment of patients with MB involving the or intracoronary injection of nitroglycerin. Several
LAD, suggesting a pragmatic clinical approach to factors have been postulated to account for the re-
this entity. ported mismatch between the rates of tunneled
From the aDepartment of Cardiac, Thoracic and Vascular Sciences, University of Padua, Padova, Italy; bDepartment of Radiology,
Erasmus Medical Center University, Rotterdam, the Netherlands; and the cDepartment of Radiology, Montréal Heart Institute,
Universitè de Montréal, Montreal, Quebec, Canada. Prof. Tarantini received lecture fees from St. Jude and Volcano. Dr. Migliore is
a consultant for Boston Scientific. Prof. Cademartiri is a consultant for SIEMENS, Guerbet, and SOMAHLUTION. All other authors
have reported that they have no relationships relevant to the contents of this paper to disclose.
Manuscript received May 29, 2016; revised manuscript received August 28, 2016, accepted September 27, 2016.
2888 Tarantini et al.
LAD Coronary Artery Myocardial Bridging
ABBREVIATIONS arteries observed at necropsy compared
AND ACRONYMS with observations from angiography. These
include the thickness and the length of the
CCT = cardiac computed
tomography
MB, the reciprocal orientation of the coro-
nary artery and myocardial fibers, the pres-
CFR = coronary flow reserve
ence of loose connective or adipose tissue
FFR = fractional flow reserve
around the bridged segment, the presence of
iFR = instantaneous wave-free
ratio
an aortic outflow tract obstruction (in which
the systolic tension that develops in the MB
IVUS = intravascular
ultrasound overcomes the intracoronary artery pres-
LAD = left anterior descending sure), the intrinsic tone of the coronary
artery artery wall, the presence of a proximal coro-
LV = left ventricle nary fixed obstruction (which causes a
MB = myocardial bridging decrease in distal intracoronary pressure),
the state of myocardial contractility and
heart rate at the time of angiography, and observer
experience (7). The use of intravascular ultrasound
(IVUS), which is more sensitive for detection of minor
compression, increases MB prevalence to
(8). More recently, the introduction of cardiac
computed tomography (CCT), with its multiplane and
3-dimensional capabilities, has significantly
proved the detection rate of MB (in vivo), even when
the milking effect and/or changes in vessel course at
conventional angiography are absent or mild. Hence,
the CCT-based prevalence of MBs rises to 5% to 76%,
depending on the intrinsic heterogeneity of the study
population, scanner types, and MB pattern (superfi-
cial vs. deep encasement) (6,7).
PATHOPHYSIOLOGY
Myocardial perfusion occurs primarily in diastole
because systolic contraction transiently impedes
coronary blood flow, especially to the
endocardium (9). Thus, MB replicates the normal
microvascular physiology of high diastolic and low
systolic flow, although at the level of the epicardial
coronary artery. Given that in normal conditions, only
15% of coronary blood flow occurs during systole, and
that the effect of MBs is a systolic event at angiog-
raphy, the clinical relevance of MBs has been ques-
tioned. However, other than the usually benign
nature of MBs, what do we know about them that is
important to clinical pathophysiology? Are all LAD-
MBs the same? What additional factors unmask and
aggravate an MB? When does a previously asymp-
tomatic patient with a congenital MB become
symptomatic? What diagnostic tests may guide man-
agement of MBs? As shown in panel A of the Central
Illustration, LAD-MBs may significantly
anatomically with respect to depth (superficial: >1 to
2 mm vs. deep: >2 mm) and length of encasement
(10). The latter seems to influence the dynamic
JACC VOL. 68, NO. 25, 2016
DECEMBER 27, 2016:2887–99
compression not only of the entrapped LAD segment,
but also of the septal branches arising from or near
the involved LAD segment (11,12). Other important
anatomic properties of LAD-MB to consider are the
concomitant number of arteries or tunneled seg-
ments, and the degree of systolic diameter reduction
or kinking.
Clinical and pathophysiological factors that may
unmask or exacerbate MB are the age of the patient,
heart rate, left ventricle (LV) hypertrophy, and the
presence of coronary atherosclerosis (9). In this re-
gard, the increase of LV diastolic dysfunction associ-
ated with aging, LV hypertrophy, and coronary
atherosclerosis may worsen not only the supply-
demand mismatch imposed by the bridge (9), but
also reduce microvascular reserve by compression of
the microvasculature. Similarly, tachycardia associ-
ated with increased sympathetic drive due to exercise
23% or emotional distress reduces flow and myocardial
perfusion by shortening diastolic perfusion time, and
also increases epicardial coronary vasoconstriction as
im- well as contraction of the MB over the tunneled
epicardial LAD (13,14) (Figure 1A). Indeed, a prolon-
gation of the MB contraction due to delayed ventric-
ular relaxation may impair the early hyperemic
diastolic flow beyond that which results simply from
tachycardia, reducing the diastolic perfusion time (15)
(Figure 1B). Additionally, this may also cause a local-
ized phasic coronary spasm that persists into diastole,
because the relaxation time of the arterial vascular
smooth muscle is delayed compared with the dura-
tion of diastole, especially with tachycardia, which
contributes to further worsening the coronary perfu-
sion (11). The resulting impairment of diastolic flow
sub- has 2 secondary pathophysiological consequences
related to heart rate and severity and duration of
epicardial arterial compression. These consequences
are the subendocardial/transmural ischemia and the
septal ischemia caused by an “intramural steal” or
“branch steal” mechanism (11,16). The latter is caused
by the depressurization of septal branches within the
MB, resulting in an intrabridge decrease in perfusion
pressure due to a Venturi effect, or simply due to a
classic fluid dynamic entrance and viscous pressure
loss in the narrowed section, causing the “branch
steal” (12,16) (Central Illustration). In this regard, mild
to moderate MB compression more frequently results
in local (septal) ischemia (due to branch steal), rather
than distal ischemia, as shown by the presence of
normal coronary flow or fractional flow reserve (FFR)
differ downstream of the epicardial coronary (16). More-
over, the reversal of systolic flow seen on Doppler
tracings, in which retrograde flow collides with
antegrade flow, causes high systolic wall shear stress
JACC VOL. 68, NO. 25, 2016 Tarantini et al. 2889
DECEMBER 27, 2016:2887–99 LAD Coronary Artery Myocardial Bridging

