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SECTION 1 Pathophysiology and investigation ofcoronary artery disease28
H-thymidine incorporation (cpm/10
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* *
1400
cells)
1200
5
1000
800
*/**
600
400
200
3
0
Control Stretch
Internal mammary artery Saphenous vein
Control Stretch
Fig.3.6.8 Effects of pulsatile stretch on vascular smooth muscle cells obtained from the internal mammary artery or saphenous vein. Proliferation
of smooth muscle cells (left) is quantified by 3H- thymidine incorporation (right). Note the much more pronounced proliferative response of vascular
smooth muscle cells of the saphenous vein (grey squares) compared to those of the mammary artery (open squares). * P < 0.05 saphenous vein versus
internal mammary artery; ** P <0.05 saphenous vein stretch versus saphenous vein control.
Reproduced from Lüscher T, Predel H, Yang Z, Bühler F, von Segesser L , Turina M.Implications of pulsatile stretch on growth of saphenous vein and mammary artery smooth muscle.
The Lancet. 1992;340(8824):878– 9 with permission from Elsevier.
trial used an ex vivo transfection of harvested vein gras with an
E2F decoy oligonucleotide and showed a 70– 74% decrease in the
level of proliferating cell nuclear antigen (PCNA) and c- myc mRNA
expressed by the smooth muscle cells in the vein. However, this did
not translate into improved clinical endpoints in a large randomized
controlled trial. More eective transfection of a biologically crucial
gene such as NOS3 using an adenovirus or novel transfection techniques available such as CRISPR may provide greater benet and
should be further tested in clinical trials.
REFERENCES
1. Loop FD, Lytle BW, Cosgrove DM, Stewart RW, Goormastic M,
Williams GW, etal. Inuence of the internal- mammary- artery
gra on 10- year survival and other cardiac events. N Engl J Med.
1986;314(1):1– 6.
2. Li XN, Stulz P, Siebenmann RP, Yang Z, Lüscher TF. Dierent
eects of activated platelets in the right gastroepiploic and internal
mammary arteries. Implications for coronary artery graing. J
orac Cardiovasc Surg. 1992;104(5):1294– 302.
3. Yang Z, Siebenmann R, Studer M, Eglo L, Lüscher TF. Similar
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endothelium- dependent relaxation, but enhanced contractility,
of the right gastroepiploic artery as compared with the internal
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Biological properties of bypass gras critically determine their function when implanted into the coronary circulation. Both the biology
of endothelial and smooth muscle cells of venous and arterial gras
markedly dier, explaining the remarkable dierences in their patency rates and associated clinical outcomes. Genetic engineering
of venous bypass tissue according to the expression prole of mammary arteries may be a promising approach to prevent venous bypass gra failure in the future.
4. Lüscher TF, Vanhoutte PM. e endothelium:modulator of
cardiovascular function. Boca Raton, FL:CRC Press; 1991.
5. Lüscher TF. Vascular biology of coronary bypass gras. Coron
Artery Dis. 1992;3(2):157– 65.
6. Yang Z, Diederich D, Schneider K, Siebenmann R, Stulz P,
Von Segesser L, etal. Endothelium- derived relaxing factor
and protection against contractions induced by histamine and
serotonin in the human internal mammary artery and in the
saphenous vein. Circulation. 1989;80(4):1041– 8.
Acknowledgments
Original data by the author reported in this book chapter have
been supported by the Swiss National Research Foundation and
the Foundation for Cardiovascular Research (Zurich Heart House,
Zurich, Switzerland).
7. Yang Z, Von Segesser L, Bauer E, Stulz P, Turina M, Lüscher T.
Dierent activation of the endothelial L- arginine and cyclooxygenase
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8. Seo B, Oemar BS, Siebenmann R, Von Segesser L, Lüscher T. Both
ETA and ETB receptors mediate contraction to endothelin- 1 in
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9. Dohi Z, Hahn A, Boulanger C, Lüscher T. Vascular renin
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10. Forstermann U, Sessa WC. Nitric oxide synthases:regulation and
function. Eur Heart J. 2012;33(7):829– 37.
11. Lüscher TF, Diederich D, Siebenmann R, Lehmann K, Stulz P,
von Segesser L, etal. Dierence between endothelium- dependent
relaxation in arterial and in venous coronary bypass gras. N
Engl J Med. 1988;319(8):462– 7.
12. Yang ZH, Stulz P, von Segesser L, Bauer E, Turina M, Lüscher
TF. Dierent interactions of platelets with arterial and venous
coronary bypass vessels. Lancet. 1991;337(8747):939– 43.
