Chapter 2: Coronary Artery Ectasia

Chapter (2)

Coronary Artery Ectasia

Coronary artery ectasia (CAE) has been observed by pathologists

and cardiologists for more than two centuries. This coronary anomaly was
first described by Morgagni in 1761. Bourgon was the first to describe the
postmortem finding of right coronary artery (RCA) dilatation in a patient
who experienced sudden death in 1812 (Dilu et al., 2014).

The term ectasia was first used by Bjork in 1966 to describe dilated
coronary arteries .The literature prior to this date consisted of only
postmortem reports (Björk, 1966).

Coronary angiography and new diagnostic tools have enabled

clinicians to discover more cases of ectasia. However, not all patients
with ectasia are symptomatic and receive coronary angiography
examination;hence, the real incidence is unknown. The reported
incidence is between 0.3% and 4.9% at autopsy and during coronary
angiography (Hsu et al., 2014).

Zeina et al determined that the prevalence of CAE in consecutive

participants who underwent coronary multidetector computed to
mography (MDCT) was 8% (Zeina et al., 2007).

The incidence as high as 12% in Indian population , which may have

different demographic characteristics.There is a male preponderance,
with a male-to female ratio of 3:1 (Boles et al., 2010) .

The proximal and middle parts of the RCA are most commonly
affected by ectasia, although the reasons for this are not clear.

1
Chapter 2: Coronary Artery Ectasia

Involvement of the left anterior descending artery and left circumflex

artery is variable (Zografos et al., 2013).

The left main coronary artery is less commonly involved. Most cases
of CAE involve only a single vessel. Disturbance in blood flow filling and
washout are major characteristics of CAE. Delayed antegrade filling, a
segmental back flow phenomenon, and local deposition of dye (stasis) in
the dilated coronary segment have been observed during imaging
(Zografos et al., 2013).

Definition and classification:

There are various methods for defining CAE. Hartnell et al defined

CAE as an arterial segment with a diameter at least 1.5 times the diameter
of the adjacent normal coronary artery. Markis et al provided the
following classification of CAE based on the extent of coronary
involvement: type I, diffuse ectasia of two or three vessels; type II, diffuse
disease in one vessel and localized disease in another vessel; type III,
diffuse ectasia of one vessel only; and type IV, localized or segmental
ectasia. This classification is used extensively (Eitan and Roguin, 2016).

Plehn et al preferred to use the term coronary artery aneurysm for

segmental ectasia, reserving the term ectasia for diffuse vessel
involvement (Plehn et al., 2006).

They classified aneurysms as small (< 5 mm), medium (5–8 mm), or

giant (≥ 8 mm). In addition, coronary artery aneurysm has been classified
as the fusiform or saccular type based on the anatomicshape of the ecstatic
segment. There is no general concept concerning the critical diameter
required for the development of rupture. To date, only a few reports have
described the anatomic changes that occur in CAE over time. Plehn et al

2
Chapter 2: Coronary Artery Ectasia

reported a patient who presented with ectatic lesions that rapidly

progressed to aneurysmatic lesions within 3 years (Plehn et al., 2006).

The patient was treated with aneurysm ligation and coronary artery
bypass grafting (CABG). Periodic careful follow-up of patients with CAE
is recommended (Plehn et al., 2006).

Figure (7): Coronary artery ectasia classification. Drawing of

coronary artery ectasia by Markis’s classification of types I-IV. The shaded
portions of the coronary arteries represent the distribution of ectasia
(Markis et al., 1976)

Etiology and pathogenesis:

More than 50% of CAE cases are reportedly caused by

atherosclerosis (Dahi et al., 2011).

Compensatory vessel enlargement in the presence of coronary

atherosclerotic plaques is a common phenomenon that is viewed as
positive remodeling . Progressive overcompensation leading to ectasia
may be caused by an inadequate extent of media atrophy and fracture of
the internal elastic lamina, as well as atypical rearrangement of smooth
muscle cells (Singh et al., 2012).