C ENTR AL I LL U STRA T I O N LAD Coronary Artery Myocardial Bridging: Anatomic Properties and Clinical and
Pathophysiological Factors of MB of the LAD

Tarantini, G. et al. J Am Coll Cardiol. 2016;68(25):2887–99.

(A) Morphological variations in tunneling (length and depth of tunneled segment). (B) Pathophysiological factors that may unmask or exacerbate myocardial bridging
(MB). (C) Pathophysiological mechanisms that play a potential role in the genesis of the clinical factors related to MB, including “intramural steal” or “branch steal”
mechanism, coronary spasm, coronary artery disease, and coronary dissection. LAD ¼ left anterior descending artery.

upstream from the bridge entrance and seems to play
an important role in formation and spatial distribu-
tion of coronary plaques that are usually present 20 to
30 mm proximal to the entrance of MBs, where
disturbed near-wall blood flow patterns are present
(17,18). These altered biomechanical forces at the
level of the MB may also underlie other potential
complications, such as plaque vulnerability/throm-
bosis (17), increase in vasospasticity (19), and intimal
injury that may further develop into coronary
dissection (20).
Despite this, the severity and effects of MBs seem
to be more appropriately defined by (patho)physi-
ology than by anatomy. Thus, the rare MBs causing
ischemia must incur complex pathophysiological dy-
namics related to intrinsic and extrinsic factors,
which include time-varying interactions among aortic
pressure, arterial and myocardial compression, dia-
stolic flow, transmural perfusion gradients, heart rate
or diastolic perfusion time, and sympathetically-
driven myocardial contraction and coronary vaso-
constriction, all of which interact with diffuse and
2890 Tarantini et al. JACC VOL. 68, NO. 25, 2016

LAD Coronary Artery Myocardial Bridging DECEMBER 27, 2016:2887–99

F I G U R E 1 Schematic of Interaction Among Tachycardia, Coronary Artery Flow, and Transmural Distribution

A Tachycardia − No MB
B Subepicardial flow
Tachycardia − Severe MB Subendocardial flow & Peak flow delayed 20 sec

(% Maximum Mean Coronary Flow)

Rest Flow 150 Average transmural flow
Coronary Flow (cc/min)

Coronary Blood Flow

10 − 20 sec
100

50

0
Systole Diastole Time (sec) 90-sec occlusion 20 40 60 80 100 120 140 160 180 200
Seconds After Release of 90-sec LAD Occlusion