13. Yang Z, Arnet U, Bauer E, von Segesser L, Siebenmann R, Turina
M, etal. rombin- induced endothelium- dependent inhibition
and direct activation of platelet- vessel wall interaction. Role of
prostacyclin, nitric oxide, and thromboxane A2. Circulation.
1994;89(5):2266– 72.
14. Joannides R, Haefeli WE, Linder L, Richard V, Bakkali EH,
uillez C, etal. Nitric oxide is responsible for ow- dependent
dilatation of human peripheral conduit arteries in vivo.
Circulation. 1995;91(5):1314– 9.
15. Payeli SK, Latini R, Gebhard C, Patrignani A, Wagner U,
Lüscher TF, etal. Prothrombotic gene expression prole in
vascular smooth muscle cells of human saphenous vein, but
not internal mammary artery. Arterioscler romb Vasc Biol.
2008;28(4):705– 10.
16. Sims FH. e pathology of the internal thoracic artery and its
contribution to the study of atherosclerosis. In:Green GE, Singh
RN, Sosa JA, eds. Surgical revascularization of the heart:the
internal thoracic arteries. NewYork, NY:Igaku- Shoin; 1991,
pp. 18– 62.
17. Yang Z, Oemar BS, Carrel T, Kipfer B, Julmy F, Lüscher TF.
Dierent proliferative properties of smooth muscle cells of
human arterial and venous bypass vessels role of PDGF receptors,
mitogen- activated protein kinase, and cyclin- dependent kinase
inhibitors. Circulation. 1998;97(2):181– 7.
18. Lüscher T, Predel H, Yang Z, Bühler F, von Segesser L,
Turina M. Implications of pulsatile stretch on growth of
saphenous vein and mammary artery smooth muscle. Lancet.
1992;340(8824):878– 9.
19. Largiader T, Eto M, Payeli SK, Greutert H, Viswambharan H,
Lachat M, etal. Endothelial nitric oxide synthase gene transfer
inhibits human smooth muscle cell migration via inhibition of
Rho A. J Cardiovasc Pharmacol. 2008;52(4):369– 74.
20. Tanner FC, Largiadèr T, Greutert H, Yang Z, Lüscher TF. Nitric
oxide synthase gene transfer inhibits biological features of bypass
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Surg. 2004;127(1):20– 6.
21. Mangi AA, Dzau VJ. Gene therapy for human bypass gras. Ann
Med. 2001;33(3):153– 5.
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randomised, controlled trial. Lancet. 1999;354(9189):1493– 8.
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4
Anomalous coronaryarteries
Chin Siang Ong, Ronald K. Binder, Marshall L. Jacobs, and Duke E. Cameron
Introduction
blood ow to the anterior interventricular septum and may give rise to
diagonal branches, which supply the anterior and lateral free wall of the
Coronary artery anomalies have been recognized since antiquity
and were described in various anatomical treatises by Renaissance
scholars.– In the mid- 1970s, the clinical signicance of anomalies
of coronary artery origin and course with respect to sudden death
was appreciated, and the rst successful surgical unroong procedure was performed.
le ventricle. e circumex artery (CX) provides blood to the lateral
and posterior le ventricular free wall by its marginal branches.
In 50% of the general population separate origins of the RCA and its
conal branch are observed. While in most people the LAD and CX arise
from the le main coronary artery (LMCA) which originates from the
le aortic sinus, 1% show separate ostia of the LAD and CX without a
distinct LMCA. In 20% of the population the LMCA divides into three
Embryology
branches:the LAD, the CX, and an intermediate branch which is located
between the other two and supplies the le ventricular lateral free wall.
e origin of the posterior descending artery denes the domin-
During fetal development, the coronary vasculature is formed from
three elements:coronary buds from the aortic sinus, sinusoids, and
the in situ vascular endothelial network. Initially, the sinusoids communicate with the heart cavities in the loosely packed myocardium,
but later disappear as the myocardium becomes more compact.
Incomplete involution of the sinusoids leads to coronary artery stulae that connect to the heart chambers. e myocardial vascular
endothelial network which is initially connected with other medi-
ance of the coronary artery tree. Most people (85%) exhibit a right
dominant system in which the posterior descending artery arises
from the distal RCA. In 10% the posterior descending artery stems
from the CX (le dominant) and in around 5% both the RCA and
the CX supply the inferior septum (codominant system).
