1. ATHEROTHROMBOSE Stratification du risque vasculaire Marqueurs carotidiens. Emphase sur “IMT” Application pratique et Consensus canadien 2006
André Roussin MD, FRCP, Internal medicine
Director, Vascular Lab, Notre-Dame Hospital (CHUM)
Associate Professor of medicine and Researcher
University of Montreal
Chair
President
TIGC.ORG
SSVQ.ORG

2. André Roussin MD Disclosures
I have been on advisory boards or received honorarium as consultant or speaker or received research funds from the following companies:
AstraZeneca
Bristol-Myers Squibb
Boeringher-Ingelheim
GlaxoSmithKline
Leo Pharma
Merck Frosst
Pfizer
Roche Diagnostics
Schering Canada
sanofi aventis

3. HUMAN ATHEROGENESIS From yellow streak to plaque and thrombosis1 2 3 4 5 6 7
Figure 1. Initiation, progression, and complication of human coronary atherosclerotic plaque. Top, Longitudinal section of artery depicting“timeline” of human atherogenesis from normal artery (1) to atheroma that caused clinical manifestations by thrombosis or stenosis (5, 6, 7).Bottom, Cross sections of artery during various stages of atheroma evolution. 1, Normal artery. Note that in human arteries, the intimal layeris much better developed than in most other species. The intima of human arteries contains resident smooth muscle cells often as early asfirst year of life. 2, Lesion initiation occurs when endothelial cells, activated by risk factors such as hyperlipoproteinemia, express adhesionand chemoattractant molecules that recruit inflammatory leukocytes such as monocytes and T lymphocytes. Extracellular lipid begins toaccumulate in intima at this stage. 3, Evolution to fibrofatty stage. Monocytes recruited to artery wall become macrophages and expressscavenger receptors that bind modified lipoproteins. Macrophages become lipid-laden foam cells by engulfing modified lipoproteins. Leukocytesand resident vascular wall cells can secrete inflammatory cytokines and growth factors that amplify leukocyte recruitment and causesmooth muscle cell migration and proliferation. 4, As lesion progresses, inflammatory mediators cause expression of tissue factor, a potentprocoagulant, and of matrix-degrading proteinases that weaken fibrous cap of plaque. 5, If fibrous cap ruptures at point of weakening, coagulationfactors in blood can gain access to thrombogenic, tissue factor–containing lipid core, causing thrombosis on nonocclusive atheroscleroticplaque. If balance between prothrombotic and fibrinolytic mechanisms prevailing at that particular region and at that particular timeis unfavorable, occlusive thrombus causing acute coronary syndromes may result. 6, When thrombus resorbs, products associated withthrombosis such as thrombin and mediators released from degranulating platelets, including platelet-derived growth factor and transforminggrowth factor-b, can cause healing response, leading to increased collagen accumulation and smooth muscle cell growth. In this manner, thefibrofatty lesion can evolve into advanced fibrous and often calcified plaque, one that may cause significant stenosis, and produce symptomsof stable angina pectoris. 7, In some cases, occlusive thrombi arise not from fracture of fibrous cap but from superficial erosion of endotheliallayer. Resulting mural thrombus, again dependent on local prothrombotic and fibrinolytic balance, can cause acute myocardial infarction.Superficial erosions often complicate advanced and stenotic lesions, as shown here. However, superficial erosions do not necessarily occurafter fibrous cap rupture, as depicted in this idealized diagram.
Libby P. Circulation. 2001;104:

4. Inflammation markers Koenig W, Khuseyinova N. ATVB 2007; 27: 15-26
Markers of inflammation and plaque instability: from foam cell to
plaque rupture (modified after reference 2) *Biomarkers, which
are covered in this review. IL indicates interleukin, TNF-!, tumor
necrosis factor-!; MCP-1, monocyte chemoattractant protein-1;
sICAM, soluble intercellular adhesion molecule-1; sVCAM, soluble
vascular cell adhesion molecule; oxLDL, oxidized low density
lipoprotein; Lp-PLA2, lipoprotein associated phospholipase
A2; GPx-1, glutathione peroxidase; MPO, myeloperoxidase;
MMPs, matrix metalloproteinases; PlGF, placental growth factor;
PAPP-A, pregnancy-associated plasma protein-A; sCD40L, soluble
CD40 ligand; CRP, C-reactive protein; sPLA2, secretory
type II phospholipase A2; SAA, serum amyloid A; WBCC, white
blood cell count.
Koenig W, Khuseyinova N. ATVB 2007; 27: 15-26