(A) Schematic of coronary artery flow. Coronary artery flow at rest (dotted blue line) and during stress hyperemia and tachycardia in the absence of a significant
myocardial bridging (MB) (solid blue line). The stress hyperemic response may be severely blunted (solid orange line) by severe MB compression of the epicardial artery
and dynamic severe stenosis that limits coronary flow reserve with low distal fractional flow reserve. (B) Differential perfusion of the subepicardium and subendocardium in
a normal nonstenosis experimental model. The rate of increase in coronary blood flow in early diastole is fastest in the epicardium and slowest in the subendocardium. The
time delay in subendocardial hyperemia after subepicardial hyperemia is significant (range 10 to 20 s), and at the time that the initially high subepicardial hyperemia
peaks, subendocardial hyperemia has reached only about 50% of its peak. Many factors may impede this rapid early diastolic hyperemia including (rarely) MBs. As the
diastolic perfusion time shortens because of tachycardia, there is not enough time between serial systoles for the impeded and slowly increasing diastolic coronary blood
flow to adequately supply the subendocardium. Adapted with permission from Gould and Johnson (14). LAD ¼ left anterior descending artery.

focal atherosclerotic disease that is beyond anatomic standard for diagnosing MB, a number of diagnostic
description. modalities have been used to assess its anatomic/
morphological and functional significance (Table 1).
CLINICAL PRESENTATION
At coronary angiography, the MB typically appears
as a systolic narrowing, or “milking” of the vessel,
An MB of the LAD is usually an incidental finding on
with a “step-down” and “step-up” demarcating the
angiography or autopsy. Nevertheless, patients with
affected area, and complete or partial decompression
MB may present with stable (exercise-induced)
in diastole (Figures 2A and 2B) (25). The reduction in
symptomatic or silent myocardial ischemia, as well as
diastolic coronary arterial diameter ranges from 24%
with acute coronary syndrome due to complications
to 58%, compared with the 71% to 99% systolic
potentially related to the presence of an MB, such as
reduction (26). Systolic narrowing at the bridge can be
coronary spasm, thrombosis, and coronary dissection
accentuated by intracoronary injection of nitroglyc-
(20) (Central Illustration). Other reported clinical pre-
erin, which vasodilates adjacent nonbridged coronary
sentations are syndrome X, myocardial stunning or
segments (27). Adjunctive intravascular imaging
transient ventricular dysfunction, Takotsubo syn-
might be useful to improve the detection rate, and to
drome/cardiomyopathy, and life-threatening ven-
better characterize the length, thickness, and location
tricular arrhythmias and sudden death (4,21–24).
of the MB. The IVUS hallmark of the presence of a
Given the low prevalence of these clinical findings,
tunneled segment of LAD is a variable degree of
the correlation with data from diagnostic testing to
compression that persists into diastole, with the
identify whether this broad spectrum of clinical
typical finding of the “half-moon phenomenon,” an
ischemic symptoms are related directly to MB, or
echolucent area present only between the bridged
indirectly to concomitant vasospasm, atherosclerosis,
coronary segment and epicardial tissue throughout
or none of the preceding, is extremely challenging.
the cardiac cycle (28). The etiology of this phenome-
MORPHOLOGICAL ASSESSMENT non is not well understood, presumably representing
the intramyocardial course of the LAD, but it could
The original definition and classification of MB has also result from the fiber optic probe bending at the
been developed with invasive coronary angiography MB site. Regardless, this finding remains highly
(2). However, because of the lack of a true gold specific because it can be detected only in the MB
JACC VOL. 68, NO. 25, 2016
DECEMBER 27, 2016:2887–99
segment with systolic compression, and not in adja-
cent reference segments without compression (28).
IVUS also remains an important diagnostic tool to
characterize the presence, severity, and distribution
of subangiographic atherosclerosis, coronary dissec-
tion, or other complications that might be associated
with MB, with their inherent treatment implications
(e.g., appropriate stent selection and placement)
(8,29). Few data exist on optical coherence
tomography, although this technique may theoreti-
cally improve the characterization of the vessel
wall, providing more information on pathological
changes (30).
The clinical implementation and widespread use of
CCT has also improved the characterization and un-
derstanding of MBs (31). The advantage of CCT in the
assessment of MB is related to its fully 3-dimensional
capability, which is associated with high spatial and
contrast resolution. CCT can easily visualize the cor-
onary lumen, the vessel wall, and the myocardial
wall, hence allowing accurate definition of the MB’s
morphological features (31). The CCT scan protocol is
not different from the conventional protocol used to
assess coronary artery stenosis. Post-processing
software is helpful for the precise definition of the
length and depth of the MB. CCT-based reclassi-
fication of the LAD’s anatomic course includes normal
(within the epicardial fat), superficial intra-
myocardial, and deep intramyocardial courses
(Figure 3). A field in which CCT has shown evidence of
the importance of MB is Takotsubo syndrome. This
syndrome has been shown to be associated with a
significantly higher prevalence of MB on the LAD (21).
Cardiac magnetic resonance can provide anatomic
coronary imaging, but because of limitations in
spatial resolution and technical failures, it cannot
provide reliable and robust insight into the intra-
myocardial depth of the LAD.
FUNCTIONAL ASSESSMENT
As in fixed stenosis, intracoronary physiology tech-
niques represent a valuable alternative to coronary
angiography. However, these diagnostic tools are
hampered by the complex hemodynamics, cyclic
changes in luminal dimensions, and noncircular
lumen morphology of the bridged LAD. Because
these dynamic stenoses are dependent on the degree
of extravascular compression and intramyocardial
tension and are unmasked by chronotropic and
inotropic stimulation, their invasive assessment
should not be limited to resting conditions. Accord-
ingly, although the traditional use of FFR, requiring
only 2 mean pressures to be obtained during maximal
Tarantini et al. 2891
LAD Coronary Artery Myocardial Bridging
(adenosine-induced) hyperemia, is accepted as the
gold standard for assessment of fixed coronary le-
sions, this is largely inadequate for assessment of the
hemodynamic significance of an MB (32,33). More-
over, MB may cause significant diastolic pressure
gradients and artificially normal or negative systolic
pressure gradients (systolic distal pressure is greater
than systolic proximal pressure) as a result of systolic
pressure overshooting; this is completely different
from fixed stenosis, in which the difference between
mean and diastolic pressure gradient values across
the lesion are not significant (Figure 4) (33). This
phenomenon may produce an artificial elevation in
the mean pressure used by traditional FFR (average
systole and diastole), resulting in an underestimation
of hemodynamic significance of the MB (Figures 2C
to 2G) (33). Diastolic FFR with the use of dobut-
amine challenge is a more appropriate approach for
testing the hemodynamic significance of MB because
the MB has less influence on diastole, whereas FFR on
the basis of mean pressures should be used with
caution (34). Escaned et al. (34) demonstrated that
combining low-dose intracoronary adenosine (20 m g)
with moderate-dose intravenous dobutamine infu-
sion (20 m g/kg/min) increased the likelihood of
unmasking larger diastolic pressure gradients in pa-
tients with LAD-MB and ischemia in noninvasive
tests, showing that diastolic FFR identifies a signifi-
cant proportion of hemodynamically relevant MBs
that conventional FFR did not identify. The investi-
gators also found that the angiographic severity of
MB was modified by dobutamine. Another small
study of 18 patients with MB reported that the use of
dobutamine-diastolic FFR resulted in larger gradients
in 3 patients; however, the investigators failed to find
a correlation with major adverse cardiac events (12).
Besides these 2, there are no other studies correlating
diastolic FFR using adenosine, dobutamine, or both
with noninvasive parameters of ischemia, or with
clinical outcomes (35). Recently, the instantaneous
wave-free ratio (iFR), a pressure-only index that takes
an alternative approach to the isolation of the he-
modynamics of a stenosis from the microcirculation,
has been introduced. It does not need the adminis-
tration of vasodilators; instead, it samples intra-
coronary pressure during the diastolic “wave-free”
period—a period in the cardiac cycle when intrabeat
microvascular resistance is inherently stable and
minimized, and the flow is at its highest compared
with the whole cycle (36). The iFR is a diastolic-
specific index, and for this reason, it appears prom-
ising in MB physiological evaluation. Also, iFR allows
anatomic mapping by means of coregistration (iFR
Scout). Figure 2 shows a typical clinical example that

