1

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y

Armed Forces In

stitute of Pathology

D e p a r t m e n t o fD i a g n o s t i c R a d i o l o g yB a l t i m o r e , M a r y l a n dB a l t i m o r e , M a r y l a n dI m a g i n g o fC o r o n a r y A r t e r yD i s e a s e : I

Jean Jeudy, MD

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yNORMAL

Asymptomaticatherosclerosis

High RiskVulnerable Plaque

ThrombosedPlaque

1. Asymptomatic

2. Stable angina

pectoris

3. Acute

coronary

syndrome U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yE v o l u t i o n o f a t h e r o s c l e r o t i c p l a q u e

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yE v o l u t i o n o f t h r o m b o s i s

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yA t h e r o t h r o m b o t i c p l a q u e sM a i n c o m p o n e n t s1. Connective tissue extracellular matrix (collagen

proteoglycans, fibronectin)

2. Crystalline cholesterol, cholesterol esters, phospholipids

3. Smooth muscle cells, T-lymphocytes, macrophages

4. Thrombotic material with platelets and fibrin deposition

2

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yA H A P l a q u e C l a s s i f i c a t i o n

Preatheroma:

increased extracellular lipid deposits

Fatty streaks:

little intracellular lipid, deposits of

SMC

Normal intima or minimal intimal

thickening

Type III

Type II

Type I

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yA H A P l a q u e C l a s s i f i c a t i o n

Fibroatheroma

Atheroma:

Massive confluent lipid

deposits

Type V

Type IV

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yA H A P l a q u e C l a s s i f i c a t i o n

Fibrous plaque

Calcified plaque

Type IV or V lesion with surface defect and/or hematoma, thrombotic deposit

Type VIII

Type VII

Type VI

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yM o d i f i e d A H A C l a s s i f i c a t i o nIntimal Xanthoma

(Type I, II)

• Not primarily

associated with

atherosclerosis

• Potential to regress

“Fatty streak”

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yM o d i f i e d A H A C l a s s i f i c a t i o nIntimal thickening

(Type III)

• Most likely precursor of atherosclerotic disease

• Intimal thickening with ill defined fibrous cap of smooth muscle cells

Intimal mass U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yM o d i f i e d A H A C l a s s i f i c a t i o nIntimal thickening

(Type III)

• Extracellular lipid

pools

Preatheroma

3

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yM o d i f i e d A H A C l a s s i f i c a t i o nFibrous Cap Atheroma

(Type IV, V)

• Lipid core rich in cellular debris lined by a cap of smooth muscle cells

• Varying degrees of infiltration– Macrophages and lymphocytes Atheromatous plaque,

fibroatheroma U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yT h i n C a p F i b r o u s A t h e r o m a• Fibrous cap < 65 µm thick

• Series of 41 ruptured plaques in which 95% were < 64 µm in thickness

• Compared to other fibrous cap atheromasthere is loss of SMC extracellular matrix and lymphocytes

Burke et al 1998

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yT h i n C a p F i b r o u s A t h e r o m a• Series of >400 sudden death cases

• Appx 60% of acute thrombi resulted from

rupture of thin cap fibrous atheromata

(TCFA)

• TCFA without rupture were found in 70%

Burke et al 2006 U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yC o m p l e x l e s i o n s• Complex plaque morphologies are thought to be the most common cause of coronary thrombosis

• morphologically distinguished as encompassing one of 3 processes:– Plaque rupture

– Plaque erosion

– Calcified nodule

Burke et al 1998

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yP l a q u e r u p t u r eFibrous cap disruption

– overlying thrombus is continuoous with underlying necrotic core

– Cap infiltrated by macrophages and lymphocytes

– Sparse SMC U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yP l a q u e r u p t u r e• Found in 60% of sudden deaths

• Most frequent cause of death – men <50 yrs

– women >50 yrs

• Assoc w/ hypercholesterolemia, high total cholesterol

4

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yT C F A v s P l a q u e r u p t u r e• TCFA most resembles plaque rupture in morphology

• Precursor lesion – “vulnerable plaque”

• Most frequently observed in proximal coronary arteries

• Demonstrate positive remodeling U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y

P l a q u e e r o s i o n• when evaluation of a thrombosed lesion fails to demonstrate fibrous cap rupture

• As opposed to rupture, exposed intima has predominant SMC and minimal inflammation