In two- thirds of cases the sinus node artery originates from the
RCA, in 20% from the CX, and in 10% both the RCA and the CX
supply the sinus node.
astinal vessels later connects with the coronary buds of the aortic
sinus. Incomplete involution of the former connections may persist
as coronary stulae to other thoracic vessels. Abnormal origins of
coronary arteries stem from deviations of the connections between
the endothelial buds arising from the base of the truncus and the
vascular endothelial network. In the normal spectrum of variation,
diverse numbers and locations of coronary ostia and courses of
coronary arteries are observed, many without clinical signicance.
Normal can be dened as any anatomy that occurs in more than 1%
of subjects of an unselected sample of the healthy general population.
Coronary artery anomalies and their
classification
e prevalence of coronary anomalies is approximately 1% in the general population. e majority of coronary anomalies are clinically silent. However, in young athletes coronary anomalies are the second
most common causes of sudden cardiac death (SCD). According to
their clinical signicance, coronary anomalies may be classied as
(1) not causing ischaemia (the majority), (2) obligatory ischaemia
Normal coronaryanatomy
(e.g. aberrant origins from the pulmonary artery (PA)), and (3)occasionally causing ischaemia (e.g. origin of the le coronary artery
from the right aortic sinus with an intramural or interarterial course
Nomenclature of the coronary arteries is based on the myocardial
territory they supply and not their origin. e right coronary artery
(RCA) provides blood ow to the right ventricular free wall und usually originates from the right aortic sinus. e posterior descending
artery supplies the inferior interventricular septum and usually originates from the RCA. e le anterior descending artery (LAD) provides
between the aortic and the PA). e anatomical classication of coronary anomalies is based on the ostium (e.g. atresia), the origin (e.g.
from the PA or from the opposite aortic sinus), the course (e.g. anterior
to the PA, interarterial, posterior to the aorta, intraseptal or posterior
to the tricuspid and mitral valves), duplication (e.g. double LAD), the
congenital absence or hypoplasia, and the termination (e.g. stula).
SECTION 1 Pathophysiology and investigation ofcoronary artery disease32
A
L
P
P
L
R
P
(a) (b)
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RCA
LAD
LMCA
CX
(a) (b)
L
L
LAD
R
CX
P
LMCA
R
A
RCA
R
R
L
L
LAD
LMCA
CX
A
RCA
R
L
R
Fig.4.1 Wrong sinus origin of anomalous coronary arteries. Normal coronary pattern, upper left. (a)Left coronary from right sinus. (b)Right coronary
from left sinus. A, anterior; L , left; P, posterior; R, right.
Created by Bona Kim, Copyright Duke Cameron.
e most common anomalous aortic origin of a coronary artery (AAOCA) is the CX arising from the RCA or right aortic sinus
(incidence 0.3%), which is felt to be of no clinical signicance, except when it courses at the bottom of the non- coronary sinus and
is at risk during surgical aortotomy. More important are the origins of the RCA, LAD, or LMCA from the opposite aortic sinus
with an interarterial or intramural course (Fig. 4.1). e clinical
LAD
LMCA
CX
A
R
L
P
Fig.4.2 Interarterial (a)versus intramural (b)course of anomalous coronary arteries. A, anterior; L, left; P, posterior; R, right.
Created by Bona Kim, Copyright Duke Cameron.
RCA
presentation may be stable or exertional angina, syncope especially
with exercise, or sudden cardiac arrest. e pathophysiology of ischaemia in these anomalies is still debated and several mechanisms
have been theorized. Compression of the aberrant coronary artery
(whether in an interarterial or intramural course) due to distension
of the great vessels during exercise has been postulated (Fig. 4.2).
erefore, screening for ischaemia should be performed using a
A
RCA
R
LAD
L
R
LMCA
CX
L
4 Anomalous coronaryarteries 33
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physical exercise stress test with imaging rather than a pharmacological stress test. Surgical correction is recommended in the case of
symptoms or proof of ischaemia. In general, management of asymptomatic subjects with high- risk anatomies is more controversial.
Anomalous origin of one or more coronary arteries from the PA
leads to myocardial ischaemia because of the low perfusion pressure
and low oxygen saturation of the PA blood. As a collateral circulation develops, a coronary steal phenomenon may develop with ow
reversal of the proximal anomalous coronary, which compromises
the collateral circulation. Surgical correction of anomalous origin
of a coronary artery from the PA is warranted because of the risk
of ischaemic cardiomyopathy and heart failure. Treatment options
include reimplantation of the anomalous vessel into the aorta,
simple ligation, ligation with coronary artery bypass, and baing
the anomalous coronary ostium within the PA to a surgically created
aortopulmonary window (Takeuchi repair). Direct aortic implantation is usually possible in infants and small children, but is more
dicult to achieve in adults.
