Journal of the American College of Cardiology

Volume 78, Issue 22, 30 November 2021, Pages 2196-2212

The Present and Future

JACC State-of-the-Art Review

Myocardial Bridging: Diagnosis, Functional

Assessment, and Management: JACC State-
of-the-Art Review
David Sternheim MD a ∗, David A. Power MD a ∗ , Rajeev Samtani MD a,
Anapoorna Kini MD a, Valentin Fuster MD, PhD a b, Samin Sharma MD a

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Highlights
• Myocardial bridging is a common coronary anomaly in which a coronary
artery segment traverses through the myocardium, but functional imaging
and hemodynamic characterization in symptomatic patients are necessary
to identify those who benefit from treatment.

• Medical management with beta-blockers and calcium-channel blockers

are first-line therapeutic strategies, reserving revascularization for those
who do not respond sufficiently to medication therapy.
 • Percutaneous coronary intervention and surgical myotomy are the
revascularization strategies of choice, depending on lesion length, depth,
concomitant atherosclerosis, operator expertise, and patient preference.

Abstract
Myocardial bridging (MB) is a congenital coronary anomaly in which a segment of the
epicardial coronary artery traverses through the myocardium for a portion of its
length. The muscle overlying the artery is termed a myocardial bridge, and the
intramyocardial segment is referred to as a tunneled artery. MB can occur in any
coronary artery, although is most commonly seen in the left anterior descending
artery. Although traditionally considered benign in nature, increasing attention is
being given to specific subsets of MB associated with ischemic symptomatology. The
advent of contemporary functional and anatomic imaging modalities, both invasive
and noninvasive, have dramatically improved our understanding of dynamic
pathophysiology associated with MBs. This review provides a contemporary overview
of epidemiology, pathobiology, diagnosis, functional assessment, and management of
MBs.

Central Illustration
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Key Words
myocardial bridge; myocardial bridging; state-of-the-art review
Abbreviations and Acronyms
BMS, bare-metal stents; CA, coronary angiography; CAD, coronary artery disease;
CCTA, coronary computed tomography angiography; FFR, fractional flow reserve; iFR,
instantaneous wave-free ratio; ISR, in-stent restenosis; IVUS, intravascular ultrasound;
LAD, left anterior descending artery; MB, myocardial bridging; OCT, optical coherence
tomography; PCI, percutaneous coronary intervention; TLR, target lesion
revascularization

The coronary arteries typically course between the peri- and epicardium. A partial or
total encasement of the coronary arteries by myocardial fibers is termed myocardial
bridging (MB). The muscle overlying the artery is termed a “myocardial bridge,” and
the intramyocardial segment of the artery is referred to as a “tunneled artery.” The
first autopsy description of MB dates to physician Henric Reyman (1) in 1732, during
which time it was thought to be a benign cardiovascular anomaly. MB may occur in
any epicardial coronary artery but most often arises in the left anterior descending
artery (LAD). Although MB is benign in most cases, it represents a diagnostic and
therapeutic challenge in a subset of symptomatic patients.

Epidemiology
The true prevalence of MB is not accurately known; however, MB is likely present to
some degree in approximately 1 in 3 adults (2). Rates of MB detection vary
significantly according to the imaging modality used to identify these coronary
variants. The most commonly studied methods to determine prevalence in the general
population include coronary angiography (CA), coronary computed tomography
angiography (CCTA), and autopsy studies. The reported prevalence of MB is between
2% and 6% for CA and 19% and 22% for CCTA (2,3). The variation in prevalence among
imaging modalities across individual studies depends largely on heterogeneous target
populations, type of imaging device used, and the inclusion versus exclusion of
“superficial” MB (4, 5, 6). Autopsy studies are considered the gold standard in
identification of MB, with a prevalence approaching 33%-42% (2,7,8). In terms of
anatomical location, 67%-98% of MBs are located in the LAD, most commonly in the
proximal- and mid-LAD segments. The left circumflex and right coronary artery are
less commonly affected (9).

Considering the high rate of MB detected at autopsy, CCTA is considered the more
sensitive modality, compared with CA and intravascular imaging, for general
diagnostic purposes. Several factors have been identified to account for the significant
discordance in prevalence of MB across imaging modalities; these include the highly
variable length and depth of myocardial mass overlying the tunneled artery, the axial
orientation of the coronary artery alongside myocardial fibers, the presence of a fixed
stenosis proximal to the MB, the existence of connective or adipose tissue opposing
the tunneled segment, a concomitant aortic outflow obstruction, intrinsic tone of the
coronary artery wall, significant hypotension, vasopressor use at the time of imaging,
and intraobserver variability (10). Nitroglycerin also notably augments the degree of
systolic compression during angiography, potentially influencing the detection and
perceived severity of MB (11). Alternatively, the use of intravascular ultrasound (IVUS)
may increase the detected prevalence of MB during CA up to 23% in some dedicated
studies (3,12).

Pathophysiology
For many years, MB was considered an entirely benign phenomenon. This was chiefly
based on the observation that almost all (∼85%) coronary blood flow occurs during
diastole, while MB is characterized by systolic arterial compression. Therefore, only
approximately 15% of coronary blood flow is at risk of being compromised by
significant MB, a seemingly clinically irrelevant fraction. The reality, however, is more
complex and is characterized by the interplay between anatomic and physiologic
factors that influence each other dynamically, not only throughout the cardiac cycle,
but also during the life of the patient.

MB is a congenital anatomic anomaly characterized by a length of tunneled artery

beneath a section of myocardium. The depth of the tunneled segment and the length
of the segment play an integral role in providing the substrate that eventually leads to
ischemic symptoms in some cases. The depth of the tunneled artery (1-2 mm
superficial, >2 mm deep) (13) is related to (but not the sole determinant of) the degree
of systolic compression and course of the artery. The depth of the MB also has
implications for treatment, especially when considering surgical intervention. The
length of the tunneled segment is important not only as it relates to the amount of the
affected artery, but also to the number of branches affected by the MB. This is
especially clinically relevant when considering LAD MBs that affect diagonal or septal
branches.

