ESC coronary ectasia review 2006

Review

European Heart Journal (2006) 27, 1026–1031
doi:10.1093/eurheartj/ehi725

Coronary artery ectasias: imaging, functional
assessment and clinical implications
Athanassios Manginas* and Dennis V. Cokkinos
First Department of Cardiology, Onassis Cardiac Surgery Center, 356 Syngrou Avenue, Athens 17674, Greece
Received 22 September 2005; revised 1 December 2005; accepted 23 December 2005; online publish-ahead-of-print 16 January 2006

KEYWORDS

Coronary artery ectasia is a relatively common entity characterized by inappropriate dilatation of the
coronary vasculature. The exact mechanism of its development is unknown, but evidence suggests a
combination of genetic predisposition, common risk factors for coronary artery disease and abnormal
vessel wall metabolism. It frequently coexists with aneurysms elsewhere, mostly involving the aorta.
In this review, the flow disturbances that are associated with this condition and the imaging modalities,
which can be used for diagnosis and prospective follow-up are described. The prognosis of coronary
ectasias is controversial and prospective studies focusing on conservative or invasive strategies to
prevent cardiac complications are needed.

Introduction
Coronary artery ectasia (CAE) has been observed by
pathologists and cardiologists for more than two centuries.
As its first description by Morgagni1 this not so infrequent
form of coronary artery disease has puzzled the clinicians
regarding its cause, clinical sequelae and treatment. In
the current review we searched the MEDLINE database for
all relevant articles, containing the key words ‘coronary
ectasia’ and ‘coronary aneurysm’ without specific selection

criteria. The reference list of identified papers was also
searched. With the widespread use of coronary angiography
the incidence of CAE in patients undergoing this diagnostic
procedure was clearly delineated. Although the incidence
may overestimate the true frequency in the general
population, CAE has been found in 1–5% during coronary
angiography.2–7 In the largest series from the CASS registry,
Swaye et al. 2 found CAE in 4.9% of more than 20 000 coronary angiograms they reviewed. The incidence of CAE in an
Indian patient cohort with ischaemic heart disease has
been reported to exceed 10%.8
The most commonly used angiographic definition of CAE,
albeit arbitrary, is the diameter of the ectatic segment
being more than 1.5 times larger compared with an adjacent
healthy reference segment.2–3 However, as the distribution
of CAE is quite variable and not always focal, normal reference segments may not be readily apparent, and this definition potentially underestimates the true incidence of the
disease. More detailed definition characteristics, for
example employing larger diameter ratio or incorporating
angiographic flow alterations, may enhance detection

* Corresponding author. Tel: þ30 210 9493341; fax: þ30 210 9493235.
E-mail address:

accuracy during angiography but also may further underestimate the true incidence of the disease.
More than half of CAE are due to coronary atherosclerosis,
but occasionally they are related to other pathological entities.9 As the first report of coronary dilatation in a patient
with syphilitic aortitis,1 CAE has been observed in association with connective tissue disorders such as scleroderma,10 Ehlers–Danlos syndrome11 and polyarteritis
nodosa12 but also with bacterial infections13 and the
Kawasaki disease.14 In a small percentage of patients CAE
can be congenital in origin.15 The differentiation between
congenital and acquired coronary aneurysms may often be

difficult, despite the exclusion of other associated diseases.9
Acquired CAE should also be differentiated from coronary
aneurysms following coronary interventions. These include
true or pseudo-aneurysms during coronary balloon angioplasty, but more importantly following coronary stent placement, atherectomy and brachytherapy.16–18 Occasionally
large ulcerated coronary plaques can be misinterpreted
angiographically as coronary aneurysms. Their true cause
can be usually revealed with intravascular ultrasound
(IVUS).19
Recent studies have documented the association of CAE
with the presence of aneurysms in other vascular beds as
well, probably owing to a common underlying pathogenetic
mechanism. CAE has been seen more frequently in patients
with aneurysms of the abdominal and ascending aorta, the
popliteal arteries, veins, and the pulmonary artery.20 In a
retrospective study by Stajduhar et al.,21 20.8% of patients
operated on for abdominal aortic aneurysm had CAE,
compared with 2.9% of patients who were operated on
for occlusive peripheral vascular disease. Similar findings
have been reported by most,22–24 but not all investigators.2,5 Our group recently extended this association to
patients operated on for aneurysm of the ascending aorta,

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Coronary artery disease;
Ectasia;
Aneurysm;
Coronary flow

Coronary artery ectasias

reporting a five-fold increase in the frequency of angiographically detected CAE, compared with a concomitantly
studied cohort of patients with suspected coronary artery
disease.25