Classification
Given the heterogeneity of coronary artery anomalies, multiple classication systems have been proposed, based on anatomy, function,
or clinical signicance.– With the intent of creating a unied database, the STS- Congenital Heart Surgery Database Committee and
representatives from the European Association for Cardiothoracic
Surgery proposed a standard nomenclature and categorization of
anomalies,:
• AAOCA.
• Anomalous pulmonary origin of coronary arteries (includes
anomalous origin of the le coronary artery from the PA; Bland–
Garland– White syndrome).
• Coronary artery stula.
• Coronary artery aneurysm.
• Other coronary artery anomalies (such as myocardial bridges,
stenoses, and secondary variations).
Coronary artery stulae are most oen inconsequential incidental
ndings discovered during coronary angiography. When the shunt
is large, coronary steal is possible, though rare in adults, and therapeutic interruption may be indicated. In infants, the stulae may be
large and lead to congestive heart failure.
Anomalous origin from the PA is similarly rare and of clinical importance mainly in small children. Reimplantation into the aorta is
preferred unless the vessel is diminutive. Details on management of
these anomalies is beyond the scope of this chapter.
risks remains elusive. For the remainder of this chapter, we shall use
AAORCA to indicate anomalous aortic origin of the RCA, most
oen from the le sinus of Valsalva, and we shall use AAOLCA to
indicate anomalous aortic origin of the LMCA, most oen from the
right, or anterior sinus of Valsalva. Instances where only the LAD
branch or only the CX coronary artery has anomalous origin in general are managed similarly to situations where the le main arises
anomalously.
An important distinction is the dierence between interarterial
and intramural anomalous coronary arteries (Fig. 4.2). In the
former, the anomalous coronary lies between the aorta and pulmonary and theoretically can be compressed between the two. In
the latter, the anomalous vessel travels within the aortic wall from
the wrong aortic sinus and is thought to be compressed mainly in its
intramural segment.
A landmark paper that demonstrated the association of AAOCA
with SCD was published in 1974 by Cheitlin and associates from
the Armed Forces Institute of Pathology in Washington, DC. ey
reviewed all cases of single coronary artery origin or both coronary
arteries arising from the same sinus of Valsalva from autopsy cases.
ey found a total of 51 cases of AAOCA out of 475,000 records.
Among patients in whom both coronary arteries arose from the
anterior (‘right coronary’) sinus (AAOLCA), 27% (9/ 33) had experienced SCD. ere were no cases of SCD among the 18 patients
in whom the RCA arose from the le coronary sinus (AAORCA).
e authors noted that a slit- like orice and intramural course were
commonly seen in cases with SCD. ey proposed that these features (wrong sinus origin and slit- like orice) were the mechanism
for sudden death.
Basso etal. reviewed two registries of young competitive athletes
in the United States and Italy who died suddenly during exercise and
found 27 athletes with coronary anomalies (24 AAOLCA and three
AAORCA, 22 men and ve women, ages 9– 32years). Ten of these
athletes had experienced pre- mortem symptoms (e.g. chest pain,
syncope, palpitations). Twelve athletes had normal testing in life, including all ten symptomatic patients. On pathological examination,
every heart had a slit- like orice and an intramural course, albeit of
variable length.
Maron and associates reviewed the distribution of causes of
sudden cardiovascular death in 1435 athletes in the United States
less than 35years of age between 1980 and 2005; they reported that
17% were due to coronary artery anomalies. e only cardiovascular anomaly associated with a larger number of cases of sudden
death was hypertrophic obstructive cardiomyopathy.
ere have been a number of possible underlying mechanisms for
sudden death in AAOCA including aortic pressure on an intra-
Anomalous aortic origin ofa coronaryartery
AAOCA can be subdivided into anomalous LMCA from the right
aortic sinus of Valsalva (RASV), anomalous RCA from the le aortic
sinus of Valsalva, CX from RASV or RCA, and inverted coronary
arteries (rare). ‘Wrong sinus origin’ of the RCA is more common
than ‘wrong sinus origin’ of the le coronary artery, by ratios ranging from 3:1, to as high as 9:1 in various reports, (Fig. 4.1). e
risk of sudden death is widely acknowledged to be higher when the
LMCA arises from the RASV than when the RCA arises from the le
aortic sinus of Valsalva, though precise estimation of these relative
mural segment (Fig. 4.3), a slit- like orice ‘closed’ by increased aortic
pressure, kinking or sharp angulation at take- o, an interarterial
segment ‘squeezed’ by the aorta and PA, and spasm of the AAOCA.