T A B L E 1 Myocardial Bridging and Imaging Modalities
Imaging
Modality Description
Invasive
CAG Invasive technique using
selective catheterization of
coronary arteries.
IVUS Invasive technique using
selective catheterization of
coronary arteries, and
insertion of the probe across
the region of interest.
Intracoronary Invasive technique using
Doppler selective catheterization of
coronary arteries and
insertion of a wire across the
region of interest.
FFR Invasive technique using
selective catheterization of
coronary arteries and
insertion of a wire across the
region of interest.
iFR Invasive technique using
selective catheterization of
coronary arteries and
insertion of a wire across the
region of interest.
Noninvasive
CCT 3D noninvasive technique
performed on outpatient
basis; not technically
different from any other
contrast-enhanced CT.
TAG Noninvasive technique
performed on outpatient
basis; not technically
different from any other
contrast-enhanced CT.
FFRct Noninvasive technique
performed on outpatient
basis; not technically
different from any other
contrast-enhanced CT.
Semiology
2D visualization of the anatomy
of the coronary arteries
through luminography that
allows the measurements of
lumen diameter.
3D visualization of the anatomy
of the coronary artery that
allows accurate
measurements of lumen
diameter/area and of the
vessel wall.
Evidence of specific altered
functional patterns of
hemodynamic significance
associated with MB.
Determination of a reduction of
the ratio between the
maximum achievable blood
flow in a diseased coronary
artery and the theoretical
maximum flow in a normal
coronary artery.
Ratio of proximal and distal
coronary pressures over the
wave-free period in diastole.
Accurate visualization of the
course of coronary arteries
into the epicardial fat and
within the myocardial wall;
can define degree of radial
involvement of coronary
wall and myocardial wall.
Linear regression coefficient
between luminal attenuation
and axial distance from the
coronary ostium.
CT-derived computational fluid
dynamics application.
Resembles invasive FFR
concept. Not performed
during stress.
2892
Pharm
Diagnostic Criteria Pros Cons X-Rays Contrast Stress
LAD Coronary Artery Myocardial Bridging
Tarantini et al.
Milking effect Most frequently used. No functional value þþ þþ 
Anatomic/dynamic assessment.
Half-moon Identify: Not commonly used þþþ þþ 
 Proximal plaque No functional value
 Negative arterial
remodeling
 Extent of phasic arterial
compression
Fingertip  Functional evaluation of Longer procedural time þþþ þþ þþ
coronary lesions and Pharmacological side effects.
microvascular disease No standard cutoff with Ade
 Simulation of dynamic or Dob
myocardial obstruction Off-label use of acetylcholine
 Endothelial function
testing/coronary
vasospasm assessment.
FFR <0.75–0.80 Functional evaluation of: Longer procedural time þþþ þþ þþ; Ade
 Fixed lesions (gold Adenosine is mandatory
standard) Pharmacological side effects
 Dynamic coronary Pd/Pa as average of systole
obstruction and diastole
iFR <0.86 (gray zone Functional evaluation of: Longer procedural time þþþ þþ þ/
0.86–0.93)  Fixed lesions Further validation needed
 Dynamic coronary
obstruction
Diastolic specific index
Ade not mandatory
At least 1mm of myocardium More accurate than Not readily available þ þþ 
covering the coronary artery angiography. No functional value
(i.e., deep intramyocardial Shows atherosclerosis within
course). the coronary segment.
Widely tested for the detection
and definition of MBs.
Drop in HU per 10 mm length of The same of CCT þ additional Not tested on MBs þ þþ 
coronary artery; variable functional assessment
DECEMBER 27, 2016:2887–99
thresholds depending on at rest.
JACC VOL. 68, NO. 25, 2016
different methods
FFR <0.75–0.80 The same of CCT þ additional Not tested on MBs þ þþ 
functional assessment at
rest.
Continued on the next page
 DECEMBER 27, 2016:2887–99