Underlying pathology and causative
mechanisms
The specific causative mechanisms of abnormal luminar dilatation in CAE are essentially unknown. However, as the histopathological characteristics are similar to coronary
atherosclerosis, it is not surprising that the hypotheses for
the origin of CAE revolve around the vascular endothelium
and the biological properties of the arterial wall.
Virmani23 and other investigators have provided detailed
pathological characterization of CAE, including lipid deposition with foam cells, fibrous caps and significant loss of
musculoelastic vascular wall components as main histological abnormalities.4,22 CAE has to be differentiated from
post-stenotic dilatation, in which an increase in wall
stress, added to the atherosclerotic destruction of the
media, may result in progressive arterial dilatation.26 In a
minority of cases, CAE is observed in the absence of significant atheromatous burden. Despite the intact intima,
extensive media degeneration and hyalinization, possibly
as a result of chronic vascular inflammation, are stressed
as the common denominator in all cases with CAE.27
On a pathophysiological basis, Sorrell28 suggested a probable mechanism that can predispose to ectasia, i.e. chronic
overstimulation of endothelium by NO or NO donors.
Enhanced NO production has also been documented, via
the iNOS pathway, following an increase in the local interstitial concentration of acetylcholine.29 ‘Clustering’ of CAE has
been observed in Vietnam veterans exposed to Agent
Orange,30 suggesting a possible link between NO overstimulation and medial thinning leading to CAE. The components
of this chemical compound, directly or indirectly, antagonizes acetylcholinesterase, thus producing higher levels of

acetylcholine and enhanced NO production. Although
contra intuitive, ectatic coronary segments can undergo
intense coronary spasm in response to exogenous administration of vasoreactive medications such as ergonovine and
acetylcholine. Despite controversy, if spasm may occur
within the CAE31 or at its borders,32 this phenomenon,
together with possible distal microembolization, may
account for the rare development of acute coronary syndromes in patients with CAE without coronary stenoses
(‘dilated coronaropathy’), who also manifest ischaemia at
exercise.9
Another mechanism, proposed by Lamblin et al.,24 focuses
on the system of metalloproteinases, which are actively
involved in the proteolysis of the extracellular matrix proteins. These investigators found in patients with CAE, compared with to patients with obstructive coronary lesions,
a higher percentage of the 5A/5A polymorphism of the
metalloproteinase-3 (MMP-3). Although the serum levels of
the MMP-3 were not measured, it is possible that overexpression of MMP-3 may lead to enhanced vessel wall
degradation of various matrix proteins, such as proteoglycans, laminin, fibronectin and collagen Types III, IV, V, and
IX and subsequent excessive vessel wall dilatation. These
results are in line with recent evidence suggesting the

1027

presence of higher MMP-3 levels and an imbalance of
MMP/TIMP in patients with generalized CAE.33 As CAE commonly coexist with coronary stenoses, overproduction of
the MMPs may contribute to the development of acute coronary syndromes, and these findings if verified may offer in
the future therapeutic insights through MMP inhibition.
In addition, the inflammatory vascular hypothesis is
further strengthened by observations linking the presence
of CAE with elevated plasma levels of hsCRP,34,35 Il-636 and
V-CAM, I-CAM, and E-selectin.37
Taken all the above findings together, one might speculate

that CAE occurs due to two different mechanisms in two distinct patient groups: (i) rarely in subjects without coronary
atherosclerosis as a result of exogenous interstitial NO vascular overstimulation and (ii) commonly in patients with
concomitant coronary artery disease due to severe and
chronic arterial inflammation.

Imaging
For the last four decades, since Daoud22 stated ‘indeed no
case of coronary aneurysm has yet been diagnosed antemortem’, coronary angiography remains the gold standard for
the assessment of CAE. In order to clarify anatomical
variations, Markis proposed a classification of CAE based
on the extent of ectatic involvement. In decreasing order
of severity, diffuse ectasia of two or three vessels was classified as Type I, diffuse disease in one vessel and localized
disease in another vessel as Type II, diffuse ectasia of one
vessel only as Type III and localized or segmental ectasia
as Type IV.4 In addition, CAE has been classified according
to the anatomical shape of the ectatic segment in fusiform
or saccular types.20 Older studies preferred the term ‘coronary aneurysm’ for the more discrete and saccular-type
ectatic segments, reserving the term ‘ectasia’ for the
fusiform diffuse vessel involvement.4,38 All three coronary
vessels can be affected by CAE, but in 75% of patients an
isolated artery is ectatic.3 In patients with concomitant
coronary artery disease, the proximal and mid segments of
the right coronary artery are the most frequently involved,
followed by the left anterior descending artery and the
circumflex artery.2,3 The reason for the higher right coronary
artery predisposition to CAE is not well understood. Of
interest, diffuse, fusiform type CAE tends to have more
frequently bilateral distribution and association with
abdominal aortic aneurysms but it coexists with obstructive
coronary lesions less frequently, compared with discrete