Unlike classic atherosclerotic plaque that produces a fixed stenosis, MB produces a

dynamic effect that varies with cardiac cycle, heart rate, and sympathetic tone.
Despite being considered a chiefly systolic phenomenon, angiographic ultrasound and
IVUS studies have shown vessel compression in systole is followed by a delay in the
increase in luminal diameter during diastole (14,15). This may be due to localized
phasic artery spasm caused by myocardial bridge contraction. This delay impedes
rapid early-diastolic hyperemia most significantly in the sub-endocardium (16) that is
more subject to ischemia. The phenomenon is drastically exaggerated in the presence
of high sympathetic tone (as seen with exercise or dobutamine infusion) for a few
reasons. Increased sympathetic tone increases heart rate and thereby decreases
diastolic perfusion time. In addition, increased strength of contraction across the MB
delays relaxation beyond systole into the early-diastolic phase, further impairing flow.
Finally, high sympathetic tone also increases coronary vasoconstriction. In the setting
of high sympathetic tone, the MB-induced delay in rapid early-diastolic coronary flow
serves to severely attenuate the natural stress hyperemia response, thereby
exacerbating supply-demand mismatch (17). For these reasons, it is imperative that
accurate clinical assessment of MB uses a modality that incorporates the milieu of
high sympathetic tone.

Another important pathophysiological consequence of MB is that of “branch steal,”

which is most apparent in the case of septal perforator arteries. As blood flows
through the tunneled artery in end systole/early diastole, it passes through a
constricted segment that serves to increase fluid velocity, thereby decreasing
perfusion pressure at the ostium of the septal branch due to the Venturi effect. Others,
however, point out that the relatively modest increases in velocity seen in vivo in
Doppler flow velocity measurements are unlikely to result in large enough pressure
gradients across side-branch arteries to account for the observed effect. Instead, they
argue that the phenomenon follows chiefly from classic fluid dynamic entrance and
viscous pressure loss in the narrowed segment (17). In either case, the presence of
“branch steal” in MB is supported by studies that show lower diastolic pressures in the
intrabridge segment than in the distal artery (14), as well as the observation that mild-
moderate MBs more often result in local/septal ischemia as compared with ischemia
in the distal myocardium. This observation is further supported by the distinctive
abnormality of focal septal buckling with apical sparing seen in patients with MB
during exercise echocardiography (18).

Coronary atherosclerosis and MB

The development of atherosclerotic coronary disease has been associated with MB.
Recent studies have elucidated how biomechanical forces from MB affect the coronary
artery over time and may help to explain both the characteristic pattern of
atherosclerosis progression associated with MB and several of the clinical
presentations. Under normal conditions, coronary arteries are subject to multiple
mechanical forces, including compressive stress, tensile stress, and shear stress (19).
Shear stress or wall shear stress (WSS) is the frictional force that acts tangentially to
flow and has been shown to play a role in the development of endothelial dysfunction
and atherosclerosis (20,21), possibly by inducing alterations in several inflammatory
pathways. Doppler studies of MBs show that systolic compression of the tunneled
artery produce retrograde flow proximal to the MB (22). This results in abrupt
breakage of the propagating antegrade systolic wave and creates an area of low WSS
that has been posited to explain the development of atherosclerotic plaque
immediately proximal to the MB (23,24). However, these altered biomechanical forces
are also potentially responsible for some nonatherosclerotic complications associated
with MB. It is likely that high compressive stress exerted by the MB on the tunneled
artery could cause intimal injury that could propagate to dissection (25).

Another frequently seen characteristic of MB is the relative freedom from plaque

within the tunneled segment of the artery. This can be explained by a few
observations. First, MB results in separation of the bridged segment from perivascular
adipose tissue in the epicardium that is associated with proinflammatory signaling
pathways (26). Furthermore, optical coherence tomography (OCT) imaging has
identified a lack of adventitial vaso vasorum, which normally act as a conduit for
diffusing inflammatory cells and cytokines from the perivascular adipose tissue, at MB
(27). Second, compression of the tunneled artery may improve lymphatic drainage
(28), and finally, the tunneled segment is exposed to high or physiologic WSS as a
result of elevated velocities that have been associated with atheroprotective pathways
in vitro (29). As a counterpoint to the development of CAD, some authors have
proposed that MB may instead act as a potentially protective element against severe
obstructive CAD elsewhere in the coronary system; however, mechanisms and robust
data are as of yet lacking (30).

These many pathophysiological factors interact together with clinical variables such as
advancing age and comorbid conditions resulting in new symptoms of ischemia in
previously asymptomatic patients. Atherosclerotic plaque occurring proximal to the
MB results in decreased pressure downstream that exacerbates ischemia caused by
the MB. Second, left ventricular diastolic dysfunction and left ventricular hypertrophy
worsen supply-demand mismatch, as well as reduce microvascular reserve via
compression of the microvasculature. Third, coronary vasospasm and endothelial
dysfunction associated with the MB can cause myocardial ischemia (31).

Overall, it is the rare patient with the right combination of physiologic, rather than
anatomic, changes related to MB who develops symptomatic disease. The process that
underlies this develops over the course of years in a complex interplay related to MB
length/depth, fluid dynamics and their long-term biologic effects, CAD, and left
ventricular changes.

Classification
The Schwarz classification (2009) has been proposed as a guide for directing therapy
for MB. In their retrospective study of 157 patients with MB at 5-year follow-up,
patients with type A MB, defined as those with clinical symptoms but no objective
signs of ischemia (incidental finding on angiography), did well with reassurance alone
(80% reported improved symptoms). Type B patients with objective signs of ischemia
by noninvasive testing and type C patients with altered intracoronary hemodynamics
(quantitative CA/coronary flow reserve/intracoronary Doppler) were treated with
beta-blockers or calcium-channel blockers. Of those with type C lesions (n = 37), 24
patients (65%) required stenting with bare-metal stents (BMS) due to lack of
improvement with medical therapy. Four cases of in-stent restenosis (ISR) were
identified at the prescribed 7-week angiographic follow-up requiring target lesion
revascularization (TLR), but all were symptom- and event-free at 2- and 5-year follow-
up. Based on this, the authors propose that patients with type A MB receive
reassurance or medical therapy for persistent symptoms; patients with type B receive
medical therapy followed by invasive hemodynamic assessment and possible stenting
for refractory symptoms; and patients with type C receive medical therapy (even in
the absence of ischemia on noninvasive test) followed by stenting for refractory
symptoms (32). This simple treatment schema has recently been brought into
question with iterative advancements in the pathobiology of MB.

