Coronary ectasia

CORONARY ECTASIA/ ANEURYSMS (CEA)
DR.NILESH TAWADE
JHRC MUMBAI

What is Coronary Artery Ectasia/ANEURYSM (CEA)?
Relatively common entity
inappropriate dilatation of the coronary
vasculature
Etiology  unknown
Multifactorial:
genetic predisposition
risk factors for coronary artery disease
abnormal vessel wall metabolism.

INTRODUCTION
Coronary artery ectasia (CAE)
represents a form of atherosclerotic
coronary artery disease seen in 1.5-
8% of patients undergoing coronary
angiography.
The presence of ectatic segments
produces sluggish blood flow, with
exercise- induced angina and
myocardial infarction, regardless of
the severity of coexisting stenotic

CEA, or aneurismal
coronary artery disease,
is defined as
dilatation of an arterial
segment to a diameter
at least 1.5 times that of
the adjacent normal
coronary artery
HARTNELL et al.1985
Hartnell GG, Parnell BM, Pridie RB. Coronary artery ectasia, its prevalence and clinical significance in 4993 patients.
Br Heart J. 1985: 54; 392-395.
Suzuki et al. recommended expanding Hartnell’s
definition to
include
those arteries that are 1.5 or more times greater than
the mean diameter of the proximal and distal portions
of the
ectatic area
•Suzuki H, : Coronary spasm in patients with coronary
ectasia.Carhete cardio vasc diagnostics 1994

Coronary Artery Aneurysm
 defined as a localized, irreversible dilatation of the
blood vessel lumen that exceeds the diameter of
the adjacent normal segment by more than 1.5-
fold (Falsett & Carrol, 1978; Swaye et al. 1983; Syed
& Lesch, 1997).
 In contrast, ectasia is used to describe a diffuse
dilatation of coronary arteries that involves 50% or
more of the length of the artery; this
classification is made according to the
appearance and number of vessels involved
(Markis et al, 1976).

The first case report of a coronary
artery aneurysm was by Bourgon
(1812)who described the postmortem
finding of a
right coronary artery dilatation in a
patient who died suddenly.’

Atherosclerosis
Atherosclerosis is the most common
cause of CEA causing morbidity and
mortality worldwide.
characterized by chronic inflammatory
and intimal lesions, called atheromas or
fibrofatty plaques, which protrude into
the lumen, weaken the underlying media
and
undergo a series of complications
affecting primarily elastic arteries and larger
and medium sized muscular arteries, such as
coronary arteries (Libby, 2002)

Histopathological findings.
an intimal proliferation with spreading of plaque
material into the vessel media leading to
destruction.
As a patho mechanism for the development of pre- and
poststenotic CEA, 
an increase in wall stress to which the artery is exposed
with the thinning and atherosclerotic destruction of the
vessel media resulting in progressive vessel dilation has been
proposed.

Extra cardiac vessel dilations were
reported by Daoud et al. and Stajduhar
et al., who described an
over proportional coincidence of
coronary artery aneurysms
with aneurysms of the abdominal aorta.
Daoud AS, Pankin D, Tulgan H, Florentin RA. Aneurysms of the
coronary arteries, report of ten cases and review of the literature. Am J
Cardiol 1963;11:228–37

Thrombogenesis in CE/A
 The combination of a proximal stenosis and an immediately
adjacent region of slower coronary blood flow within an aneurysm
represents a powerful stimulus promoting thrombus
formation.
 Additionally, turbulent poststenotic flow within
the coronary aneurysm likely promotes endothelial activation.
 the presence of chronic thrombosis within an aneurysm may also
promote thrombogenesis by providing clotting precursors and
fibrin as nidus for new clot.
 Hence, CEA thrombosis is mediated both from platelet and
endothelial derived pathophysiologic mechanisms and which is
further propagated in the presence of chronic thrombus .

 The presence of aneurismal/ectatic segments due
to their sluggish or turbulent blood flow, associated
with increased incidence
of typical exercise-induced angina pectoris and
acute coronary syndromes , regardless of the severity
of coexisting stenotic coronary disease.
 This is due to the
repeated dissemination of micro emboli to segments
distal to the ectasia, or to thrombotic occlusion of the
dilated vessel
 Slow blood flow in the coronary
artery may also be a causative factor.
Clinical symptoms and
pathophysiological explanations.

 Micro embolisms with consecutive disturbance
of coronary perfusion may account for
ventricular arrhythmias and even sudden
cardiac death;
 The occlusion of major coronary vessels may
result in acute ventricular dysfunction due to
acute myocardial infarction.
Clinical symptoms and pathophysiological
explanations.

Therapeutic management.
• No specific guidelines
• Customized treatment
The coronary morphology of CEA is
heterogeneous;  for this reason,
pharmacological, interventional and surgical
therapy specific to the cause is required.
In addition to the determination of the
cause, therapeutic management depends
on possible or manifest complications.

Medical management
 The application of platelet inhibitors as a prophylaxis
against ischemic syndromes attributed to fibrin thrombus
formation and micro emboli showering is crucial in all forms of
CEA.
 Anticoagulation with cumarin has been propagated, although a
therapeutic superiority compared with aspirin has not yet been
evaluated and not established by evidence based medicine
 Study by Krueger et al (1) strongly suggest that NTG has no
therapeutic benefit in “dilated coronaropathy,” on contrary it
may lower the ischemic threshold. Consequently, the
administration of nitrates in “dilated coronaropathy” should be
avoided
 a reasonable therapeutic approach might be the administration
of beta-blockers due to their negative chronotropic effect and
reduction of myocardial oxygen consumption in the absence of
vasodilation
1.Krueger et al. Myocardial Ischemia in Dilated CoronaropathyJACC
November 1, 1999:1461–70.