Additional morphological features that are associated with increased risk of ischaemic events are the length of the intramural segment, abnormally high take- o from the aorta, and an exaggerated
degree of ‘ellipticity’ (i.e. non- roundness) of the proximal segment
of the coronary artery., Conversely, within the entire spectrum
of AAOCA with ‘wrong sinus origin’, there are a number of variants
that are thought to be relatively benign, for example, AAOCA with
posterior looping course or anterior ‘pre- pulmonic course’, as well as
AAOLCA with ‘intraseptal’ or ‘intraconal’ course.
SECTION 1 Pathophysiology and investigation ofcoronary artery disease34
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L
P
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AAORCA patients had a longer intramural course compared to
non- ischaemic patients.
Diagnosis ofanomalous aortic origin ofa
coronaryartery
e initial diagnosis of AAOCA is usually made by echocardiography, with exceptions being coronary angiography or chest computed tomography scan in adults or by incidental discovery during
cardiac operations for other lesions. However, there are limitations of
LAD
RCA
R
echocardiography compared to computed tomography or magnetic
resonance imaging, such as lower spatial resolution. ere is no
LMCA
CX
universal consensus regarding the optimal evaluation of AAOCA
and use of various imaging modalities for evaluation is based on
physician preference. It is generally agreed that an echocardiographic diagnosis should be conrmed by tomographic scans to elucidate morphological details that can be helpful for risk stratication
and surgical planning. Stress testing is also important, providing
Fig.4.3 Intramural course as a mechanism of coronary ischaemia in
AAOCA. A, anterior; L , left; P, posterior; R, right.
Created by Bona Kim, Copyright Duke Cameron.
functional assessment to assess for provocation of ischaemia, and
as a baseline for follow- up and postoperative assessment.
Indications forsurgery
In the most recent 2017 expert consensus guidelines for AAOCA,
In possibly the largest series of patients with anomalies of coronary artery origin and course, the Congenital Heart Surgeons’
Society AAOCA registry has 560 patients less than 30years of
age at diagnosis who were enrolled from 40 institutions between
January 1998 and December 2016. ere were 415 AAORCA
patients, 128 AAOLCA patients, and 17 patients with anomalous origin of both the le and right coronaries, most oen a
single coronary origin outside the sinus of Valsalva and above the
‘intercoronary’ commissure. Of these, 55% of AAORCA patients,
64% of AAOLCA patients, and 41% of anomalous right/ le coronary artery patients underwent surgery (i.e. 57% of all patients).
Operated and unoperated patients in this registry are all being followed longitudinally, with the hope of shedding light on both the
natural and ‘unnatural’ (i.e. operated) history of these anomalies,
and possibly to address unanswered questions about risk stratication and indications for surgery in certain subgroups. Arecent analysis of this registry by Jegatheeswaran and associates
sought to characterize patients with ischaemia or a sudden event
(sudden cardiac arrest or SCD) at presentation. Characteristics
among those who had documented ischaemia (i.e. 49 patients
with sudden death, aborted sudden death, lethal arrhythmia, syncope with exercise, or positive exercise stress test documenting
ischaemia) were compared to those who had undergone exercise
stress tests without ischaemia (n=236 patients). e remainder,
who had not been subjected to provocative physiological stress
testing, were not included in the analysis. Of the 49 patients in
the ischaemia group, 28/ 49 (57%) had AAOLCA, 20/ 49 (41%) had
AAORCA, and 1/ 49 (2%) had anomalous aortic origin of both the
LMCA and RCA. Anomalous le outnumbered anomalous right
by approximately 1.4 to 1.In the smaller subgroup who had experienced sudden events (sudden cardiac arrest or SCD, 18 patients), 12/ 18 (67%) had AAOLCA and 6/ 18 (33%) had AAORCA.