Clinical Presentation
MB is typically an asymptomatic, benign finding discovered during CA. Although the
vast majority of MBs are “normal variants,” numerous case reports and series have
documented the association between MB and angina or angina-equivalent syndromes.
Patients with MB may present with stable or unstable angina, vasospastic angina, or
acute coronary syndrome (ACS) related to MB complications (33,34). ACS
presentations in MB are thought to be the result of coronary spasm, thrombosis,
coronary dissection, or the development of focal atherosclerosis immediately
proximal to the MB (35). A study of 298,558 patients undergoing CA revealed that
patients with MB were younger, had higher rates of smoking, and lower rates of
cardiovascular risk factors such as diabetes, chronic kidney disease, prior myocardial
infarction, and prior percutaneous coronary intervention (PCI). In a subset of patients
presenting with ACS, patients with MB were more likely to present with unstable
angina rather than troponin-positive myocardial infarction such as ST-segment
elevation or non–ST-segment elevation myocardial infarction. The higher incidence of
MB among smokers may be associated with increased tendency toward coronary
artery spasm with cigarette smoking (36). Less common syndromes that have been
associated with MB include exercise-induced ventricular dysrhythmias, ventricular
rupture, angina with normal coronary arteries, sudden cardiac death, Takotsubo
cardiomyopathy, left ventricular dysfunction, and Wellens syndrome (37, 38, 39, 40,
41). Clinically, the surface electrocardiogram rarely shows abnormalities in
asymptomatic, resting patients, although repolarization abnormalities may
infrequently be seen during exercise stress testing (42). Practically, there is a
significant diagnostic challenge in attributing whether symptoms in a patient with MB
are: 1) directly related to the MB; 2) indirectly related to coronary vasospasm; 3)
related to atherosclerotic coronary disease; or 4) clinically unrelated to the MB
(10,23).

Angiographic and Functional Assessment

Numerous invasive techniques can be used in the catheterization laboratory for
detailed assessment of MB, including angiography, IVUS, OCT, Doppler flow wire
(DFW), and pressure wire methods (Figure 1) (43). The classic angiographic finding of
MB is the systolic narrowing or “milking” of the vessel. This is associated with a “step-
down” and “step-up” demarcating the affected coronary segment with either
complete or partial decompression in diastole. A significant “milking effect” is present
when there is a visual ≥70% reduction in the minimal luminal diameter during systole
and persistent ≥35% reduction in minimal luminal diameter during mid- to late-
diastole. Importantly, routine CA is an insensitive imaging modality for the detection
of MB, with most bridges not visible on angiography and only 5% demonstrating the
classic milking effect. The use of intracoronary vasodilators, such as nitroglycerin, can
increase angiographic sensitivity significantly by augmenting the severity of the
compression related to MB; therefore, nitroglycerin should be administered
immediately before CA for the purposes of detailed MB assessment if hemodynamics
allow (44). Furthermore, important consideration should be paid to optimal
angiographic views. CA is hampered by the presence of complex hemodynamics at the
MB site, cyclical changes in lumen dimensions, and noncircular lumen morphology
poorly delineated on 2-dimensional angiography.

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Figure 1. Invasive and Noninvasive Imaging Modalities of MB

Select invasive and noninvasive imaging modalities for the anatomic and functional
characterization of MB. The classic finding of MB during invasive coronary
angiography is systolic compression of the tunneled arterial segment with a “step-
down” or “step-up” demarcating the affected area followed by decompression in
diastole that may be complete or partial. Positive findings for each respective imaging
modality are detailed with descriptions of classic and/or pathognomonic findings.
CCTA = coronary computed tomographic angiography; CTFFR = computed tomography
fractional flow reserve; FFR = fractional flow reserve; IC = intracoronary;
iFR = intracoronary wave-free ratio; IVUS = intravascular ultrasound; MB = myocardial
bridging; MPI = myocardial perfusion imaging; OCT = optical coherence tomography;
TTE = transthoracic echocardiography.

IVUS has been used throughout a multitude of studies in the angiographic assessment
of MB. Three-dimensional visualization of the anatomy at the site of MB allows for
accurate measurements of the lumen diameter and vessel wall morphology. The
characteristic finding is a “half-moon” sign, representing an echolucent area present
immediately adjacent to the vessel lumen that persists throughout the cardiac cycle.
Although there has been debate as to the nature of the “half-moon” echolucency,
Yamada et al (45) demonstrated in a cadaveric study using IVUS and histo-
pathological assessment that the echolucency identified by IVUS did indeed represent
a muscle band overlying the tunneled arterial segment. IVUS allows for objective
measurement and quantification of the phasic compression of the tunneled arterial
segment (45). Nonetheless, the key limitation of IVUS in the assessment of MB
revolves around a lack of functional information relating to coronary arterial flow
(Video 1).

Compared with CA, OCT can provide more information about MBs, specifically,
enabling the examination of vulnerable plaque and more detailed observation of the
morphology of the coronary arteries. The resolution of OCT is approximately 10 µm,
approximately 10 times greater than that achieved with standard IVUS systems (46).
Use of OCT may therefore be associated with improved detection and anatomic
characterization of atherosclerotic lesions compared with IVUS. In one series
examining the safety and feasibility of OCT for the detection of MB, varying degrees of
fibrous intimal hyperplasia were seen in the vascular segments immediately proximal
to the MB, but not in the middle and distal arterial segments. Given the focality and
phasic systolic compression of MB, close attention must be paid to ensure that the
proximal and distal portions of the bridge are not missed. Pullback protocols using
both IVUS and OCT risk underestimating the length of MB, particularly if rapid
pullback is performed. This effect may be even more pronounced in bradycardic
patients. Despite its higher resolution, OCT may not be the optimal imaging modality
to detect MB, mainly because of its limited penetration and rapid OCT fiber pullback
and image acquisition (20 mm/s vs 0.5 mm/s in IVUS). OCT can be performed
manually with the fiberoptic lens left stationary in the MB; however, this is not
routinely performed. IVUS is therefore preferred over OCT for the intracoronary
assessment of MB, and should be ideally performed using a slow pullback with
manual technique (Figure 2).
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Figure 2. IVUS and OCT of LAD Myocardial Bridge

(A) IVUS image of LAD myocardial bridging (MB) demonstrating the characteristic
“half-moon” phenomenon (yellow asterisk). (B) OCT demonstrating a mid-LAD MB
heterogeneous signal-poor fusiform area with well-delineated borders (white
asterisk). (C) Coronary computed tomography imaging of a mid-LAD MB (arrow)
overlying a tunneled arterial segment. IVUS = intravascular ultrasound; LAD = left
anterior descending; OCT = optical coherence tomography.