 Medications with vasodilating
properties against coronary spasm have also been
proposed.
 At present, there
are no vasoactive medications that have already
been tested and can be widely recommended to
patients with CEA.

 In cases of CEA where coronary ischemia persists despite
medical optimization, surgical or percutaneous
revascularization may be required.
 Multiple authors have reported the excellent acute and long-
term results of balloon angioplasty as well as USE OF BMS/DES in
lesions adjacent to coronary aneurysm $$;
 Special attention should be paid to the need
for adequate stent expansion and wall stabilization
in these vessels.
 The implantation of covered versus BMS/DES offers a superior
acute angiographic result, excluding the ectatic segment, but
the long-term benefit has not been adequately proven.
?$$ Ochiai M, Yamaguchi T, Taguchi J, et al. Angioplasty of stenoses adjacent to aneurysmal coronary
artery disease. Jpn Heart J. 2007; 31: 749-757

CEA AND ACS
 PCI in the instance of thrombosis, may represent several technical
challenges.
 Two important potential complications include distal embolization
of thrombus and stent malapposition.
 Yip et al reported no-reflow phenomenon (defied as ≤ TIMI-2 flw)
and distal embolization after primary PCI in 68.2% and 70% in
patients with visibly thrombosed CEA.
 Placement of a stent within an aneurysmal segment poses a
technical challenge, since apposition of stent struts to a vessel of
large and irregularly-variable caliber may not be feasible.
 Leaving unopposed stent struts — whether bare metal or drug
eluting —
may represent a nidus for thrombosis.
Yip H-K, Chen M-C, Wu C-J, et al. Clinical features and outcome of coronary artery
aneurysm in patients with acute myocardial infarction undergoing a primary percutaneous coronary intervention. Cardiology.
2002;98(3):132-140

PTFE (Covered )STENT AND
CEA
 The use of PTFE-covered stents may also pose unique
challenges:
 deployment of a covered stent in CEA may result
in occlusion of branch arteries that originate within
the subtended aneurysm;
 Incomplete coverage of the aneurysm may result in
persistent “leak” into the aneurysm sac; and, PTFE-covered
coronary stents pose risk for thrombosis or in-stent restenosis.
 Stent length and aneurysm caliber (diameter >10 mm) have
also been reported as independent risk factors for future
restenosis with PTFE-covered stents

Many authors suggests that the
exclusion of the aneurysm with a PTFE-
covered stent graft would eliminate
sluggish flow through the (previously)
aneurysmal segment, and would reduce
the likelihood of aneurysm thrombosis,
enlargement, or future rupture.

 Surgery may be indicated in the presence of
aneurysms three to four times the original
vessel diameter (giant CEA),
 involvement of the left main, bifurcation
lesions, or multivessel involvement.
 Surgical treatment entails coronary artery
bypass with or without aneurysm ligation or
resection

1. Initial Management: Antiplatelet and
Anticoagulant therapy
Antiplatelet
therapy should
be initiated
immediately
upon
the
identification of
CAA with ACS if
not previously
administered.
Anticoagulation
with intravenous
weight-based
unfractionated
heparin (UFH) or
subcutaneous
LMWH should be
added to
antiplatelet
therapy.
If copious
thrombus is noted
within CAA during
angiography,
recommend
additional
consideration of
glycoprotein
IIb/IIIa
inhibitor infusion for
24-48 hours.
Glycoprotein
IIb/IIIa infusion
should be
accompanied
by close
monitoring for
thrombocytope
nia, anemia, or
bleeding.

2. Conservative Versus Invasive
Strategy
Similar to the AHA/ACC guidelines for the management of
patients with unstable angina and non-ST segment elevation
myocardial infarction ,Pts with CEA should be treated
invasively
Most patients presenting with ACS in the context of culprit
CEA identified at coronary angiography should be managed
conservatively with antiplatelet and antithrombotic therapies.

Recommended ; that patients with the
following be considered for revascularization:
(1) TIMI 0 or 1 flow in the aneurysmal vessel;
(2) Patients with recurrent angina or ischemia;
(3) Sustained ventricular tachycardia; or
(4) Hemodynamic instability including sustained
hypotension

Invasive Strategy: Percutaneous Versus
Surgical Revascularization
 a soft-tipped coronary guidewire should be manipulated
meticulously through the CAA, taking care not to
coil the wire tip in the body of the aneurysm;
 distal embolic protection could be considered, particularly in
the context of copious thrombus;
 aspiration Thrombectomy is often necessary to reduce
thrombus burden and improve coronary flow.
 The use of IVUS or optical coherence tomography (OCT)
may further define the lesion characteristics including vessel
diameter, presence of thrombus, and relationship of the CAA
to branch vessels.

Discharge Antiplatelet and Anticoagulation
Strategies
 In patients with giant CEA or with other indications for
chronic systemic anticoagulation, chronic therapy with
aspirin 81 mg daily and warfarin to target an international
normalized ratio (INR) of 2.0-3.0 Should be preferred
 In the majority of other cases, however, we recommend
dual-antiplatelet therapy with aspirin 81 mg daily and
clopidogrel, prasugrel, or ticagrelor, regardless of whether
conservative or invasive strategy is pursued.
 The duration of dual-antiplatelet therapy in patients
presenting with ACS and CAA is unclear, and should be
tailored to the patient, lesion, and treatment approach.

 The role of the novel oral anticoagulants for
treatment of CAA is unknown at this time and
is not likely to be studied given the paucity of
patients with CAA and ACS.
 Off-label
use may be considered following discussion
with the patient, including careful
consideration of potential risks and benefits.

Coronary ectasia

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Coronary ectasia

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