us, in the sudden event subgroup, anomalous le outnumbered
anomalous right coronary artery by 2:1. Ischaemic AAOLCA patients were more likely to have an intramural course, high orice, or slit- like orice, than non- ischaemic patients. Ischaemic
intervention is recommended for symptomatic AAOCA individuals
(e.g. chest pain or syncope suspected to be due to myocardial ischaemia or proven/ suspected cardiac arrhythmias), or when there
is a history of aborted SCD. ese patients should have their activity
restricted until repair. Surgical repair is indicated for symptomatic
patients or for a history of SCD (classI, level of evidence B); catheterbased intervention (stenting of the intramural course) may be considered if surgical risk is deemed too high (classIIb, level of evidence
C). Asymptomatic individuals with the LMCA arising from the right
sinus of Valsalva should be oered surgery (classI, level of evidence
B) because of the elevated risk of sudden death. Individuals with an
anomalous origin of the RCA from the le sinus of Valsalva should
be evaluated for inducible ischaemia (classIIa, level of evidence
C). Based on the expert consensus guidelines, if the stress testing is
negative and the patient is counselled regarding the risk of sudden
death, the patient may participate in competitive sports (classIIa,
level of evidence C). However, there are many questions that remain
unanswered in these guidelines, such as whether there is a lower or
upper age limit for surgery, and whether to perform corrective procedures if the anomaly is found incidentally at the time of surgery.
Management of asymptomatic patients with AAORCA remains
controversial. Practices vary from centre to centre, and treatment
may be tailored based on patient factors. For example, in the management of asymptomatic patients with AAORCA, the Coronary
Anomalies Program at the Texas Children’s Hospital takes into consideration ‘high- risk anatomy’ such as long intramural course,
abnormal ostium, dynamic changes of ostium and proximal course
during the cardiac cycle, as well as signicant family anxiety, desire
to participate in competitive sports, and coronary vessel dominance.
Types ofsurgicalrepair
e pathophysiology of AAOCA is that of ischaemia occurring
when myocardial oxygen demand exceeds supply. is may be related to multiple surgically correctable anatomical factors,, such
as interarterial course, ostial morphology (i.e. a round, oval, slit- like,
pinhole), ostial location, peri- commissural origin, acute angulation
(a)
(b) (c)
(a) (b) (c)
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Fig.4.4 Repair of AAOCA by unroofing (a), creation of a neo-ostium (b), or reimplantation (c).
Created by Bona Kim, Copyright Duke Cameron.
4 Anomalous coronaryarteries 35
of origin, right– le ostial relationship, and the presence and length
of intramural course. As such, the aim of surgical repair is to reduce the likelihood of myocardial ischaemia. is can be achieved
by establishing or restoring a coronary origin within the ‘appropriate
sinus’, optimizing the ostial size and morphology, eliminating the
interarterial course, and eliminating intramurality, while minimizing the likelihood of sclerosis or scarring. Alternatively, the critical
features of morphology may occasionally be le in place while providing an extra- anatomical source of myocardial blood supply.
ere are several surgical options for treating AAOCA:(1) unroong the intramural segment (Fig. 4.4a), (2)creation of a ‘neoostium’ in the appropriate sinus (Fig. 4.4b), (3)translocation of
ostium (i.e. reimplantation) (Fig. 4.4c), (4)translocation of PA (Fig.
4.5), and (5)anatomical repair by pericardial patch enlargement of
the aorta and proximal anomalous coronary artery (Vouhe repair)
either alone or in combination with translocation of ostium or PA
(Fig. 4.6). Simple coronary bypass using internal thoracic arteries or
autologous saphenous vein is occasionally used to provide an extraanatomical source of blood ow to the myocardium, but is not generally recommended because of the concern that competitive ow
from the usually normal ow in the anomalous coronary will lead
to gra failure.
Unroong is the most commonly performed operation and is the
simplest, both technically and conceptually. rough a median
sternotomy, the pericardium is opened and conventional cardiopulmonary bypass is established. Aer cardioplegic arrest, the ascending
aorta is opened either by an oblique aortotomy or by transecting
well above the coronary origins, to allow for the identication of the
orice(s) from which the coronary arteries arise. e courses of the
coronary arteries are ascertained by gentle probing. If there is an
intramural course above the commissures, a sharp scalpel incision
is made over the probe or small right- angle clamp inserted into the
coronary. Asection of the common wall between aorta and coronary
is oen excised. Precautions are taken to prevent a transaortic or
transcoronary incision to the outside of the heart. Polypropylene sutures of 6- 0 or 7- 0 are then placed along the course of the unroong
to prevent delamination and dissection of the coronary artery.
If the intramural course of the anomalous coronary lies low and
below the commissure, the unroong is performed separately in the
correct sinus, with tacking sutures then placed at the neo- orice
(Fig. 4.4b). is technique, which is oen referred to as ‘neo- ostial
creation’, avoids the need to take down and later resuspend the valve
commissure, which in some series has been associated with late
aortic insuciency. e aorta is repaired, the heart is reperfused,
and the patient is rewarmed. During this time, electrocardiographic
ndings are examined closely for changes suggesting myocardial ischaemia, and transoesophageal echocardiography is performed to
assess the function of the aortic valve.