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yP l a q u e e r o s i o n• Erosions constitute appx 40% of cases of thrombotic sudden death

• More common in young womwn and men <50 years of age

• Associated smoking U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yC a l c i f i e d n o d u l e• Fibrous cap

disruption and

thrombus associated

with a dense calcific

nodule

• associated with

healed plaques

• Infrequent cause of

thrombotic occlusion

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yR o l e o f I m a g i n g• Most common cause of coronary thrombosis is plaque rupture followed by plaque erosion, whereas calcified nodule is infrequent

• Techniques evaluating calcified coronary plaque give insight into plaque burden

• Newer techniques focus on identifying vulnerable plaque U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y

C a l c i u m m e a s u r e m e n t b y M D C T• Histology studies have demonstrated a high

correlation between coronary artery

calcium and overall magnitude of

atherosclerotic plaque burden

• Coronary plaques with healed ruptures

invariably contain calcium, whereas plaque

erosions are frequently not calcified

Sangiorgi et al, JACC 31(1):126

5

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yC a l c i u m m e a s u r e m e n t b y M D C T• Coronary calcium is detected in majority of

patients with ACS in substantially greater

numbers than matched subjects without

CAD

• Provide indirect evidence of underlying

plaque biology and propensity for future

plaque rupture U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yC a l c i u m s c o r i n gA g a t s t o n m e t h o d• Slice-by-slice analysis

• Multiply area of calcified lesion x weighting factor dependent on the peak attenuation of the lesion

• Individual scores are calculated for each main coronary artery segment

• The sum of all scores yields a total coronary score

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yC a l c i u m s c o r i n gA g a t s t o n m e t h o d• 35,246 subjects

Hoff JA et al, 2001 U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yC a l c i u m s c o r i n gA g a t s t o n m e t h o d

Calcium score = 500

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yC a l c i u m s c o r i n gEBCT vs MDCT• EBCT and MDCT have equivalenentreproducibility for measuring CAC

Agatston vs Mass score• Evaluation of calcium volume has found to be reproducible than Agatston score– Clinical relevance

Stanford et al, 2004

Detrano et al, 2005 U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yC a l c i u m s c o r i n g• Studies have reported a regression effect on

calcified lesions after initiating lipid-lowering

therapies

Achenbach et al, 2002

6

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g ySOFT PLAQUE IN PROXIMAL LAD70% LUMINAL STENOSIS

CALCIUM SCORE = 0

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yC a l c i u m s c o r i n g• 15% of patients without evidence of CAC on

screening are ultimately found to have

noncalcified coronary plaque

• Majority of vulnerable plaques are poor in

calcium thus would potentially be missed on

screening

Nikolaou et al, 2003

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yC o r o n a r y C T A• Potential for MDCT to characterize in vivo noncalcified coronary plaque

• Primary challenges:

– Resolution

– Range of density

– Motion

– Body mass index U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yLAD RCA

C u r v e d M P R o f c o r o n a r i e s1 6 - M D C T

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yLAD RCA LCx

C u r v e d M P R o f c o r o n a r i e s6 4 - M D C TU n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y

Q u a n t i t a t i v e S t e n o s i s A s s e s s m e n t

7

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yM D C T v s C o n v e n t i o n a l A n g i o g r a p h yR e v i e w o f L i t e r a t u r e

Specificity %Sensitivity %N

958670Raff et al.

977359Leber et al.

979467Leschka et al.

64-MDCTA

947630Cordeiro et al.

32-MDCTA

918834Dewey et al.

988964Martuscelli et al.

969450Achenbach et al.

989551Mollet et al.

988272Kuettner et al.

16-MDCTA

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yKopp et al, 2001

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yO u r t e m p l a t e

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yO v e r v i e wCLINICAL HISTORY: 38 year-old M with hyperlipidemia and

coronary artery disease.

TECHNIQUE: Prospective and retrospective ECG gated images of the heart were obtained in a volumetric acquisition from the aortic arch to the upper abdomen both before and after the administration of intravenous contrast. The field of view was constrained to evaluate the heart.

• Curved multiplanar, 3-D MIP, and volume rendered images were later reconstructed at an independent workstation.

STUDY PREP: 0.4 mg of sublingual nitroglycerin was administered to the patient in preparation for the study.

COMPARISON: No prior studies are available for comparison.

