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Morphological features in myocardial bridging

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Rom J Leg Med [18] 163 170 [2010]
DOI: 10.4323/rjlm.2010.163
2010 Romanian Society of Legal Medicine

Morphological features in myocardial bridging

Dan Dermengiu1*, Iason Vovolis2, Sorin Hostiuc3,George Cristian Curc4,


Mugurel Constantin Rusu5, Lcrmioara Luca3

____________________________________________________________________________
Abstract: Myocardial bridging is a common coronary anomaly characterized by the presence of a muscle bridge
above an epicardial artery. Although its involvement in the development of severe cardiovascular pathologies is disputed
there are many proofs that it may possibly be associated, in particular circumstances, with sudden cardiac death, the
development of malignant arrhythmias, atherosclerosis, myocardial infarction, hibernation or stunning, etc. The
development of cardiovascular complications is mainly dependent upon the presence of a significant hemodynamic
obstruction. In order for a myocardial bridging to determine such an obstruction it must present some specific
morphological characteristics which we will present in this article.
Key words: Myocardial bridging, Sudden cardiac death, Cardiovascular pathologies

A though myocardial bridging is a common coronary anomaly, with a prevalence in general


population averaging 30% (with limits from below 1% [1-3] obtained in angiography
series to 86% [4] obtained in anatomical studies) its cardiovascular consequences are still disputed.
Various studies revealed an association between myocardial bridging and sudden cardiac death [5-17],
myocardial infarction [18-31], arrhythmias [27, 32-33], myocardial ischemia [10, 15, 32, 34-48],
myocardial stunning [20, 32, 37, 49-50], myocardial hibernation [32, 37], etc. The incidence seems
higher in patients with hypertrophic cardiomyopathy (CMH); children with CMH and MB seem to
have an increased risk of increased QTc dispersion, myocardial infarction and sudden cardiac
death[17]; in adults, although in association with HCM MB is proportionally more frequent, the
cardiovascular consequences are uncertain. Although empirically men seemed more predispose to MB
than women, clinica studies couldnt find significant differences; by analyzing however seven studies
together and cross tabulating their results a significant difference was found (Chi square value of 7.44,
in the 95 confidence interval with a p value of 0.006, see Table 1).

Myocardial bridging position


The most frequent location of MB is on the left anterior descending artery (anterior
interventricular artery AIVA). Anatomic studies depicted a medium incidence of AIVA MB ranging
around 58% (data obtained by computing the results from [4, 36, 52-54, 56-63] (Figure 1) whilst
angiographic studies revealed an incidence of over 98% (data obtained by computing the results
obtained from [1, 17, 60, 64-73]. Data obtained from MSCT varies - 16-section MSCT has results
closer to angiography while 64-section MSCT is closer to anatomical studies. Myocardial fibers
covering AIVA originate from the pulmonary infundibulum and cross the artery on a perpendicular
________________________
*1) Corresponding author; Professor, MD, PhD, National Institute of Legal Medicine Mina Minovici,
Sos. Vitan Birzesti 9, Sector 4, 042122 Bucharest, Bucharest, Romania, e-mail: danderme@legmed.ro
2) University of Medicine and Pharmacy Carol Davila
3) MD, National Institute of Legal Medicine Mina Minovici, Bucharest
4) Associate Professor, MD, PhD, Chair of Legal Medicine, University of Medicine and Pharmacy Carol Davila
5) MD, PhD, PI, Senior Lecturer, Chair of Anatomy, University of Medicine and Pharmacy Carol Davila
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Dermengiu D et al Morphological features in myocardial bridging

course. The medium width of the myocardial bridge is around 2-3 mm[4, 55, 74-75], higher in
particular subgroups (hypertrophic cardiomyopathy, cases of sudden cardiac death, etc.); medium
length is about 10-30 mm[15, 74], and usually the bridging is located in the middle third of the AIVA,
more than half the cases analyzed by [1, 17, 55-56, 58, 60-61, 69, 71, 73, 76] being located here (see
Figure 2).

Myocardial bridging on the right coronary (Figure 3) and left circumflex artery (Figure 4) are
only rarely described in angiographic
Study Men Women studies; anatomical studies found them in
T P T P about 15% of MB cases (RCA) and 6%
Fereirra[51] 56 32 34 18 (LCx). These results may underestimate
Bellesteros Acuna[52] 125 54 29 8 the true incidence of these bridges, the
Bezerra[36] 30 25 20 14 main reason being related to their width,
Kosinski[53] 59 25 41 16 much smaller than the ones on AIVA or its
Reig[54] 10 10 2 2 branches, making them harder to identify.
Konen[55] 107 32 11 4 Usually these bridges are super-
Ishi[56] 345 165 297 105 ficial, with minimum hemodynamic
Total 732 343 434 167 impact, the origin of the fibers being atrial
Chi Square (Yates) 7.44 P=0.0063 myocardium.
Table 1. Sex ratio in various studies: T total number of cases; P
positive cases
Other branches, like the diagonal,
the obtuse marginal, etc., account for 19% of all MB cases. Often branches located on the free margin
of the left ventricle plunge into the myocardium, take a direction parallel with myocardial fibers and
never resurface [74].