Fig.4.5 Pulmonary translocation repair of AAOCA. (a)Left main compressed by pulmonary artery. (b)Main pulmonary artery translocated to left.
(c)Right pulmonary artery brought in front of aorta (LeCompte manoeuvre).
Created by Bona Kim, Copyright Duke Cameron.
SECTION 1 Pathophysiology and investigation ofcoronary artery disease36
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(b)
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Fig.4.6 Vouhe repair of AAOCA. Incision and patching of extramural portion of anomalous coronary, usually the left.
Created by Bona Kim, Copyright Duke Cameron.
Methods other than unroong can also be applied. Cubero etal.
opined that the major limitation of unroong is that it does not eliminate the interarterial segment of the anomalous coronary artery and
has uncertain value when there is only a short intramural segment.
In instances with only a short intramural segment, unroong may
still leave the coronary artery origin in the ‘wrong sinus’, with persistence of an interarterial segment. In such cases, PA relocation may
be performed (Fig. 4.5). Additionally, unroong may require takedown and resuspension of the valve commissure, which may predispose to late aortic regurgitation. Reimplantation can be performed,
such as in the case of AAORCA from the le coronary sinus with
interarterial course and intramural segment (Fig. 4.4c). e RCA
is divided immediately distal to the intramural segment and is directly reimplanted in an end- to- side fashion, without button, into
the RASV., Reimplantation of the AAOLCA is felt by some to be
more technically dicult, and unroong is believed by most surgeons to be more suitable for AAOLCA from the RASV.
An anatomical surgical repair has been suggested by Gaudin
etal. and is also known as the Vouhe repair (Fig. 4.6). In this procedure, the aorta and pulmonary trunk are transected to expose the
course of the anomalous LMCA. e proximal epicardial course
of the anomalous LMCA is incised and a patch of autologous pericardium or saphenous vein is used to fashion a neo- ostium in the
appropriate sinus, with incorporation of the patch into the aortic suture line. Proponents of this technique point out that the abnormal
interarterial and/ or intramural segment is le intact but is essentially bypassed. Anew, enlarged coronary ostium is created in the
appropriate sinus, restoring a normal angle of take- o.
In AAOCA patients with a single coronary ostium and no intramural component, a PA translocation can be performed, either as
an anterior PA translocation (i.e. LeCompte manoeuvre) or a lateral PA translocation (Fig. 4.5b). In a variation of the LeCompte
manoeuvre, the right PA is transected, mobilized, and translocated
anterior to the aorta and re- anastomosed to the main PA, with patch
augmentation (Fig. 4.5c). PA translocation has been proposed by
the Stanford group,– for instances in which unroong of a relatively short intramural segment results in the ostium remaining in
the wrong sinus, and persistence of an interarterial course. Repairs
that rely upon extra- anatomical sources of coronary blood ow such
as coronary artery bypass graing using either saphenous vein gras
or internal thoracic artery gras are generally not preferred in children and young adults, due to long- term gra patency concerns, but
may be considered in older adults, particularly if there is a xed
proximal stenosis. Other less common methods not covered in this
chapter include simple ostioplasty without unroong, creation of
ostial window (i.e. partial unroong to fashion a neo- ostium in the
distal intramural segment), and aortocoronary anastomosis from
outside the aorta without unroong.
Surgicaloutcomes
Turner et al. from Duke University (Durham, NC, USA) reviewed 53 AAOCA patients from 1995 to 2009, with a mean age
of 13.9 years (range 4– 65 years). ere were 40 patients with
AAORCA and 13 with AAOLCA. ere were symptoms of angina or syncope in 58% of the AAORCA patients, and 46% of the
AAOLCA patients. e lack of an intramural course was noted
intraoperatively in ve AAORCA patients and two AAOLCA patients, with transthoracic echocardiography accurately predicting
an intra/ extramural course in 92.5% of cases. ere were no mortalities with a mean follow- up of 29months, with complications
in 9.4% of all patients (aortic insuciency, pneumothorax, pleural
eusion, and bleeding).
Mainwaring etal. from Stanford University (Stanford, CA, USA)
reviewed 50 AAOCA patients from 1999 to 2010. e Stanford institutional approach was to recommend surgical treatment for all patients identied with AAOCA between the ages of 10 and 30years.