In contrast to CA, IVUS, and OCT, DFW, and pressure wire techniques can be used to
assess MB both functionally and physiologically. MBs are dynamic stenoses,
dependent on the degree of extravascular compression, and it is generally posited that
their assessment should not be limited to anatomic or morphologic characteristics
alone. The introduction of chronotropic or inotropic stressors (whether pharmacologic
or exercise related) into the comprehensive assessment of MBs are of crucial
importance.

An intracoronary DFW involves selective catheterization of the suspected MB segment

with passage of the wire distal to the lesion segment. The characteristic velocity
pattern, termed the “fingertip phenomenon” is observed at the MB segment,
representing 3 distinct phases: 1) rapid early-diastolic flow acceleration; 2) rapid mid-
diastolic deceleration; and 3) a mid-to-late diastolic plateau phase. An additional flow
pattern, consisting of retrograde systolic arterial flow immediately proximal to the
bridged segment, also may be seen. Multiple pharmacologic agents can be used
alongside DFW to simulate the effect of coronary vasospasm or vigorous systolic
myocardial obstruction, including dobutamine, adenosine, or acetylcholine (47).

Fractional flow reserve (FFR) has been widely used for the assessment of MB using a
pressure wire and infusion of adenosine. Although FFR is generally accepted as the
gold standard for the functional assessment of obstructive atherosclerotic plaque, its
use in dynamic MBs is unfortunately inadequate. In fixed stenotic lesions, the
difference between mean and diastolic FFR (dFFR) values has been demonstrated to be
nonsignificant. However, for dynamic obstruction related to MB, the properties of
dFFR present certain theoretical advantages over conventional “mean pressure” FFR
(48). First, the restriction of measurements to diastole avoids the influence of negative
intracoronary gradients on overall pressure measurements, and second, it allows
identification and quantification of the MB on diastolic coronary blood flow. Prior data
from Tarantini et al (49) demonstrated that following dobutamine infusion, when
coronary compression was maximal and patients developed symptoms/ischemic
changes, median FFR did not significantly change. This finding potentially relates to
the artificial reduction in systolic pressure gradients due to distal pressure
overshooting. With this in mind, dFFR has proven to be an overall more sensitive
modality for functional assessment of MB than conventional FFR. An FFR of ≤0.75 has
previously been identified as a cutoff in predicting those likely to have MB-related
ischemia, with similar cutoffs proposed for dFFR (≤0.76). The use of intravenous
dobutamine also has been investigated as a pharmacological adjunct for use during
FFR to increase the strength of myocardial contraction. Prior studies have
demonstrated that the combination of intravenous dobutamine with intracoronary
adenosine can increase the likelihood of unmasking larger diastolic pressure gradients
in MB (45,50). Unfortunately, although conventional FFR has become a ubiquitous
assessment tool across contemporary catheterization labs for the evaluation of fixed
stenoses, the use of dFFR remains cumbersome and time-consuming, and is not
routinely performed in most laboratories.
Instantaneous wave-free ratio (iFR) has been increasingly used in the functional
assessment of MB over the past 5 years. The iFR has numerous benefits that may be
particularly advantageous in the assessment of MB. Namely, it is a diastolic-specific
flow index and it allows for anatomic mapping via coregistration software (iFR scout;
Philips). In a physiological study comparing FFR and iFR for the evaluation of MB, use
of iFR was associated with a significantly higher proportion of positive obstructive
bridges. Under nonhyperemic conditions, the iFR wire is advanced past the MB and
measurement of the diastolic wave-free period is possible, a period in which the
intrabeat microvascular resistance is constant and coronary flow is at its peak. Of note,
iFR has only been formally validated in resting conditions with a cutoff value
considered ≤0.89. The use of a inotropic infusion with iFR to measure MB
hemodynamics in both rest and stress states remains experimental (47). Some centers
have also reported using iFR both pre- and postintervention to demonstrate
normalization of the MB segment after revascularization, although evidence is lacking
to support this approach.

Noninvasive Assessment
Although there is no gold standard for diagnosing MB in vivo, the original definition
and classification was developed using CA. Since then, other modalities have been
used to assess the clinical and anatomic significance of MB. The use of CCTA to
investigate chest pain syndromes has been increasing rapidly. The advantage of CCTA
advantage lies in its high spatial resolution and the ability to easily visualize not only
the coronary artery lumen, but also all surrounding structures in 3 dimensions (51).
This allows accurate assessment of the vessel wall and the surrounding myocardium
as well as the lumen. Using CCTA, the rate of detection of MB has been reported to be
up to 58% (5,52). CCTA is useful for classifying the course of the artery as normal
(within the epicardial fat), superficial intramyocardial, or deep intramyocardial, which
may have ramifications for treatment (4). Superficial and shorter-length MBs are likely
more amenable to PCI. On the other hand, very deep (≥5 mm) or long (≥25 mm) MBs
are presumably better treated with a surgical approach, although data are lacking.

Technical limitations, including reduced temporal resolution, restrict the use of CCTA
in assessing physiological significance of an MB. Typically, a patient undergoing CCTA
receives some combination of beta-blockers, calcium-channel blockers, and/or
ivabradine as well as nitroglycerin (usually sublingual) before scanning. This serves to
improve the quality of the film by prolonging diastasis and inducing vasodilation of
the coronaries. The use of dobutamine and/or exercise to induce the physiologic
milieu in which MBs are most likely to produce symptoms therefore presents a
significant technical challenge. Indeed, some studies exploring the clinical relevance
of MB assessed by CCTA have concluded that MBs cause little to no impairment in
coronary blood flow (13). However, these limitations, as well as patient selection, may
have influenced study results (53). Finally, the use of CCTA is limited by radiation and
contrast exposure. New advances in computational fluid dynamics have increased
with use of CT-derived FFR. Although this has been applied to studying MB, more
research is needed to validate this approach, which may be curbed by some of the
same limitations that apply to both CCTA and classic invasive FFR (54) (Table 1).