saccular type CAE.3,9,21 In a small percentage of patients,
CAE does not coexist with coronary stenoses. In this subgroup, more frequently involves part or the whole length
of the artery in a diffuse form (‘dilated coronaropathy’).9
Coronary angiography by documenting the severity and
extent of concomitant coronary artery disease may also
provide significant prognostic information, as discussed
subsequently. To date, there are no studies examining the
anatomical changes that may occur in CAE over time.
From a small angiographic series of nine patients, we
noted that the CAE diameter remained stable over a mean
follow-up of 36 months. Although speculative, this finding
may suggest that the pathophysiological mechanisms
responsible for their development operated temporarily
long before their angiographic documentation (unpublished
data).


1028

IVUS is an excellent tool to assess luminal size and characterize arterial wall changes. Ge et al.,19 observed a significant atheromatous burden in the majority of CAE, with
plaque areas evenly distributed between proximal and
distal reference segments, as well as within the aneurysmal
segment. Percent stenosis, however, was significantly lower
within the CAE, due to larger vessel area, stressing the difficulty in assessing the degree of stenosis when it appears
within an ectatic segment. Of importance, IVUS correctly
differentiated true from false aneurysms caused by plaque
rupture.39 Emptied plaque cavities may appear angiographically as CAE and the distinction are of clinical importance,
as false aneurysms may lead to acute coronary syndromes.40
Recently, magnetic resonance imaging (MRI) has been successfully used to assess coronary anatomy in patients with
CAE41 (Figure 1) and Kawasaki syndrome.42 This modality,

together with electron beam computerized tomography, may
prove to be of particular value for the non-invasive prospective evaluation of CAE, as regards both morphology and flow.

Flow alterations
Disturbances in blood flow filling and washout are an
inherent characteristic of CAE. They represent the direct
result of inappropriate coronary dilatation and are clearly
associated with the severity of CAE.9 Angiographic signs of
turbulent and stagnant flow include delayed antegrade dye
filling, a segmental back flow phenomenon and local deposition of dye (stasis) in the dilated coronary segment.4,9
Slow flow has been recently directly evaluated. In a
detailed study, Akyurek et al. 43 used the Doppler wire
(Flowire) to measure blood flow velocity and coronary flow
reserve in patients with isolated CAE and in a control
group. They reported within the CAE, compared with the
control group, a trend for lower resting blood flow velocity.
Following intracoronary administration of papaverine, a
potent hyperemic stimulus, the coronary flow reserve was
1.51 in the CAE compared with 2.67 in the control arteries
(P , 0.001), suggesting a combination of epicardial flow disturbances and microvascular dysfunction as the cause of
myocardial ischaemia. A point of interest was the estimated
resting absolute volumetric flow within the CAE, found
approximately 3 times higher compared with control
patients. On a conceptual basis, this finding contradicts previous data using coronary sinus lactate and exercise stress

A. Manginas and D.V. Cokkinos

test, that documented myocardial ischaemia in areas supplied by ectatic arteries.9,44 A possible explanation may be
the spurious estimation of volumetric flow with the
Flowire in a dilated coronary segment with obviously nonlaminar flow.9

Recently, we used the TIMI frame count method (TFC), an
index of coronary flow velocity along the entire epicardial
coronary artery and reported a higher TFC (slower flow) in
CAE.45 We subsequently reported similar findings using magnetic resonance flow velocity.46 More studies are needed in
this aspect, including transthoracic Doppler evaluation, as
the acceleration of slow flow may be a therapeutic target.

Clinical sequelae and prognosis
In the majority of cases (85%), CAE accompanies atherosclerotic coronary disease.2–4,6 The clinical presentation
and the long-term cardiac complications are mostly associated with the severity of the coexisting coronary lesions.
In this population, it has been repeatedly shown that CAE
does not confer an additional risk to that which is attributed
to coexisting coronary stenoses.2–4 In the largest series from
the CASS study, the presence of CAE did not affect the
adjusted 5-year survival of patients with coronary artery
disease (75 vs. 81%).2
In a recent report from our group corresponding to more
modern medical management, the 2-year survival in the
two groups, with and without CAE, was also similar (96.7
vs. 94.8%).3 Very recently, Baman et al.,47 using more stringent criteria for identifying patients with CAE, reported a
significant adverse outcome among 276 patients they
studied, with a 5-year mortality of 29.1%. Although
autopsy reports frequently document thrombus within a
CAE, the true incidence of thrombotic occlusion is
unknown, requiring a large prospective angiographic study.
Non-invasive methods, especially MRI, may offer a means
of prospectively following these patients.
The clinical course of the patients with isolated CAE (with
no or non-significant coronary stenoses) deserves special
attention. Despite the absence of flow limiting coronary

lesions in this small group of patients, Krueger et al. 9 convincingly documented the presence of angina, positive exercise stress test and pacing-induced myocardial ischaemia in
patients with ‘dilated coronaropathy’. In addition, unstable
coronary syndromes may occur despite absence of stenoses:

Figure 1 Coronary magnetic resonance angiograms employing ‘black blood’ (left) or ‘white blood’ (middle) contrast and a corresponding coronary angiogram
(right) from a patient with an ectatic right coronary artery (maximum diameter of the ectatic segment 5.2 mm). Adapted with permission from Mavrogeni et al. 41


Coronary artery ectasias

1029

Figure 2 Coronary angiogram of the left anterior descending artery (right anterior oblique projection) showing a severe mid-segment stenosis (black arrow)
adjacent to a coronary ectatic segment, before stent placement (left), after stent placement (middle), and intracoronary ultrasound image (right) within
the proximal ectatic segment exhibiting inadequate apposition of stent struts (asterisks) against the vessel wall (white arrows) despite stent overexpansion.

In our study, 38.7% of patients with isolated CAE were
reported as having a history of myocardial infarction in the
corresponding myocardial territory.3 Overall, however,
cardiac event rate in this patient group appears to be low
and clinical follow-up suggests a relatively favorable prognosis. As reported previously2 mortality approximates 2% per
year.

Treatment
Contrary to atherosclerotic coronary artery disease, there is
a scarcity of data adequately addressing the medical management of patients with CAE. Previous studies based on
the significant flow disturbances within the ectatic segments, suggested chronic anticoagulation as main
therapy.28,48 However, this treatment has not been prospectively tested, and could not be recommended unless supported by subsequent studies.27 Heparin infusion as well as
fibrinolysis, have been successfully used for recanalization
in isolated cases of acute thrombotic occlusions, occasionally revealing absence of flow-limiting stenoses.49,50

The coexistence of CAE with obstructive coronary lesions
in the great majority of patients and the observed incidence
of myocardial infarction, even in patients with isolated coronary ectasias, have led to the generalized administration of
aspirin in all patients with CAE.2,51 The role of combined
antiplatelet therapy, with the addition of ADP inhibitors,
has not yet been evaluated in prospective randomized
studies.
Medications with vasodilating properties against coronary
spasm have also been proposed.28 Of importance, nitrates,
presumably by causing further coronary epicardial dilation,
have been shown to exacerbate myocardial ischaemia and
are discouraged in patients with isolated CAE.9 To date,
there are no vasoactive medications that have been
tested, in order to be widely recommended to patients
with CAE.
As CAE represents a form of atherosclerotic heart disease,
intense risk factor modification for primary and secondary
prevention is obviously necessary. Sudhir et al. 52 reported
that CAE is 6 times more frequent among patients with
familial hypercholesterolemia than in a control group,
suggesting a link between abnormal lipoprotein metabolism
and aneurysmal coronary artery disease.

For patients with coexisting obstructive lesions and symptoms or signs of significant ischaemia despite medical
therapy, percutaneous and/or surgical coronary vascularization can safely and effectively restore normal myocardial
perfusion. Ochiai et al. 53 many years ago reported excellent
acute and long-term results of balloon angioplasty in lesions
adjacent to coronary aneurysms and these findings also
agree with our clinical observations. One point of special
consideration is the need for adequate stent expansion

and wall apposition. This, at times can be accomplished
only with IVUS (Figure 2). Although we did not encounter
acute complications using the IVUS, extra care is recommended during introduction and withdrawal of the
device, in order to avoid stent dislocation. The implantation
of covered vs. bare metal stents offers superior acute angiographic result excluding the ectatic segment, but long term
benefit has not been adequately proven.54 Coronary artery
bypass grafting has been used for many years for the treatment of significant coronary artery disease co-existing with
ectatic coronary segments. The presence of thrombus
within the CAE and the question of the necessity to
remove large aneurysms has led to the introduction of a
variety of operative procedures, including proximal and
distal ligation, aneurysmorrhectomy and even aneurysm
resection.55 The post-operative outcome, however, was uniformly good.56

Conclusions
CAEs represent a not uncommon form of atherosclerotic coronary artery disease, seen in 5% of patients undergoing
coronary angiography. Many unanswered questions remain
regarding their exact aetiology, prognosis and therapy. The
introduction of genetic studies, new non-invasive modalities, especially MRI, and the systematic testing of modern
antiplatelet and vasoactive medications, may offer significant means of improving their prognosis.
Conflict of interest: none declared.

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