3
Chapter 2: Coronary Artery Ectasia

Virmani et al provided a detailed pathologic characterization of

CAE, including lipid deposition with foam cells, fibrous caps and
significant loss of musculoelastic vascular wall components as the main
histological abnormalities (Ruiz-Morales et al., 2013).

The reason why stenosis develops in some individuals with

atherosclerosis while dilatation occurs in others is unknown. Genetic
susceptibility is likely to explain why certain individuals are at risk of
developing CAE (Taimur et al., 2012).

Many other clinical entities can cause dilation of the coronary

arteries, such as syphilis, mycotic or bacterial infection, Kawasaki disease,
trauma, congenital heart disease, inflammatory disorders, connective
tissue disorders such as Marfan syndrome, scleroderma, systemic lupus,
Ehlers-Danlos syndrome, periarteritis nodosa, Behcet’s disease and
congenital defects (Taimur et al., 2012).

Prolonged exposure to herbicides such as 2,4,5-T

(trichlorophenoxyacetic acid) and 2,4-D (dichlorophenoxyacetic acid) has
been associated with CAE These herbicides, which contain
acetylcholinesterase inhibitors, can increase the levels of acetylcholine and
stimulate the production of nitric oxide (Lin et al., 2008).

Nitric oxide can stimulate relaxation of the coronary artery. At

present, it is not known whether or not chronic relaxation of the smooth
muscle layer of the coronary artery causes CAE (Chen et al., 2010).

CAE can also be iatrogenic in origin, for example after percutaneous

coronary intervention (PCI). Chiuet al reported a patient who developed
coronary artery aneurysm after successful stent implantation for a chronic
totally occluded lesion (Chiu et al., 2007).

4
Chapter 2: Coronary Artery Ectasia

Interestingly, the aneurysm spontaneously regressed a few months

later without further intervention. It was thought that the most likely
mechanism for this was shear stress inducing vessel positive remodeling
after an intervention procedure, with subsequent negative remodeling
when the shear stress returned to baseline. Lamblin et al found that
patients with CAE had a higher percentage of the 5A/5A polymorphism
of metalloproteinase-3 (MMP-3), which is actively involved in the
proteolysis of extracellular matrix proteins (Freeman et al., 2011).

The levels of inflammatory markers such as plasma interleukin-6, C-

reactive protein, V-CAM, I-CAM and E-selectin are elevated in CAE
patients (Schlesinger and Bendas, 2015).

This suggests a role for the inflammatory process in this setting.

Pinar et al determined that CAE was associated with the classical
cardiovascular risk factors except for diabetes, which was rare in patients
with isolated CAE (Boles et al., 2012).

This negative correlation between diabetes and CAE has also been
reported by others. Williams et al found impaired nitric oxide-mediated
vasodilatation in patients with non- insulin-dependent diabetes (Williams
et al., 1996).

However, Zeina et al demonstrated that there was no apparent

correlation between CAE and hypertension, hyperlipidemia, diabetes,
smoking and a family history of coronary artery disease. The actual
relationship between CAE and traditional cardiovascular risk factors still
needs to be clarified by further study (Zeina et al., 2007).

5
Chapter 2: Coronary Artery Ectasia

Considering all of the above findings, Manginas and Cokkinos

speculated that CAE occurs due to two different mechanisms in two
distinct patient groups:

 Commonly in patients with concomitant coronary artery disease due

to severe and chronic arterial inflammation.

 Rarely in subjects without coronary atherosclerosis as a result of

exogenous interstitial nitric oxide vascular overestimation (Manginas
and Cokkinos, 2006)

Clinical manifestations:

Although it has been shown that more than half of patients with CAE
have underlying coronary artery stenosis, the symptoms do not directly
correlate with the degree of stenosis. It was founded that CAE subjects
patients to a higher risk of myocardial ischemia irrespective of the extent
of stenosis (Aboeata et al., 2012).

On the contrary, the Coronary Artery Surgery Study database

showed no difference in 5-year survival for patients with both CAE and
coronary artery disease compared with those with only coronary artery
disease (Mavrogeni, 2010).