Myocardial bridging width


Depending on its width MB was usually classified as superficial (Figure 5) and deep (Figure 6)
[51]; Fereirra described these two variants on the AIVA only a MB is superficial if AIVA runs
within the interventricular groove and is crossed perpendicularly or at an acute angle by the bridged
fibers and deep if the AIVA was deviated towards the right ventricle, is deeply situated within the
interventricular septum and is crossed helically, obliquely or transversally by longitudinal fibers
originating from the right ventricle and inserting into the interventricular septum [51].
Mohlenkamp updated this classification by adding incomplete myocardial bridging as a third
type, defined by the presence of a tunneled artery covered partially by myocardial fibers and partially
by fatty, fibrous or nervous tissue; this type can cause systolic compression and determine myocardial
ischemia [77] and is somehow similar to the myocardial loops described by von Polacek [4].
Other authors relied more on MB width to differentiate superficial from deep MB Jodocy for
example gave as a cut-off value for deep MB a width of two millimeters [78]; although these two
definitions of superficial/deep MN are similar they are not identical as sometimes a deep Fereirra MB
can have less than two millimeters and vice versa. Konen has united Ferreira and Jodocy variants and
classified MB in superficial, deep and right ventricular types [55], whilst other described a fourth type,
intracavitary or subendocardial coronary artery (Figure 7) [9, 79-83].
First description of an intracavitary coronary artery was made by McAlpine in 1975 who
described both intracavitary AIVA (into the right ventricle) and RCA (into the right atrium) [84]. First
case of subendocardial LCx/LCx branch was described by Dermengiu et al. who identified a
subendocardial sinus node artery originating from the LCx [9]. Oschner found the incidence for
intracavitary RCA to be 0.09% and for intracavitary AIVA 0.2% [79].
The intracavitary LAD usually enters the right ventricle close to its origin, in an acute angle
and reemerges after a long intramyocardial and subendocardial loop [79, 81]. RCA enters the right
atrial myocardium in an acute angle, makes a subendocardial or intracavitary loop of about 1.5-3

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centimeters and then resurfaces [83-84]. A study realized on 100 cases found 29 intramyocardial
branches from the RCA, suggesting a much higher occurrence of this variant than was believed
previously [83].
As possible explanations are cited the thickness of the atrial myocardium and a higher origin
for the coronary artery [83].
For the current clinical use, Jodocy variant seems more useful and easier to determine; also, it
can be used in other MB locations. A deep MB is usually considered to have the potential to determine
significant hemodynamic effects and be
associated with sudden cardiac death.
Morales for example separated his MB
cases in two subgroups with and without
myocardial fibrosis in the group with
myocardial fibrosis medium MB width
was 3.8 +/- 1.8 mm and SCD was present
in 13 out of 19 cases whilst in the groups
without myocardial fibrosis medium MB
width was 1.9 +/ 0.9 mm. and there was no
SCD case [47, 85].

Myocardial bridging length


The length of a typical MB is
usually within the 10 to 30 mm range, only
rarely exceeding 40 mm (Figure 3). A Fig. 1. Location of Myocardial Bridging (AIVA anterior
interventricular artery, LCx left circumflex artery, RCA right
longer MB seems to be associated with coronary artery, RI Ramus intermedius)
more significant hemodynamic effects, and
more severe clinical symptoms. For example Feldman [86] found, by increasing the length of a
coronary obstruction and maintaining constant the resting and reactive hyperemic flow, the pressure
gradient between aorta and the distal coronary artery to be increased; therefore a smaller dynamic
stenosis can be associated with increased hemodynamic effects during at rest and reactive hyperemia if
the length of the stenotic segment is increased. Other authors however couldnt find a correlation
between MB length and the severity of cardiac symptoms[69]. Typically longer bridges thicker and
situated more closer to the origin [51, 87].

Myocardial Bridging angle


The angle between the direction of
myocardial fibers and that of the tunneled coronary
artery depends upon the direction of the coronary
artery and the distribution of the bridged myocardial
fibers.
According to Baptista [57] average angle
values () were: for AIVA 81.5 degrees (range 400-
900), for AIVA branches 400 (range 10-900), PIVA
(posterior interventricular artery) 600 (range 400-
800), left marginal 100 (range 10-200), and ramus
diagonalis 430 (range 300-600).

Fig. 2. Myocardial Bridging location on AIVA During systolic contraction the most
important hemodynamic effect is obtained during the
perpendicular shortening over the tunneled artery. If the bridging is perpendicular on the tunneled
artery the effect is dependent upon the difference between diastole and systolic length of the
myocardial fibers. If the bridge is not perpendicular on the tunneled artery the effect is dependent upon

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Dermengiu D et al Morphological features in myocardial bridging

the difference between diastole and systolic length of the myocardial fibers multiplied with the sinus
of the angle made by the direction of the artery and the bridge (lsin) (Figure 8). Even though a
correlation between the angle and clinical symptoms/morphological signs wasnt yet researched, the
fact that the highest angle is associated with the location where MB is correlated with the most severe
signs/symptoms (AIVA) might suggest a possible correlation. Specific studies are needed to clarify
this problem.