Table 1. Diagnostic Imaging Modalities for Myocardial Bridging

Imaging Description Diagnostic Advantages Disadvantages

Modality Criteria

Invasive techniques

Coronary Selective Milking effect • Frequently used • Invasive

angiography catheterization of
• Anatomic • No physiological value
coronary arteries
assessment
with contrast
injection; can be • Quantification of
used with systolic
nitroglycerin compression

Intravascular Selective Half-moon • Identifies • No physiological value

ultrasound catheterization of sign proximal plaque
• May underestimate
coronary arteries
• Quantification of the length of a bridge
with insertion of
arterial if rapid pullback
a probe across
compression and
the lesion of
MLA
interest; allows
for 3D arterial • Identifies negative
visualization arterial
remodeling

Optical Selective Fusiform,

coherence catheterization of signal poor
tomography coronary arteries border with • Identifies • High pullback velocity
and insertion of a systolic proximal plaque and pullback protocols
fiberoptic probe compression risk misidentifying
• Identifies
across the lesion proximal and distal
neoatherosclerosis
MB edges

• Quantification of
• Stationary OCT
MB arc thickness
assessment is not
widely used

Intracoronary Selective Fingertip sign • Functional • Pharmacotherapies

Doppler wire catheterization of evaluation of required
coronary arteries coronary lesions
• Longer procedural
and insertion of a
• Assessment of time
pressure wire
microvascular
across the lesion • Pharmacotherapy side
disease
of interest effects
• Can simulate
• No standardized
dynamic systolic
cutoffs for
obstruction
dobutamine/adenosine
• Endothelial
function testing

Fractional flow Selective FFR ≤0.75 • Functional • Longer procedural

reserve catheterization of evaluation of: time
coronary arteries i) Fixed lesions
• Pharmacotherapies
and insertion of a
ii) Dynamic required (adenosine)
pressure wire
lesions
across the lesion • Pharmacotherapy side
of interest effects
• Widely available

• Diastolic FFR not

commonly accessible
(Pd/Pa may
underestimate
severity)
Instantaneous Selective iFR ≤0.85 • Diastolic-specific • Longer procedural
free wave ratio catheterization of index time
coronary arteries
• Functional
and insertion of a
evaluation of both
wire across the
fixed and dynamic
lesion of interest
lesions

• Adenosine not
mandatory

Noninvasive techniques

Cardiac Contrast- ≥1 mm of • More accurate • Overdetection of

computed enhanced CT myocardium anatomic minor MB may lead to
tomographic allowing for 3D overlying the assessment unnecessary
angiography reconstruction coronary compared with downstream testing
and visualization artery defines CAG
• Relation of symptom
of the coronary “any MB”
• Well validated severity to depth of
arteries ≥2 mm defines
MB unclear
“deep MB” • Shows
≥5 mm defines concomitant
“very deep atherosclerosis
MB”
• Highly sensitive

Computed Contrast- FFR ≤0.75 • Functional • Tested only in patients

tomographic enhanced CT (Gray Zone assessment of with proximal MB
fraction flow with 0.75-0.80) ischemia at rest stenosis
reserve computational
• Requires contrast
fluid dynamics to
injection
estimate
myocardial
stenosis

Single-photon Nuclear imaging Reversible or • No anatomic value

emission test that allows segmental
computed for functional perfusion
tomography myocardial defects during • Physiological • Low spatial resolution
perfusion stress assessment of for subendocardial
imaging functional effect defects
of MB
• Requires radioactive
• Readily available tracer injection

Positron Nuclear imaging Reversible or • Physiological • No anatomic value

emission test that allows segmental assessment of
• Low spatial resolution
tomography for functional and perfusion functional effect
for subendocardial
quantitative defects during of MB
defects
myocardial stress
• Readily available
perfusion • Requires radioactive
imaging tracer injection

Stress Echocardiography Segmental • Physiological • No anatomic value

transthoracic stress imaging hypokinesis assessment of
• Requires ultrasound
echocardiography using ultrasound during stress functional effect
enhancing agent
enhancing agents of MB
to assess for
• Readily available
myocardial
hypokinesis

Cardiac magnetic MRI imaging to Segmental • Physiological • No anatomic value

resonance assess for subendocardial assessment of
• Contrast exposure
imaging segmental perfusion functional effect
myocardial defects during of MB
perfusion defects stress

CAG = coronary angiography; CT = computed tomography; FFR = fractional flow reserve;

iFR = instantaneous free wave ratio; MB = myocardial bridging; MLA = minimal luminal area;
MRI = magnetic resonance imaging; OCT = optical coherence tomography; Pd/Pa = Distal coronary
pressure/Proximal coronary pressure; 3D = 3-dimensional.

Cardiac magnetic resonance imaging (MRI) can also provide anatomic information and
has been used to interrogate MB in the setting of hypertrophic cardiomyopathy (55);
however, its routine use is limited by technical challenges and lack of spatial
resolution (56).

Myocardial perfusion imaging (MPI) is frequently performed to interrogate chest pain

syndromes as well as to assess for ischemia related to MBs. MPI can be performed
using various imaging techniques (single-photon emission computed tomography
[SPECT], positron emission tomography, MRI), as well as various stress protocols (eg,
exercise, dobutamine, adenosine, regadenoson, dipyridamole). In a study of SPECT in
MB, Gawor et al (56) related the amount of ischemia detected to the degree of systolic
luminal narrowing on CA; however, the routine use of MPI has been limited by the
heterogeneity of approaches as well as lower spatial resolution for subendocardial
defects (57).

Stress echocardiography can be helpful in assessing MB. In addition to identifying

reversible stress-induced myocardial hypokinesis in the distribution of the affected
coronary artery, a unique pattern of septal buckling with apical sparing has been
described that is associated with LAD MB (19). This represents a promising
noninvasive avenue for assessing hemodynamic relevance of MB (58). In addition,
studies using echocardiographic strain imaging (speckle tracking) have shown that
hemodynamically significant LAD MB as determined by invasive dFFR have lower
septal longitudinal strain with exercise when compared with matched controls (35)
(Figure 3).
Download : Download high-res image (388KB)
Download : Download full-size image

Figure 3. Angiography, IVUS, and CCTA of a Diffuse Mid-LAD Myocardial Bridge

(A and B) Coronary angiography demonstrating a classic “milking effect” of the LAD

coronary artery. Extrinsic myocardial compression occurs during systole, leading to
luminal narrowing of the tunneled vascular segment (yellow lines). (C and D) IVUS
images of MB (yellow asterisks) corresponding to diastole (C) and systole (D). (E and
F) Coronary computed tomography images of LAD myocardial bridge in diastole (E)
and systole (F) demonstrating systolic compression of the tunneled artery (arrows).
MLA = minimal lumen area; other abbreviations as in Figures 1 and 2.