Angina is the most common symptom in patient with CAE; ST-

elevation myocardial infarction, non-ST elevation myocardial infarction,
heart failure, and severe arrhythmias such as ventricular tachycardia and
fibrillation have also been reported. Ovalı and Morrad demonstrated that
ectatic arteries are prone to spasm (Ovalı and Morrad, 2017).

Heuser et al used computer analysis to evaluate the effects of ergo

ovine- and acetylcholine-induced spasm . They found that the actual

6
Chapter 2: Coronary Artery Ectasia

narrowing induce by these agents usually occurred adjacent to the ectatic

portion and less commonly within the ectatic area (Heuser et al., 1999).

Giacoppo et al reported a case of large spontaneous dissection of an

ectatic right coronary artery in a patient with out-of- hospital cardiac
death (Giacoppo et al., 2014).

Taimur et al described a patient who presented with sudden onset of

shortness of breath followed by respiratory arrest, in whom coronary
angiography showed type 1 CAE and two-vessel disease (Taimur et al.,
2012).

Tuzun et al found that stiffness parameters in the aorta are impaired

in patients with CAE as well as in those with coronary artery disease
(Tuzun et al., 2007).

The increased stiffness may be responsible for left ventricle diastolic

dysfunction, which is very important because it might play a key role in
the development of heart failure. CAE has been reported to be associated
with aortic aneurysm and patients present with abdominal pain. Nordon et
al, reported that CAE and abdominal aortic aneurysm share similar
histologic features with prominent medial elastin degeneration .Some
patients with CAE are asymptomatic and the disease is found incidentally
during catheterization (Nordon et al., 2011).

Diagnostic methods:

Coronary angiography is now the criterion standard for diagnosing

CAE. Coronary angiography offers a detailed definition of coronary
anatomy, making it possible to characterize the distribution and size of
coronary aneurysms and also to detect coronary stenosis (Aboeata et al.,
2012).

7
Chapter 2: Coronary Artery Ectasia

A treadmill exercise test and thallium-201 myocardial perfusion scan

can be used to evaluate myocardial ischemia caused by CAE (Aboeata et
al., 2012).

Intravascular ultrasound can be used to assess the luminal size and

condition of the arterial walls, and also to differentiate true from false
aneurysms caused by plaque rupture (Aboeata et al., 2012).

Magnetic resonance imaging (MRI) has been successfully used to

assess coronary anatomy in patients with CAE. Greil et al reported a small
series of adolescents and young adults with Kawasaki disease, who were
diagnosed by coronary magnetic resonance angiography (Greil et al., 2007).

Multi-slice Detector Computed Tomography (MDCT) is one of the

newest tools used to diagnose CAE, and it is not invasive like coronary
angiography. Zeina et al found a high prevalence (8%) of CAE when
using MDCT as a diagnostic tool (Zeina et al., 2007). The first congenital
CAE diagnosed by MDCT was reported by Ayusawa et al in 2008 (Ayusawa
et al., 2008).

Figure(8):. Magnetic resonance imaging of an ectatic left anterior descending

coronary artery (A) and an ectatic right coronary artery (B). (Zeina et al., 2007).

8
Chapter 2: Coronary Artery Ectasia

Therapeutic approach:

CAE is not a benign coronary anomaly, it is suggested to treat CAE

patients with: (Taimur et al., 2012)

 Anticoagulation therapy, utilizing chronic warfarin therapy to offset

the risk of thrombus formation and to keep the international
normalized ratio at around 2.0–2.5.

 Antiplatelet therapy, utilizing aspirin (80–360 mg/day) to minimize

platelet aggregation.

 Antispasm therapy, utilizing calcium-channel blockers .

 Nitrates could also be used, but added care should be emphasized to

provide a nitrate-free ―holiday‖ and prevent chronic exposure to
these agents

Therapy should be tailored to each individual patient because of the

serious bleeding complications associated with warfarin use. Tuncer et al
reported two cases of CAE, one in a patient with myocardial infarction and
one with unstable angina (Tuncer et al., 2008).