JACC VOL. 68, NO. 25, 2016

T A B L E 1 Continued

Imaging Pharm
Modality Description Semiology Diagnostic Criteria Pros Cons X-Rays Contrast Stress

CTP Noninvasive technique
performed on outpatient
basis that provides stress
perfusion information.
SPECT Noninvasive technique
performed on outpatient
basis that provides stress
perfusion information.
PET Noninvasive technique
performed on outpatient
basis that provides
quantitative stress perfusion
information.
CMR Noninvasive technique
performed on outpatient
basis that provides stress
perfusion information.
Stress TTE Noninvasive technique
performed on outpatient
basis that provides stress
kinetic information.
TDE Noninvasive technique
performed on outpatient
basis that provides stress
perfusion information.
Reversible stress-induced
myocardial perfusion defect
in the absence of
angiographic coronary artery
disease.
Reversible stress-induced
myocardial perfusion defect
in the absence of
angiographic coronary artery
disease.
Reversible stress-induced
myocardial perfusion defect
in the absence of
angiographic coronary artery
disease. Provides global and
regional CFR quantitative
values.
Reversible stress-induced
myocardial perfusion defect
in the absence of
angiographic coronary artery
disease.
Reversible stress-induced
myocardial hypokinesia in
the absence of angiographic
coronary artery disease.
Reversible stress-induced
myocardial perfusion defect
in the absence of
angiographic coronary artery
disease.
Provides regional (mostly LAD)
CFR qualitative assessment.
Segmental subendocardial Usually combined with CCT can Not readily available þþþ þþþ þþ; Ade
perfusion defect provide anatomic and Not tested on MBs
functional assessment of the
effect of MB.
Segmental perfusion defect Physiological assessment of Not readily available þþþ þþ þþ; Ade, Dyp,
functional effect of MB. No anatomic value Dob
Low spatial resolution for
subendocardial defects
Segmental perfusion defect Physiological assessment of Not readily available þþ þþ þþ
functional effect of MB. No anatomic value
Not tested on MBs
Low spatial resolution for
subendocardial defects
Segmental subendocardial Physiological assessment of Not readily available  þþ þþ; Ade
perfusion defect functional effect of MB. No anatomic value
Not tested on MBs
Segmental hypokinesia Physiological assessment of No anatomic value   þþ; Dyp, Dob
functional effect of MB.
Readily available.
Segmental perfusion defect Physiological assessment of No anatomic value  þþ þþ; Dyp, Dob
functional effect of MB.
Readily available.