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yO v e r v i e wFINDINGS:

CALCIUM SCORING: Calcium scoring by Agatston method = 85.8. This score places the patient between the 50th and 75th percentile for risk, adjusted for age and gender.

CORONARY CT ANGIOGRAPHY: The anatomy of the coronary arteries are normal, best illustrated on the 3-D reconstructed images. Right-sided dominance is observed.

• LEFT MAIN: No evidence of significant calcified or noncalcified coronary plaque.

• LEFT ANTERIOR DESCENDING: There are several areas of mixed calcified and noncalcified plaque in the proximal and mid left anterior descending artery. U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y

O v e r v i e wFUNCTIONAL ASSESSMENT:

• Ejection Fraction = 48%

• The left atrium and left ventricle are mildly dilated. No abnormal myocardial perfusion or wall motion abnormalities are observed.

• No intracardiac masses are noted. There is no pericardial effusion.

OTHER CARDIOTHORACIC:

• No abnormal filling defects are observed in the pulmonary vasculature. The aorta is normal in its course and caliber.

• Evaluation of the lungs demonstrates no focal pleural or parenchymal abnormality. The remaining osseous and soft tissue structures are grossly unremarkable.

8

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yO v e r v i e wIMPRESSION:

• 1. Multiple segmental areas of calcified and noncalcifiedcoronary plaque in the left anterior descending coronary artery. Two primary segments demonstrate at least a 50% decrease in luminal diameter. A focal area of myocardial bridging is also incidentally observed involving the mid LAD.

• 2. Calcium scoring by Agatston method = 85.8. (score places patient between the 50th and 75th percentile for risk, adjusted for age and gender by Agatston method)

• 3. EF = 48%. Normal wall motion is observed.

• 4. No evidence of pleural or parenchymal abnormality. U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yMIXED CORONARY PLAQUE 50-70% LUMINAL STENOSIS

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y2D MPR MAP U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yOCCLUSION OF LAD AT MIDPORTION

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yCORONARYPLAQUE IN LCXNONSIGNICANT STENOSIS U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yPATENT CORONARY STENT

9

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yOCCLUSION OF LCXCORONARY STENT U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y

• Stents >3mm

• Narrowing of contrast column

distally suggests

in-stent stenosis

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yC u r v e d M P R / C r o s s - s e c t i o n sA = 13 mm2 A = 9.8 mm2 A = 6.2 mm2 A = 3.3 mm2

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yP l a q u e c h a r a c t e r i z a t i o n

Soft plaque

Calcified plaque

Intraluminal

contrast

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y−−−−>300Calcium

± to −± to ++±100Fibrous

±−++50Lipid

+− to ±− to ±+ to ±20Recent thrombus

TOFT2WPDWT1WHUPLAQUE

MRICT

C o m p o n e n t s o fA t h e r o t h r o m b o t i c P l a q u eC o n t r a s t e n h a n c e d C T a n d M R IScroeder et al, 2005

Leber, et al, 2005

Fayad et al, 2005 U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yBecker et al, 2002

10

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y

C o m p u t e d T o m o g r a p h y ( C T ) v sI n t r a v a s c u l a r U l t r a s o u n d ( I V U S )Motoyama et al, 2007

Soft plaque

(4-12 HU)

Fibrous plaque

(90-123 HU)

Calcified plaque(318-384 HU) U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y

C T a s s e s s m e n t o f p l a q u e16-MDCT

• Achenbach et al (N=22)

– Sensitivity 94%

– Specificity 92%

• Leber et al (N=37)

– Sensitivity 95%

– Specificity 94%

Sensitivity 53%

Sensitivity 78%

NONCALCIFIED

PLAQUE

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yC T a s s e s s m e n t o f p l a q u e64-MDCT

• Leber et al (N=59)

– Sensitivity 84%

– Specificity 91%

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yP l a q u e r e m o d e l i n g• Glagov et al, 1987

• Eccentric enlargement in cross-sectional area acts to delay luminal narrowing

• Recent studies have demonstrated high sensitivity and specificity for detection of positive remodeling

Caussin et al, 2004

Leber et al, 2005

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yP l a q u e r e m o d e l i n g• Glagov et al, 1987

• Eccentric enlargement in cross-sectional area acts to delay luminal narrowing

• Recent studies have demonstrated high sensitivity and specificity for detection of positive remodeling

Caussin et al, 2004

Leber et al, 2005 U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yP l a q u e r e m o d e l i n gPROXIMAL RCA