A large thrombus was seen in both patients and they were treated
with aspirin, warfarin and metoprolol. One patient received Multi- slice
Detector Computed Tomography (MDCT) after follow-up, which
revealed that the thrombus had almost completely dissolved after 3
months (Taimur et al., 2012)

Warfarin was then discontinued in both cases and clopidogrel was

given. But these treatment strategies have not been studied prospectively.
Heparin and thrombolytic therapy have been successfully used for
recanalization (Taimur et al., 2012).

9
Chapter 2: Coronary Artery Ectasia

For patients with coexisting obstructive lesions and refractory angina

despite medical treatment, PCI can be performed. But there can be
difficulties during stent deployment because the ectatic arteries are usually
much larger than normal arteries. Selection of a stent of adequate size and
its expansion are very important, and can be determined by intravascular
ultrasound. Rha et al reported a challenging case of implantation of two 3.5
˜ 18 sirolimuseluting stents parallel to each other in a large ectatic
coronary artery (Rha et al., 2009). They suggested that in lesion which
have a large reference diameter, the clinician can consider parallel stenting
using drug-eluting stents as a new intervention strategy.

Coronary artery bypass graft (CABG) has been used for many years
for the treatment of significant coronary artery disease coexisting with
CAE, and the postoperative outcome is uniformly good In our opinion,
treatment should be tailored according to clinical manifestations and the
number and involvement of the coronary arteries (Taimur et al., 2012).

Medical therapy is recommended for patients with symptomatic

nonobstructive CAE. Surgery (CABG, aneurysm ligation, or
aneurysmorrhectomy) is a better choice for patients who are refractory to
coronary medical therapy and not suited for PCI.

In summary treatment of coronary artery ectasia:- (Taimur et al.,

2012)

Warfarin , keep INR from 2 to 2.5, to minimize thrombus

formation & aspirin, 80-360 mg daily, to minimize platelets
aggregation and diltiazem to minimize arterial spasm (INR =
International Normalized Ratio.)

10
Chapter 2: Coronary Artery Ectasia

Prognosis:

There are different opinions about the prognosis of CAE . Lam et al

reported an annual mortality rate of 15% during a mean follow-up period
of 24 months (Lam and Ho, 2004).

Baman et al reported significant adverse outcome among the 276

CAE patients they studied, with a 5-year mortality rate of 29.1% (Baman
et al., 2004).

Recently, because the techniques and equipment for

revascularization have significantly improved, the prognosis of CAE
seems to be better. Valente et al reported that the prognosis of CAE was
good with a low mortality rate (2%) (Valente et al., 2007), possibly
because their patients with ST-elevated myocardial infarction and acute
coronary syndrome all underwent PCI and the most severe cases with
coexisting coronary stenosis underwent coronary artery bypass graft
(CABG) (Valente et al., 2007).

Thrombolysis In Myocardial Infarction (TIMI):

The TIMI risk scores for UA/NSTEMI and for STEMI patients are
simple, integer-based scores derived from selected clinical-trial cohorts
(Aragam et al., 2009).

a. TIMI risk score for unstable angina / non

ST elevation MI:
The TIMI risk score for UA/NSTEMI is a simple prognostication
scheme that enables a clinician to categorize a patient’s risk of risk of
death and ischemic events at the critical initial evaluation. A promising
clinical application of this score is identification of a patient for whom

11
Chapter 2: Coronary Artery Ectasia

new antithrombotic therapies would be especially effective (Antman et

al., 2001).

Table (): TIMI risk score for UA and NSTEMI (Antman et al., 2000).

Risk Score Characteristic

History
1 Age ≥ 65 y
1 At least 3 risk factors for coronary heart disease
1 Previous coronary stenosis ≥50%
1 Use of aspirin in previous 7 d
Presentation
1 At least 2 anginal episodes in the previous 24 h
1 ST-segment deviation on admission ECG
1 Elevated levels of serum biomarkers
0-7 Total Score
Application of TIMI risk score:
The ability of the TIMI risk score to predict outcomes other than all-
cause mortality, MI, or urgent revascularization was assessed in TIMI
11B. In the entire trial population, there were progressive, significant
(P=0.001) increases in the rates of all-cause mortality, MI, urgent
revascularization, and the composite of all-cause mortality or nonfatal MI
as the TIMI risk score increased. The event rates stratified by risk score
for the UFH and enoxaparin groups in TIMI 11B there was a consistent,
significant increase in the rate of events for each outcome with increasing
risk score (Making, 2000).