2D ¼ 2-dimensional; 3D ¼ 3-dimensional; Ade ¼ adenosine; CAG ¼ coronary angiography; CCT ¼ cardiac computed tomography; CFR ¼ coronary flow reserve; CMR ¼ cardiac magnetic resonance; CT ¼ computed tomography; CTP ¼ cardiac computed tomography
perfusion; Dob ¼ dobutamine; Dyp ¼ dypiridamole; FFR ¼ fractional flow reserve; FFRct ¼ computed tomography–derived fractional flow reserve; iFR ¼ instantaneous wave-free ratio; LAD ¼ left anterior descending; MB ¼ myocardial bridge; Pa ¼ proximal pressure;
Pd ¼ distal pressure; PET ¼ positron emission tomography; Pharm Stress ¼ pharmacological stress; SPECT ¼ single-photon emission computed tomography; TAG ¼ transluminal attenuation gradient; TDE ¼ transthoracic Doppler echocardiography; TTE ¼ transthoracic

LAD Coronary Artery Myocardial Bridging

echocardiography.

Tarantini et al.
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2894 Tarantini et al. JACC VOL. 68, NO. 25, 2016

LAD Coronary Artery Myocardial Bridging DECEMBER 27, 2016:2887–99

highlights the differences in LAD-MB functional

F I G U R E 2 Intracoronary Hemodynamics From a Patient With MB
evaluation between FFR (mean pressure) and iFR
(diastolic pressure) with anatomic mapping, both at
BASAL DOBUTAMINE STRESS
rest and after dobutamine. However, the use of iFR in
this setting remains to be validated.
Finally, the use of Doppler-tipped guidewires for
measurements of intracoronary flow velocity and
coronary flow reserve may reveal both: 1) the retro-
grade flow during systole immediately proximal
to the bridged segment; and 2) the “fingertip
phenomenon,” an abrupt early diastolic flow accel-
eration, rapid mid-diastolic flow deceleration, and a
mid-to-late diastolic plateau (“spike-and-dome”
pattern) (37).
When invasive tools to evaluate ischemic poten-
tial of MB are not available, functional noninva-
sive imaging tests may be helpful. Stress
echocardiography, stress cardiac magnetic reso-
nance, single-photon emission computed tomogra-
phy, and positron emission tomography can detect
the functional effect of an MB of the LAD (38).
Compared with the others, cardiac magnetic reso-
nance has a better spatial resolution to detect
segmental and subendocardial perfusion defects.
More recently, new post-processing techniques are
available for the derivation of functional information
from the anatomic assessment provided by CCT.
These techniques are mostly post-processing algo-
rithms: transluminal attenuation gradient and
computed tomography (CT)–derived FFR (39). The
former corresponds to the linear regression coeffi-
cient between luminal attenuation and axial dis-
tance from the coronary ostium (40). The CT-derived
FFR is a computational fluid dynamics simulation of
adenosine-mediated hyperemia applied to CCT im-
aging, and is on the basis of attenuation through the
coronary artery associated with morphology of the

F I G U R E 2 Continued

(A and B) Diastolic and systolic angiographic appearance,

respectively, of an LAD-MB at resting conditions. (E and F) The
different angiographic appearance of the same vessel in dias-
tole and systole during dobutamine infusion (20 mg/kg/min).
(C and G) Proximal pressure (Pa) (red tracing) and distal
pressure (Pd) (yellow tracing) measurements from the same
patient. FFR measurements are negative and nonsignificantly
different, both at baseline (FFR 0.88) (C) and during
dobutamine/adenosine intravenous infusion (FFR 0.87) (G).
In contrast, instantaneous wave-free ratio (iFR) measurement
at rest is in the “gray zone” (iFR 0.89) (D), and becomes
definitely positive during dobutamine infusion (20 mg/kg/min)
(iFR 0.83) (H). (I) Finally, iFR with anatomic coregistration
(iFR Scout) for simultaneous MB mapping. FFR ¼ fractional flow
reserve; other abbreviations as in Figure 1.
Continued on the next column
JACC VOL. 68, NO. 25, 2016 Tarantini et al. 2895
DECEMBER 27, 2016:2887–99 LAD Coronary Artery Myocardial Bridging

vessel lumen and other parameters (41). Both

F I G U R E 3 CCT of a Patient With 2 Atypical Intramyocardial Courses of the LAD
methods have not been tested on series of patients and the LCX
with MBs. Recently, CT scanners of the latest gen-
eration have also been used to perform CT stress
perfusion. Hybrid scanners combining imaging
techniques have also been introduced, and might be
useful for a combined anatomic and functional
definition of coronary lesions and MBs. Yet, there
are no available data on the use of hybrid techniques
for the definition and characterization of MBs.

