Coronary Angiogram

Dr. Sanjiv Kler

PG Cardio
GMC Thrissur
 Patient
• 48 years old male
• Chest pain since 2-3 hours
• Severe
• Radiating to left arm
• Associated with sweating

• ECG: ST ↑ II > III, aVF, V5-V6, V7-V9; ST ↓ V1-V2

• Treated as CAD, ACS, IW + PW + LW MI Sklysed

• Taken up of Coronary Angiogram
 Coronary Artery Ectaisa
• Is a dilation of the coronary artery lumen

• Ectasia: diffuse dilation of a coronary artery

– incidence varies between 0.3% and 4.9%
– Increased prevalence in men

• Aneurysm: focal coronary artery dilation

– ≥ 1.5 times the adjacent normal segment
 Ectasia: Definition
• Dilatation exceeding > one-third of the coronary artery
length with the diameter of the dilated segment measuring
> 1.5 times the diameter of a normal adjacent segment

• This method is not applicable to patients with diffuse CAE

because of the absence of normal reference segments

• Krüger et al developed another definition of CAE that used

the mean size of each coronary segment in an age- and sex-
matched cohort without heart disease as a reference value. 
 Classification: 4 groups
• Type 1: diffuse ectasia of two or three vessels

• Type 2: diffuse ectasia in one vessel and

localized disease in another vessel

• Type 3: diffuse ectasia in one vessel only

• Type 4: localized or segmental involvement

 Size classification
• Small (vessel size under 5 mm)
• Medium (vessels size 5 to 8 mm)
• Giant (vessel size over 8 mm)
 Most common location
• Right coronary artery – 68%
• Proximal left anterior descending – 60%
• Left circumflex – 50%
 Etiology
• Acquired
– Atherosclerosis (adults)
– Kawasaki disease (children)
– Mycotic or septic emboli
– Marfan syndrome
– Arteritis from polyarteritis nodosa, Takayasu disease,
or systemic lupus erythematosus
– Iatrogenic - secondary to a PTCA, stents, directional
coronary atherectomy
• Genetic (Rarely)
 Risk Factors
• Hypertension
• Hyperlipidemia
• Smoking
• Use of illicit drugs like cocaine
 Pathophysiology
• Unknown
• Arterial remodeling can be bidirectional
• Expansion or contraction of the external elastic
membrane
• Ectasia - exaggerated expansive remodeling of the
external elastic membrane resulting in luminal expansion
• Enzymatic degradation of the extracellular matrix by
matrix metalloproteinases (MMP) and other lytic
enzymes and thinning of the tunica media associated
with severe chronic inflammation
 Histology 
• Thickened fibrotic intima with lipid deposition.
• The internal elastic laminal layer usually suffers
disruption leading to the reduction in medial
elastic tissue.
• This loss of elastic tissue is the primary cause
along with chronic vascular inflammation leading
to ectasia
 Clinical Features
• Asymptomatic
• Symptoms of underlying disease (Kawasaki, SLE, Arteritis,
etc) (< 50 years - connective tissue disorders and
vasculitides)
• Angina - Diminished coronary flow speed or stagnancy of
blood flow may cause exercise-induced angina without
coexistent stenotic coronary artery disease
• Acute coronary syndrome - Formation of intracoronary
thrombus or dissipation leading to distal emboli

• Whether the aneurysm/ectasia is a culprit for the clinical

presentation versus an incidental finding
 Evaluation
• Coronary Angiogram – Gold standard
– Distortions of flow and washout are common in CAE and
are related to the severity of ectasia.
– Signs of stagnant flow include delayed antegrade
contrast filling, segmental backflow, and stasis in the
ectatic coronary segment.
• IVUS - evaluation of characteristics and pathologies
• MRA
– For the follow up of patients, MRA is the preferred
• CTA
 Management
• When CAD coexists, intense primary and secondary risk factor
modifications
• ASA, statin, and anti-ischemic medications
– Nitrates, by causing further coronary epicardial dilation, have been shown to
exacerbate myocardial ischemia and are discouraged in patients with isolated CAE
• ACS
– Require thrombolysis (intracoronary thrombolysis), heparin administration, and
glycoprotein IIb/IIIa receptor inhibitors (intracoronary)
– Thrombus aspiration may be necessary during primary PCI
– Substantial thrombus burden
• Percutaneous and surgical interventions are often beneficial for patients
with CAE and stenotic lesions where angina persists despite maximal
medical therapy
• Optimal stent sizing is essential to prevent misplacement and embolization
of stents (Covered stents; Stent-assisted coiling; double open cell stent
implantation) (difficulties associated with landing zone sizing and delivery
of stiff high-profile devices)
 Management
• Many authors recommend chronic anticoagulation;
however, no randomized trial demonstrates its benefit in
CAE (risk benefit ratio)
• Chronic anticoagulation for selected high-risk patients
(e.g., multivessel ectasia or recurrent events despite
dual antiplatelet therapy)
• Surgery is rarely done but is sometimes a necessity in
patients who have recurring complications
– involves ligation of the proximal and distal segment of the
ectatic vessel and replacing it with a bypass graft
– No attempt to repair the ectatic vessel as the results are poor
 Complications
• Lower procedural success
• Higher incidence of no-reflow and distal embolization
• Higher rates of repeat revascularization
• Higher rates of long-term mortality
• Closed cell stents –
– offers maximal scaffolding (amount of support given to vessel wall by stent)
to the vessel wall
– have small open areas between struts
– are less flexible, may develop kinks and incomplete expansion
• Stent misplacement
• Embolization of stent
• Stent thrombosis
• Restenosis
 Differential Diagnosis
• Atherosclerosis
• Behcet’s disease
• Giant cell arteritis
• Kawasaki disease
• Mycotic aneurysm
• Septic emboli
• Ehler-Danlos syndrome
• Marfan’s syndrome
• Fibromuscular dysplasia
• Bacterial syphilis
 ACC/AHA Guidelines for Use of Warfarin in the
Management of STEMI
• Class I
– 1. Anticoagulant therapy with a vitamin K antagonist should be provided to patients
with STEMI and AF [atrial fibrillation] with CHADS2 score value greater than or equal
to 2, mechanical heart valves, venous thromboembolism, or hypercoagulable
disorder. (Level of Evidence: C)
– 2. The duration of triple antithrombotic therapy with a vitamin K antagonist, aspirin,
and a P2Y12 receptor inhibitor should be minimized to the extent possible to limit the
risk of bleeding. (Level of Evidence: C)
• Class IIa
– 1. Anticoagulant therapy with a vitamin K antagonist is reasonable for patients with
STEMI and asymptomatic LV mural thrombi. (Level of Evidence: C)
• Class IIb
– 1. Anticoagulant therapy may be considered for patients with STEMI and anterior
apical akinesis or dyskinesis. (Level of Evidence: C)
– 2. Targeting vitamin K antagonist therapy to a lower international normalized ratio
(eg, 2.0 to 2.5) might be considered in patients with STEMI who are receiving DAPT.
(Level of Evidence: C)