Hemodynamic variables were likely excluded from the TIMI

UA/NSTEMI score to restrict the use of continuous variables and
maintain risk score simplicity for routine clinical use. The absence of
heart failure parameters may be partly attributed to inherent differences
between clinical trial and community-based ACS populations. Registry
populations are generally sicker than clinical trial-derived cohorts, which

12
Chapter 2: Coronary Artery Ectasia

typically exclude patients with comorbidities such as heart failure and

renal impairment (Aragam et al., 2009).

Finally, the TIMI risk score for UA/NSTEMI offers the opportunity
for evaluation of cost-effectiveness of other drugs, such as glycoprotein
IIb/IIIa inhibitors, as well as an early invasive vs early conservative
strategy in patients with an ACS (Antman et al., 2001).

b. TIMI risk score for ST elevation MI:

The TIMI STEMI risk score (range 0-14) was derived from the
Intravenous natural tissue plasminogen activator (tPA) for Infarcting
Myocardium Early II (IN-TIME II) trial study population to predict all-
cause mortality at 30 days and includes eight variables of differing
weights. According to TIMI score, we can divide patients with ACS to
low risk (scores 0 to 4) and high risk ones (scores > 4) (table) (Antman et
al., 2000).

In STEMI patients, the TIMI STEMI score yielded c-statistics of

0.83, for in-hospital mortality. At 6-months, the TIMI STEMI score
produced a c-statistic of 0.71. Independent predictors of mortality were
added to the fitted, seven-variable TIMI UA/NSTEMI model to assess for
improvements in model discrimination. The addition of dichotomous
variables for Killip class, heart rate, and SBP (each as defined for the
TIMI STEMI risk score) independently enhanced model discrimination
for in-hospital mortality. With all three risk factors, the revised ten
variable TIMI model was well-calibrated for in-hospital mortality and
yielded a c-statistic of 0.82. Although heart rate and SBP added
minimally to model discrimination for 6-month mortality, history of
congestive heart failure (substituted for Killip class) added noticeable
discriminative power. In contrast to its UA/NSTEMI counterpart, the

13
Chapter 2: Coronary Artery Ectasia

TIMI STEMI score showed excellent discrimination for in-hospital and

6-month mortality, comparable to that of the appropriate GRACE risk
scores (Aragam et al., 2009).

Table (): TIMI STEMI risk score (Aragam et al., 2009).

Age 65–74/ > 75 2/3 point
Systolic Blood Pressure < 100 3 points
Heart Rate > 100 2 points
Killip class II-IV 2 points
Anterior STE or LBBB 1 point
Diabetes, h/o HTN, or h/o angina 1 point
Weight < 67 kg 1 point
Time to treatment > 4 hours 1 point

In fact, the sustained robustness of the TIMI STEMI score, despite

its simplicity, lends considerable support to the importance of variable
selection and model composition in the development of risk scores
(Aragam et al., 2009).

The predictive capacity of this risk score was stable over multiple
time points, in men and women, and in smokers and nonsmokers.
Furthermore, the TIMI risk score performed well in a large external data
set of patients with STEMI (Morrow et al., 2000).

(Antman et al., 2004) showed that in patients with STEMI, starting

the reperfusion therapy without wasting the time is really important and
using the scoring system for these patients can be useful.

Clear relations existed between TIMI risk score and angiography

score in patients with STEMI; thus, the meaningful relation existed
between TIMI risk score with modified Gensini risk score (Lev et al.,
2008).

So, TIMI risk score can be an excellent predictor to determine the

14
Chapter 2: Coronary Artery Ectasia

extension of CAD in patients with STEMI. And clinically useful in the

triage and management of patients eligible for fibrinolytic therapy and
serves as a valuable aid in clinical research and should be determined for
any patient entering the emergency room and this score should be
recorded in discharge letters (Lev et al., 2008).

15
Chapter 2: Coronary Artery Ectasia

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