MANAGEMENT

There is no accepted anatomic or functional clas-

sification of MBs that would provide the basis for
requiring a specific treatment for a patient. More-
over, the variability in clinical symptoms, results
of noninvasive tests, and the concomitant presence
of other conditions, such as coronary artery dis-
ease, hypertrophic cardiomyopathy, or valvular
heart disease, may independently influence treat-
ment options and outcomes of patients with MB. A
proposed management strategy for MB of the LAD
on the basis of the presence of clinical symptoms
and/or objective signs of ischemia is shown in
Figure 5.
PHARMACOLOGICAL THERAPY. Schwarz et al. (42)
proposed the following classification of MB in the
absence of coronary artery disease: type A, clinical
symptoms and no objective signs of ischemia; type B,
clinical symptoms and objective signs of ischemia by
noninvasive stress test; and type C, clinical symptoms
and objective altered intracoronary hemodynamics
(by quantitative coronary assessment/coronary flow
reserve/intracoronary Doppler). The 5-year follow-up
data on the basis of this classification showed that
types B and C responded well to b-blockers or
calcium-channel antagonists. Patients with type C MB
refractory to medical therapy were treated with
stenting of the MB. On the basis of previous patho-
physiological considerations, the mainstay of medical
treatment should focus on relieving potential triggers
and hemodynamic disturbances that aggravate the
MB, such as hypertension/hypertrophy, increased (A and B) Volume rendering images with vessel tracking; (C and D) longitudinal curved
heart rate, reduced diastolic coronary filling period, multiplane reconstructions. The intramyocardial course of the LAD (A and C) is quite
and inappropriate contractility and compression of extensive (74 mm), and involves the middle and distal segments of the vessel. It does not

the coronary arteries. Accordingly, b-blockers are show overlying myocardial tissue; therefore, it can be addressed as superficial. The
intramyocardial course of the LCX (B and D) is also quite extensive (65 mm), and
considered first-line therapy because of their nega-
involves the distal segment of the vessel. It shows overlying myocardial tissue;
tive chronotropic and inotropic effects, and because therefore, it can be addressed as deep. CCT ¼ cardiac computed tomography; LAD ¼ left
of the reduction in sympathetic drive (exertion or anterior descending artery; LCX ¼ left circumflex.
stress-induced) (4,26,42). Calcium-channel blockers
may offer additional benefit by reducing concomitant
vasospasm incremental to the aforementioned
2896 Tarantini et al. JACC VOL. 68, NO. 25, 2016

LAD Coronary Artery Myocardial Bridging DECEMBER 27, 2016:2887–99

F I G U R E 4 Intracoronary Hyperemic Pressure Measurements at Baseline and During Dobutamine Challenge in MB

Adenosine ic Adenosine + Dobutamine iv

ECG

150 110
Pa
Pressure (mm Hg)

90 Pa 70 Pa Pd

Pd Pd
30 30

Schematic of recorded ECG, Pa, and intracoronary Pd. The overshooting of Pd over Pa noted during dobutamine challenge contributes to the
characteristic negative systolic and positive protodiastolic pressure gradients. This phenomenon may produce an artificial elevation in the
mean pressure used by traditional FFR (average systole and diastole), resulting in an underestimation of hemodynamic significance of the MB.
Adapted from Escaned et al. (34). ECG ¼ electrocardiogram; ic ¼ intracoronary; iv ¼ intravenous; other abbreviations as in Figures 1 and 2.