Management
The treatment of symptomatic MB remains a clinical challenge. Consideration of the
individual patient’s symptoms, coronary and cardiac anatomy, degree of ischemia, and
comorbid conditions (in particular, the presence of CAD, hypertrophic
cardiomyopathy, valvular heart disease, and other cardiomyopathies) is critical, as
these factors may play a large role in the outcomes of patients with MB. There are no
major cardiovascular society guideline recommendations for the diagnosis or
management of MB. Medical management should be considered the initial
therapeutic strategy in the treatment of MB. Close clinical follow-up and risk factor
modification should be emphasized. If symptoms are recalcitrant to maximal medical
therapy, revascularization should be considered with either PCI or surgery, including
coronary artery bypass grafting (CABG) or myotomy. Pre-procedural anatomic
planning with CCTA is critical to guide the revascularization strategy (Central
Illustration).
Download : Download high-res image (1MB)
Download : Download full-size image

Central Illustration. Anatomic Properties of Myocardial Bridging and Overview of

Treatment Modalities

(A) An MB is present when at least 1 mm of myocardium overlies the tunneled arterial

segment. A superficial MB is defined as 1- to 2-mm depth of overlying myocardium. A
deep MB is defined as ≥2 mm of overlying myocardium. A very deep MB is defined
as ≥5 mm of overlying myocardium. A long MB is defined as ≥25 mm of overlying
myocardium. Anatomic and functional imaging are important in defining the bridge
severity and hemodynamic effect if symptoms are present and/or treatment is being
considered. (B) Treatment modalities for symptomatic MB are briefly summarized.
Medical therapy is first line for those requiring treatment. If no improvement in
symptoms despite maximally titrated medical therapy, PCI, CABG, or surgical
myotomy can be considered depending on lesion anatomy, local expertise, and patient
preference. CABG = coronary artery bypass grafting; DES = drug-eluting stent;
MB = myocardial bridging; PCI = percutaneous coronary intervention.

Pharmacologic therapy
For most patients with symptomatic MB, pharmacologic therapy remains the
mainstay of treatment. Although no randomized clinical trial data exist, beta-blockers
are generally considered first-line pharmacologic therapy because of their negative
chronotropic and inotropic effects. Beta-blockers decrease heart rate and thereby
increase diastolic filling time, allowing for decompression of the tunneled segment;
this is in addition to the advantageous reduction in overall sympathetic drive
(10,32,35). Data for this come from pioneering work by Schwarz et al (15), who
revealed that administration of esmolol during atrial pacing reversed a patient’s
symptoms and signs of ischemia during invasive hemodynamic assessment of patients
with symptomatic MB. Some studies have suggested the preferential use of nebivolol
due to its highly B1 selective nature and possible beneficial effects on endothelial
dysfunction (35).

Calcium-channel blockers are also frequently used in the treatment of symptomatic

MB and are preferred in patients with contraindications to beta-blockers such as
bronchospasm. In addition, calcium-channel blockers may have vasodilatory effects
that might be beneficial in patients with concomitant vasospasm (23).

Ivabradine, a specific inhibitor of hyperpolarization-activated cyclic nucleotide gated

channels (f-channels) in the sinoatrial node, may play a role as a second-line agent
due to its ability to lower heart rate. Ivabradine can be considered for patients unable
to tolerate beta-blockers/calcium-channel blockers or those who do not achieve an
adequately controlled heart rate despite maximally tolerated treatment with beta-
blockers/calcium-channel blockers. It is important to note that the use of ivabradine in
MB is off-label and generally should be reserved for those patients with MB also
meeting criteria according to reduced ejection fraction and advanced New York Heart
Association symptoms (59).
Vasodilating agents such as nitroglycerin should be used with extreme caution in
patients with MB. Nitrates have been shown to worsen systolic narrowing on
angiography as well as worsen clinical symptoms (60). This is likely due to
intensifying systolic compression of the tunneled artery and vasodilating coronary
segments adjacent to the bridge, thereby exacerbating retrograde flow (44). Nitrates
also can precipitate reflex tachycardia. However, nitrates have antispasmodic
properties and can decrease preload, which may be useful in the presence of
concomitant coronary vasospasm, if suspected (23).

Finally, MB has been associated with an increased risk of atherosclerosis, especially

proximal to the MB, as discussed (45). Therefore, aggressive cardiovascular risk factor
modification is recommended, and antiplatelet therapy should be considered once
atherosclerosis is detected (10,49).

Percutaneous intervention
The biopathological rationale for the use of PCI in MB is predicated on protecting the
stented arterial segment from systolic compression during exercise and physiological
stress. Randomized data are lacking for the use of PCI in the treatment of MB, and
treatment has been historically reserved for patients who have refractory anginal
symptoms despite optimal anti-anginal therapy (61). Despite this, the use of PCI for
MB is growing in the United States. Although retrospective data have demonstrated
PCI to be hemodynamically effective in MB (15,62), the availability and ease of PCI
probably constitute the key factors for its growing use in MB, rather than robust
clinical evidence (63). PCI has previously been associated with both hemodynamic and
symptom improvements in MB; however, no studies have demonstrated complete
normalization of perfusion defects following stent implantation. In addition, concerns
have previously been raised about the long-term efficacy of PCI strategies for MB.
Registry data examining PCI in MB have previously demonstrated high rates of ISR at 1
year, with rates of ISR of up to 75% for BMS and 25% for drug-eluting stents (DES) (64).
In addition, limited case series have described stent perforation rates of up to 6% in
addition to rare cases of stent fracture and stent thrombosis following PCI for MB
lesions (65, 66, 67). It should be recognized that rates of ISR described in prior studies
may be limited by the preponderance of BMS, first-generation DES, and lack of
intravascular imaging. Although data are needed, the use of high radial strength
second-generation DES combined with accurate stent sizing using intravascular
imaging may potentially improve medium- to long-term outcomes in PCI for MB.