Coronary intima
Intima of the tunneled artery has different
characteristics before, below and after the bridge.
Before the bridge the medium width of the intima is
about 406.6 m while under the bridge is about 66
m. Endothelial cells have a helical orientation
(associated with a laminar blood flow and a high
endothelial shear stress under the bridge and
polymorph, flat or polygonal shapes before the
bridge (shapes associated with low endothelial shear
stress); the latter are associated with increased
mitotic and apoptotic activity, increased MMP-2 and
MMP-9 synthesis, increased gap junctions, etc., all
pro-atherosclerotic factors. Intimal hyperplasia and
atherosclerosis are the landmarks of a
hemodynamically significant myocardial bridging in
the proximal area whilst in the distal part coronary
hypoplasia and decreased atherosclerotic disease are
the most common.
Fig. 3. Myocardial bridging on the posterior inter-
Atherosclerosis and Myocardial Bridging ventricular artery (PIVA), a branch from the right
The presence of a myocardial bridge was coronary artery.
shown to suppress atherosclerosis below the obstruction site [56, 87-89], irrespective of serum
cholesterol and blood pressure. The main cause seems to be the development of a dynamic obstruction
which proximally decreases endothelial shear stress and subsequently favors various metabolic
pathways involved in atherogenesis [90], although other factors like increased proximal wall stress or
coronary geometry can be involved as well [91].
Under and below the bridge on the other side atherosclerosis occurs rarely, due to a decreased
tensile stress, increased endothelial shear stress and decreased wall motion during the cardiac cycle
[92]. There are a few studies dealing specifically with the association between atherosclerosis and
myocardial bridging; for example La Grutta found proximal intima to be without atherosclerosis in
33%, with positive remodelling in 27%, with stenosis less than 50% in 20% and with stenosis more
than 50% in 20% of cases; distally atherosclerosis was absent in 84%, positive remodelling in 11%,
stenosis less than 50% in 3% and stenosis more than 50% in 2% [93].
Hsu, by inducing atherosclerosis on rabbit models (whose coronaries are entirely
intramyocardial) found that, even if severe atherosclerotic lesions were developed on the aorta and
other major vessels, the intramyocardial parts of the major coronary arteries were free of it [74].
Ishikawa found that atherosclerosis was more pronounced proximally, has a predilection for extension
towards the coronary ostium, augments the natural history of MB, and is a predisposing factor for
myocardial infarction [87].
Atherosclerosis under/below the bridge normally occurs in two situations: the presence of a
highly atherogenic state (e.g. congenital or acquired defects of cholesterol or plasma lipoproteins) or a
superficial/incomplete bridge without significant hemodynamic consequences. For example, Ishi found
the extent of athero-sclerotic lesions on the right coronary to be greater compared to the left anterior

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descendent in cases of myocardial bridging (RCA bridges are usually more superficial and with less
hemodynamic impact); in the general population atherosclerotic lesions on the AIVA are more
frequent than the ones found on the RCA [56].

Fig. 4. Deep LCx myocardial bridging Fig. 5. Superficial myocardial bridging on the anterior
interventricular artery

Fig. 6. Deep myocardial bridging on the ante- Fig. 7. Subendocardial sinus node artery, origina-ting
rior interventricular artery: PT pulmonary from the left circumflex artery
trunk, CxA circumflex artery, LCA left
coronary artery

Myocardial fibers
There seem to be significant differences within the myocardial structure between samples taken
from the bridging, areas vascularized by tunneled coronaries, and the rest of the myocardium. The
nuclei from bridged myocardial fibers are always smaller than the ones corresponding to myocardial
fibers from other places, suggesting that the mechanical response of these fibers is significantly
distinct, probably due to a heterogenous stretching overload determined by the particular circum-

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Dermengiu D et al Morphological features in myocardial bridging

stances of the bridge an isolated band of cardiomyocytes without circumferential contact with other
myocardial fibers leads to a reduced response to mechanical overload [54].
By comparing the characteristics of the myo-
cardium vascularized by a tunneled artery versus
myocardium vascularized by a non-tunneled artery
interstitial fibrosis, interstitial edema and hypoxia are
more severe in cases with bridging (personal,
unpublished data); these results are similar to the
ones obtained by other authors: Brodsky for example,
comparing hearts with and without MB found a
significantly increased interstitial fibrosis in samples
Fig. 8. Fibers perpendicular on the tunneled artery
obtained from the anterior wall of the left ventricle as
compared with equivalent samples from cases without MB[94]. A quantitative computerized analysis
found interstitial fibrosis to be 33% more severe in patients with myocardial bridging (significant,
p=0.0006) [94].
Theoretically, for the same systolic myocardial fiber shortening (l) the greatest effect is
obtained when the fibers are perpendicular on the tunneled artery; if the fibers are not perpendicular
the effect is equal to lsin.

Acknowledgement
This work was supported by CNCSIS UEFISCSU, project number PNII IDEI 2642/2008.

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