pharmacological effects of b-blockers. Randomized
clinical trials assessing the effect of b-blockers or
calcium-channel blockers are lacking. Pure vasodila-
tors, such as nitroglycerin, are not indicated because
they can worsen symptoms due to the increased
systolic compression of the tunneled artery, tachy-
cardia, and proximal vessel dilation, which may
aggravate the flow reversal in the proximal coronary
segment to MB (27). Ivabradine, by reduction of the
heart rate via specific inhibition of I f ion channels,
might be considered in place of or together with a
lower dose of b -blockers and calcium-channel
blockers. Aggressive risk factor modification is rec-
ommended because of the inherent risk of the MB
inducing atherosclerosis; antiplatelet therapy should
be considered when subclinical atherosclerosis is
detected.
PERCUTANEOUS OR SURGICAL TREATMENT. Other
therapeutic approaches include stents, minimally
invasive coronary artery bypass grafting (CABG), or
surgical myotomy. Although percutaneous coronary
stent implantation may ameliorate hemodynamic
abnormalities and improve symptoms (37), no studies
have demonstrated normalization of myocardial
perfusion when a perfusion defect was present before
stent implantation. Moreover, concerns related to
perforation during stent deployment (up to 6.3%)
(43), stent fracture (case reports) (44,45), in-stent
restenosis (bare-metal stents: up to 75% at 1 year;
drug-eluting stents: 25% at 1 year) (46,47), and stent
thrombosis (case reports) (48,49), have limited their
use in these settings. Available evidence on these
complications is summarized in Online Table 1.
Although the restenosis rate with bare-metal stents is
higher than that observed with drug-eluting stents,
the rate of target vessel revascularization of tunneled
arteries treated with drug-eluting stents remains
higher than that observed with atherosclerotic le-
sions, but not bridged lesions (43). When both are
present, Tsujita et al. (50) have shown that stents
extending into MBs have higher rates of target lesion
revascularization compared with those ending prox-
imal to the MB because the minimum cross-sectional
area of stents extending into the MB was significantly
smaller. Thus, recognition and location of the
maximal plaque burden with respect to the MB is of
the utmost importance (50). Whether current bio-
absorbable scaffolds may have a role in this setting
remains to be established, considering the concerns
raised about their radial strength and the negative
interaction between vessel size and in-scaffold
thrombosis. Medical therapy appears to be the treat-
ment of choice for the vast majority of patients with
MB in the absence of randomized trials comparing
optimal medical treatment versus percutaneous
coronary intervention with drug-eluting stents.
Accordingly, an ischemia-guided revascularization
using drug-eluting stents may be limited to the small
JACC VOL. 68, NO. 25, 2016 Tarantini et al. 2897
DECEMBER 27, 2016:2887–99 LAD Coronary Artery Myocardial Bridging

F I G U R E 5 Management Strategy for LAD-MB

LAD Myocardial bridging

No clinical symptoms Clinical symptoms

- Relieve potential triggers*
- Risk factors modification
(+)
- Consider antiplatelet therapy
if atherosclerosis is detected
Follow-up
and/or objective signs
of ischemia
- β-blockers/calcium channel blockers
- Consider Ivabradine together with
lower dose of β-blockers/calcium
channel blockers
- Avoid pure vasodilators
- Relieve potential triggers*
- Risk factors modification
- Consider antiplatelet therapy
if atherosclerosis is detected

Improvement

(+) (-)

Follow-up Stent/Surgical option (CABG

or supra-arterial myotomy)

Flow diagram showing proposed management strategy of MB of the LAD on the basis of the presence of clinical symptoms and/or objective
signs of ischemia. *See text. CABG ¼ coronary artery bypass grafting; other abbreviations as in Figure 1.

percentage of severely symptomatic patients who are
refractory to maximal medical treatment and who
are not surgical candidates. Surgical options for MB
are more invasive, and include either supra-arterial
myotomy (51) and/or CABG (52). Potential complica-
tions of myotomy include wall perforation, particu-
larly in the case of a deep subendocardial course,
ventricular aneurysm formation, and post-operative
bleeding (53). CABG is favored over myotomy in
cases of extensive (>25 mm) or deep (>5 mm) MB (the
risk of myotomy can be considerable), or when the
bridged coronary segment fails to
completely in diastole (myotomy is unlikely to correct
the persistent diastolic compression)
available evidence, focusing on surgical approaches
to MB, is summarized in Online Table 2. Overall, the
available data suggest that surgical therapy appears
to be safe and effective, and we recommend this
therapeutic approach in the very rare cases of
severely symptomatic patients who are refractory to
medical therapy, or when the percutaneous approach
has failed or is considered not to be safe.
REPRINT REQUESTS AND CORRESPONDENCE: Prof.
Giuseppe Tarantini, Department of Cardiac Thoracic
decompress and Vascular Sciences, University of Padua Medical
School, Via N. Giustiniani 2, 35121 Padova, Italy.
(54). The E-mail: giuseppe.tarantini.1@unipd.it.

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KEY WORDS fractional flow reserve,
instantaneous wave-free ratio, intravascular
imaging, percutaneous coronary intervention
A PP END IX For supplemental tables, please
see the online version of this article.