In patients younger than 10years or older than 30years, a more
selective approach was used, based upon symptoms or threatening
anatomy. In the initial series reported in 2011, the median age was
14years (range 5days– 47years), and there were 31 AAORCA patients, 17 AAOLCA patients, and two patients had eccentric single
coronary ostium. Overall, 52% of patients had symptoms of ischaemia, 28% had associated congenital heart diseases. ere was
a lack of intramural course observed intraoperatively in seven cases
(ve AAORCA, two AAOLCA). e surgical repair was performed
by unroong in 35 patients (70%), reimplantation in six patients
(12%), and PA translocation in nine patients (18%). ere was no
operative mortality and no late sudden deaths during a median
follow- up of 5.7years. Complications occurred in 14% and included
pleural eusion (6%), postcardiotomy syndrome (6%), and heart
block (2%). One patient with multiple previous myocardial infarctions prior to AAOCA diagnosis required cardiac transplantation
1year aer AAOCA repair. In their most recent updated report,
the Stanford group reported a total of 115 patients who underwent
surgical repair of AAOCA, including unroong of an intramural
coronary in 86 (75%), reimplantation in nine (8%), and PA translocation in 20 (17%). ere was no mortality and 57 of 59 symptomatic patients (97%) became asymptomatic aer surgery. ey
concluded that AAOCA surgery can be performed safely and is effective in relieving symptoms of myocardial ischaemia. eir report
4 Anomalous coronaryarteries 37
https://t.me/medicina_free
also described for the rst time an association between AAOCA and
myocardial bridges.
Herrmann et al. compared AAOCA perioperative management and outcomes in a paediatric versus adult centre
(Children’s Hospital of Philadelphia vs Hospital of the University
of Pennsylvania). Cardiac catheterization was utilized more frequently at the adult centre, and cardiac magnetic resonance im-
Acknowledgments
is chapter is adapted from an article originally written by
CSO, MLJ, DEC and used with permission from the Annals of
Cardiothoracic Surgery, with new illustrations by Bona Kim and
additional content by RKB.
aging was more commonly employed at the paediatric centre.
Isolated coronary unroong was performed in 19 of 20 cases at
the paediatric centre and in only two (22%) cases at the adult institution. ey found more comorbidities and more concomitant
procedures in the adult group, with longer cross- clamp times
(paediatric 28 minutes vs adult 120 minutes) and bypass times
(paediatric 42 minutes vs adult 181 minutes). Postoperatively, patients in the adult centre were extubated later (paediatric 2 hours
vs adult 15 hours) and had longer stays in the intensive care unit
(paediatric 1.6days vs adult 2.7 days) and longer hospital stays
(paediatric 3.6days vs adult 8.7days).
In view of the potential lethality of untreated AAOCA, the
American Heart Association and American College of Cardiology
have recommended that non- operated symptomatic and asymptomatic athletes with AAOLCA from the RASV, especially those
with an interarterial or intramural course, and non- operated
symptomatic athletes with AAORCA should be restricted from
participation in all competitive sports (classIII, level of evidence
B for AAOLCA; class III, level of evidence C for symptomatic
AAORCA). An exception might be made for classIA sports,
such as billiards, bowling, and golf. Asymptomatic athletes with
AAORCA from the le aortic sinus of Valsalva should undergo exercise stress testing, and those asymptomatic with negative stress
test may compete aer adequate counselling (classIIa, level of evidence C). Athletes with AAOCA may consider participation in all
sports 3months aer successful surgical repair if asymptomatic
and if an exercise stress test is negative for ischaemia or arrhythmias (classIIb, level of evidence C).
Conclusion
Anomalous aortic origin of the le or right coronary arteries
(‘wrong sinus origin’) is a rare but important anomaly with potential for exercise- related ischaemia that may present as SCD in the
young. e LMCA arising from the right coronary sinus (AAOLCA)
is a higher- risk lesion that should be repaired in nearly all patients.
e RCA from le sinus (AAORCA) is more common but may be
less serious, and operation is generally reserved for patients with
symptoms attributable to ischaemia (such as syncope with exercise),
documented ischaemia, or a history of SCD. Imaging studies to elucidate detailed anatomy of coronary origin and course should be
followed by physiological testing to assess for inducible ischaemia.
When surgery is indicated, unroong of the intramural segment
is the most commonly performed operation, though several alternative techniques are available. Asingle surgical strategy is likely
not ideal for all patients and operative techniques should be individualized on the basis of patient anatomy. All potential anatomical culprits should be addressed in patients undergoing operation.
Coronary artery bypass graing has limited application, especially
for young patients.
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