11

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yE v a l u a t i o n o f c o r o n a r y d i s e a s eM a g n e t i c R e s o n a n c e• Whole body and

coronary MR techniques

have demonstrated

relative high sensitivity

and specificity in

demonstrating luminal

narrowing

• SSFP bright blood, high-

resolution black bloodFuster and Kim, 2005 U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y

E v a l u a t i o n o f c o r o n a r y d i s e a s eM a g n e t i c R e s o n a n c e• Whole body and

coronary MR techniques

have demonstrated

relative high sensitivity

and specificity in

demonstrating luminal

narrowing

• SSFP bright blood, high-

resolution black blood

CT MR

Fayad et al, 2005

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yE v a l u a t i o n o f c o r o n a r y d i s e a s eM a g n e t i c R e s o n a n c e• 3D Whole heart imaging

– Isotropic 3D SSFP volume

• Fast heart rates and small

cardiac structures like

coronary arteries require

rigorous system

performance

1.0 x 1.0 x 1.0 mm3 U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yS u m m a r y• Most common cause of coronary thrombosis

– plaque rupture (most common)

– plaque erosion

– plaque associated with calcfied nodules

• Thin cap fibroatheromata (TCFA) is considered precursor lesion – (i.e. vulnerable plaque)

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yS u m m a r y• Most common cause of coronary thrombosis

– plaque rupture (most common)

– plaque erosion

– plaque associated with calcfied nodules

• Thin cap fibroatheromata (TCFA) is considered precursor lesion – (i.e. vulnerable plaque) U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y

S u m m a r y• Coronary calcification

correlates highly with plaque

burden but appears less a

factor in plaque stability

• Eccentric vascular

remodeling is strongly

associated with vulnerable

plaque

12

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yS u m m a r y• Coronary calcification

correlates highly with plaque

burden but appears less a

factor in plaque stability

• Eccentric vascular

remodeling is strongly

associated with vulnerable

plaque U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yS u m m a r y• CT and MR imaging have proven effective in their ability to characterize stenotic or obstructive coronary lesions

• Both modalities hold great promise to allow noninvasive characterization of vulnerable coronary plaque

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yS u m m a r y• CT and MR imaging have proven effective in their ability to characterize stenotic or obstructive coronary lesions

• Both modalities hold great promise to allow noninvasive characterization of vulnerable coronary plaque

D e p a r t m e n t o f D i a g n o s t i c R a d i o g yThank you for your attention !

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yP l a q u e M o r p h o l o g y• Type 1

– Macrophages and foam cells within

intima

• Type 2 – fatty streaks – intimal

collections of lipid-laden macrophages which may form streaks

– May regress U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y• Type 3 Preatheroma

– Zone between minimal disease and

advance lesions

– Can cause minimal intimal thickerning

• Type 4 Atheroma

– Disrupruption and disorganization of the

intima

– Crystalline cholesterol in lipid cores

– Thickened vessel wall

13

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y• Type 4 – Fibroatheroma

– Lipid core and fibrous cap containing

collagen and smooth muscle cells

– Lesion progresses to lumen reduction

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y• Type 6 – Complicated

– Fissures

– Erosions

– Hematoma/hemorrhage

– Thrmobotic deposits

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y• Type 7 – primarily calcified

• Type 8 – primarily fibrotic

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y• Stable vs Unstable plaque

• Classically defined as Type 4/5 lesions

• Plaques involve epicardial vessels NOT intramyocardial

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y• Distribution includes proximal half of LAD and LCX

• RCA may be proximal or distal

• Vascular remodeling is a

compensatory mechanism and

associated with medial atrophy U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g yU n s t a b l e P l a q u e• Plaque rupture

– Result in exposure to thrombogenic

subendothelial mediators

– Junction of plaque with adjacent

“normal” wall frequent site of involvement

• Plaque hemorrhage

– Deep intimal tears lead to hemorrhage

into core accelerating plaque

enlargement and luminal reduction

14

U n i v e r s i t y o f M a r y l a n d S c h o o l o f M e d i c i n e D e p a r t m e n t o f D i a g n o s t i c R a d i o l o g y• Thrombosis

– Thrombosis after plaque rupture may lead

to nonocculsive or occlusive thrombosis

depending on

•Exposure to underlying thrombogenic factors

•Balance between clot formation and lysis

• Flow patterns