From examining the available retrospective evidence comparing BMS with DES for the
treatment of MB, there are 2 key conclusions. First, BMS have significantly higher rates
of target vessel revascularization compared with first-generation DES, and second,
stent implantation in patients with symptomatic MB risks high rates of early ISR
potentially related to bridge-associated luminal narrowing. The ideal stent for PCI in
MB is a high radial strength drug-eluting platform. An everolimus-eluting platinum
chromium second-generation DES has recently been developed demonstrating
exceptional radial strength compared with cobalt alloy and stainless-steel platforms
(68,69). Future-generation stents may potentially achieve even greater safety profiles
related to their ability to better tolerate radial stress forces from cyclical systolic
compression. Protection of the stented vascular segment during endothelialization
may theoretically result in greater luminal gain, therefore potentially providing more
durable long-term results.

Bioresorbable stent platforms should generally be avoided given their lack of radial
strength. A “temporary” bioresorbable vascular scaffold that disappears over time was
initially considered an attractive therapeutic target given the ability to assess for
symptom improvement without committing a patient to the risks of mechanical
failure and ISR associated with metallic stent scaffolds. It was subsequently observed
that compression from the bridge appears to crush the scaffold as it loses integrity
during the process of resorption. Future bioresorbable scaffolds may be designed with
enough upfront radial strength to achieve greater luminal gain and allow for
formation of a thin fibrous endoluminal layer that withstands systolic compression
during the resorption phase. Whether scaffolds with these biomechanical properties
can be developed and withstand the scrutiny of angiographic and outcome studies
remains to be seen (70).

Taken together, there are currently no randomized data to guide the use of PCI versus
medical management in patients with symptomatic MB. Most reported complications
associated with PCI in MB have involved bare-metal or first-generation drug-eluting
scaffolds, thus significantly limiting the contemporary interpretation of these results
in the era of second-generation DES. Importantly, if treatment with coronary stenting
is planned, dobutamine challenge may be beneficial in the accurate sizing of stent
length so as to avoid incomplete coverage of the MB, which can be hazardous (63). A
second-generation DES with high radial strength should be used to maximize
resistance from cyclical systolic compression.

Given the primary concerns of ISR and stent fracture, we support the usage of these
second-generation platforms to further mitigate risk. To ensure optimal deployment
within the tunneled segment, stent inflation should be performed toward the
recommended pressure limit (10,24). Oversizing of the stent should similarly be
avoided to prevent severe complications, such as coronary perforation. There exist no
data regarding the optimal choice of dual antiplatelet therapy following PCI for MB.
Therefore, the choice of P2Y12 inhibitor is operator dependent, typically reflecting dual
antiplatelet therapy guidelines for the presenting syndrome (stable angina vs ACS).

Surgical treatment
Surgery is an effective, although invasive, treatment for symptomatic MB refractory to
maximally tolerated medical therapy. Surgical options for MB include CABG or supra-
arterial myotomy, also known as “unroofing.” CABG can be completed on or off
cardiopulmonary bypass using either arterial or saphenous vein grafts. Most
commonly, LAD MBs are bypassed using the left internal mammary artery (LIMA),
although there is some evidence to suggest that a saphenous vein graft may be
preferable in some cases (71). Complications of CABG have been well described, but in
the case of MB, the chief concern is graft failure, likely due to competitive flow (72,73).
To date, the largest retrospective study examining bypass grafting with LIMA to LAD
for MB demonstrated very high rates of arterial graft failure. Overall, only 10% of
arterial grafts were patent with competitive flow at 18 months, with 60% of grafts
demonstrating complete occlusion. Saphenous vein grafts, on the other hand,
demonstrated patency rates of almost 80%. A novel technique, “myocardial bridge
bypass grafting,” in which a free LIMA is anastomosed to the LAD proximal and distal
to the MB, has been recently described but requires further study (74).

In a myotomy, the surgeon carefully dissects the artery from the overlying
myocardium. This can be performed on or off pump, and recently has been successful
in selected cases via mini thoracotomy foregoing traditional sternotomy (75). Potential
complications include ventricular wall perforation (usually of the right ventricle with
an LAD MB and deep endomyocardial course), artery perforation, ventricular
aneurysm formation, incomplete unroofing, and postoperative bleeding.

Recently, there has been increased interest in myotomy, in both pediatric and adult
patients (75, 76, 77, 78). Myotomy has the advantage of relieving the upstream
pathophysiologic abnormality and therefore is an attractive treatment option.
However, as Hemmati et al (76,77) point out, there is a high incidence of late recurrent
chest pain after successful myotomy in adult patients, up to 60% at 3-year follow-up.
This is perhaps related to endothelial dysfunction attributable to the MB that persists
even after relief of MB compression (76,77). Therefore, myotomy may be best suited
for a pediatric population that has had less time to develop sequelae of MB.
Interestingly, IVUS examination of pediatric patients undergoing myotomy for
refractory symptomatic MB showed atherosclerotic plaque proximal to the tunneled
segment, even though the average patient age was only 15.6 years (28,78). Overall,
myotomy has been shown to be a safe and effective treatment for symptomatic MB,
especially with favorable anatomy (nontortuous artery, shorter and more superficial
intramyocardial course), thorough preoperative planning, and when performed at an
experienced center.

There is limited evidence comparing CABG to myotomy for the treatment of

symptomatic MBs. CABG has previously been favored over myotomy in cases of
extensive (>25 mm) or deep (>5 mm) myocardial bridges, or when the coronary
segment fails to decompress completely in diastole; however, there are few data to
guide this recommendation. In a recent observational study of CABG vs myotomy, Ji
et al (79) describe 54 patients who underwent surgery for symptomatic MB (31
myotomy, 23 CABG); 41% of the patients with CABG met criteria for a major adverse
cardiovascular event vs 7% in the myotomy group. On follow-up CCTA, 9 of the 23
patients who underwent LIMA to LAD grafting experienced graft failure. Notably, all 10
patients who were found to have >50% proximal stenosis on preoperative angiography
and subsequently underwent CABG were found to have patent grafts on follow-up
(79). This further supports competitive flow as a major factor contributing to bypass
graft patency in MB. The choice of surgical treatment should use an individualized
approach that considers the patient’s anatomy, clinical characteristics, and available
surgical expertise. In cases in which CABG is planned for the upfront treatment of MB,
saphenous venous grafting should be considered (80).

Therapeutic Strategy
Based on the available evidence and expert experience, we propose the following
management strategy for symptomatic MB. For patients without clinical symptoms,
therapeutic focus should be on risk factor modification, including appropriate
treatment of concomitant CAD, and relief of potential triggers. For patients with
clinical symptoms, objective signs of ischemia, and/or abnormal intracoronary
hemodynamics (iFR or dFFR with dobutamine challenge as the preferred modalities),
pharmacologic treatment should be initiated beginning with beta-blockers and/or
calcium-channel blockers. Vasodilators, such as nitrates, should generally be avoided
in all but very rare cases associated with significant vasospasm. Frequent outpatient
monitoring for clinical improvement and up-titration of oral medical therapies are
key. Similarly, consideration of other causes of angina with normal coronary arteries,
such as microvascular dysfunction, are important to rule out.

If symptoms persist despite maximally tolerated medical therapy, an interventional

option should be considered. For most patients, we suggest PCI as the upfront
interventional strategy. Noninvasive imaging with CCTA should be considered before
revascularization to assess the length, depth, and anatomic characteristics of the MB.
PCI offers a less invasive, effective option for relief of symptoms and improvement in
intracoronary hemodynamics (14). Specific factors favoring the use of PCI in MB
include shorter lesion length and more superficial depth (<2 mm) of the tunneled
segment. Deep or long MB, particularly those that cannot be addressed with a single
stent, should prompt an assessment for surgical revascularization. Although PCI of MB
has been associated with reports of stent fracture, stent thrombosis, and perforation
during stent deployment, we believe that these concerns can be reliably mitigated
using second-generation DES, accurate stent sizing aided by detailed intravascular
imaging, and preferential use of high radial strength platforms (65, 66, 67). PCI of MB
also has been associated with increased risk of ISR (64). Although the use of DES
decreases rates of TLR compared with BMS, restenosis still likely occurs more
frequently with PCI for MB than for atherosclerotic lesions. In the event of ISR
requiring TLR due to persistent symptoms refractory to medical management, we
suggest pursuing CABG. This strategy has several advantages. First, the bypass graft is
likely to be successful and durable given the lack of competitive flow from the
proximal ISR. Second, it uses widespread expertise and experience in PCI and CABG
and is therefore more accessible. Third, initial PCI can serve as a “trial” to see if
improvement in intracoronary hemodynamics leads to symptomatic relief. It is
clinically challenging to pinpoint the etiology of a patient's symptoms in many cases,
even with evidence of ischemia on noninvasive testing or abnormal intracoronary
hemodynamics. This sequence of treatments increases the likelihood that any surgical
intervention will definitively address the patient’s symptoms (Figure 4).
 MyocardialBridging

FunctionalImaging
Asymptomatic Symptomatic (Intracoronaryor
Noninvasive)

•RelieveTriggers MedicalTherapy
•RiskFactorModification •Beta-Blocker
•SmokingCessation •Calcium-ChannelBlocker
•AntiplateletsforCAD DoseIncrease
•TrialStoppingNitrates Close
•AvoidPureVasodilators
Follow-up
•RiskFactorModification
Follow-up
•AntiplateletsforCAD

ClinicalImprovement
CoronaryCTA
+ Procedural
Planning

Shorter/SuperficialMB
Longer/DeeperMB

RoutineMonitoring
PCI Myotomy* CABG

ClinicalImprovement

Download : Download high-res image (624KB)

Download : Download full-size image

Figure 4. Management Algorithm for Asymptomatic and Symptomatic MB

Flow diagram with proposed strategy for the management of asymptomatic and
symptomatic MB. Triggers include coronary vasospasm, smoking and stimulants
(cocaine), physiological stress, poor functional exercise reserve. ∗Surgical myotomy
should be considered as a first-line therapy if performed at an experienced myotomy
center and if favorable anatomy is present. CABG = coronary artery bypass grafting,
CAD = coronary artery disease; CTA = computed tomography angiography;
MB = myocardial bridging; PCI = percutaneous coronary intervention.

Alternatively, myotomy can be considered as the first-line interventional strategy in

selected cases. Patient selection should focus on favorable anatomy, including a
nontortuous affected artery with a superficial and shorter intramyocardial course, and
younger patient age, including pediatric patients. Myotomy is best performed at a
center with high-volume experience to avoid complications related to challenging
anatomy (ie, dense adhesions from prior sternotomy, right ventricle overlying the LAD,
MB abutting the right ventricular outflow tract) (75). Thorough preoperative
assessment with IVUS and CCTA may be helpful in avoiding complications during
myotomy (81).

Conclusions
MB is a common congenital anomaly encountered frequently in clinical practice.
Although generally benign, consideration should be given to identifying and treating
the subset of patients with symptomatic disease. Noninvasive imaging techniques
such as CCTA have greatly improved the anatomic characterization of MB, and
intracoronary hemodynamics (iFR, dFFR) have improved our ability to characterize
symptoms producing MB. In symptomatic patients, medical therapy is usually an
effective option. For those failing medical therapies, multimodality anatomic and
hemodynamic characterization may aid in guiding safer revascularization. PCI as the
favored revascularization technique allows for confirmation of the MB as the
symptom-producing lesion, in addition to advantageous hemodynamics for CABG in
the event of stent-related complications. Myotomy should be considered in patients
with favorable intramyocardial anatomy at experienced, high-volume MB centers.
Additional research is needed to better identify patients in whom MB is pathologic.
Randomized trials and long-term registry data are required to define the natural
history, patient selection, and optimal treatment strategies for MB.

Funding Support and Author Disclosures

Dr Sharma has received consultant fees from Abbott Vascular, Boston Scientific, and
Cardiovascular Systems, Inc. All other authors have reported that they have no
relationships relevant to the contents of this paper to disclose.

Appendix
Download : Download video (2MB)

Supplemental Video 1. Intravascular Ultrasound of Left Anterior Descending Coronary

Artery Myocardial Bridge. Intravascular ultrasound is performed using a slow, manual
pullback technique to ensure accurate approximation of the proximal and distal edges
of the myocardial bridge. A characteristic “half-moon” phenomenon is visualized
representing an overlying myocardial bridge.

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Listen to this manuscript's audio summary by Editor-in-Chief Dr. Valentin Fuster on JACC.org .
 Mahboob Alam, MD, served as Guest Associate Editor for this paper.

Christie M. Ballantyne, MD, served as Guest Editor-in-Chief for this paper.

The authors attest they are in compliance with human studies committees and animal welfare
regulations of the authors’ institutions and Food and Drug Administration guidelines, including
patient consent where appropriate. For more information, visit the Author Center .

∗ Drs Sternheim and Power contributed equally to this work.

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