5. ASO and Drug Interventions
Napoli C et al. Circulation 2006; 114:
Figure 1. Exposure to cardiovascular risk factors, partly through oxidation-sensitive mechanisms, can elicit an inflammatory response in
the arterial wall, activation of endothelial cells and platelets, and increased expression of adhesion molecules such as ICAM-1, vascular
cell adhesion molecule–1, P-selectin, and E-selectin. Subsequent monocyte infiltration and accumulation of macrophages and T lym-
phocytes facilitate propagation of oxidative stress and the inflammatory process and lead to increased vascular expression of inflam-
matory mediators like nuclear factor (NF)-
cytokines like tumor necrosis factor-
tors that are detectable in the systemic circulation, eg, CRP and IL-1 and IL-6, have been used as indices of inflammatory activity.
Several classes of drugs have shown clinical benefits that may be partly related to their anti-inflammatory properties and efficacy in
decreasing systemic levels of inflammatory markers. ACE indicates angiotensin-converting enzyme; HRT, hormone replacement ther-
apy; IFN, interferon; and GP, glycoprotein.

6. Cardiovascular disease worldwide
CVD (CAD, Stroke and PAD) is the leading cause of death worldwide1
CVD contributed in 2001 nearly one third of all global deaths1-2
3 Risk factors are responsible for > 75% of all CVD worldwide1
Elevated cholesterol
Smoking
High blood pressure
Of the three, elevated cholesterol carries the greatest attributable risk for CAD3
WHO. World Health report 2002
American Heart Association: statistical fact sheet 2003
Wilson P et al. Circ 1998; 97:

7. Risque de développer MCAS pendant la vie
0.5
Femme
0.5
Homme
0.2
0.2
1/10
1/10 65 55 40 50 60 70 80 90 40 50 60 70
Age (années)
Age (années)
Lloyd-Jones, Lancet 1999; 353: 89-92

8. Notion « traditionnelle » de risque vasculaire Consensus Canadien sur les Dyslipidémies Calcul du risque de coronaropathie à 10 ans
ASO présente
Coronaropathie (MCAS)
Maladie artérielle périphérique
ASO carotidienne (ICT, AVC isch. , plaque)
Patients > 30 ans avec Diabète sucré
Dyslipidémie sévère
Hypercholestérolémie familiale (LDL)
Hypoalphalipoprotéinémie familiale (HDL)
Tous les autres
Préciser le risque avec les tables de Framingham du NCEP III
Risque
Élevé

9. 2. Total Cholesterol (mmol/L) according to age
Risque cardiovasculaire Framingham modifié NCEP III Pour calculer le risque d’IM et de mortalité CV Points pour un homme
1. Age
2. Total Cholesterol (mmol/L) according to age
Age
Points
20-34 -9
35-39 -4
40-44
45-49 3
50-54 6
55-59 8
60-64 10
65-69 11
70-74 12
75-79 13
Points
Total
Cholesterol
Age
20-39
40-49
50-59
60-69
70-79
<4.14 4 3 2 1 7 5 9 6
>7.21 11 8

10. 3. Smoking according to age
Risque cardiovasculaire Framingham modifié NCEP III Pour calculer le risque d’IM et de mortalité CV Points pour un homme
3. Smoking according to age
Points
Age
20-39
40-49
50-59
60-69
70-79
Non-Smoker
Smoker 8 5 3 1
5. Blood Pressure according to treatment
4. HDL-C
Sys BP
Untreated
Treated
<120 1 2
>160 3
HDL-C
Points
>1.55 -1 1
<1.04 2

11. Pour calculer le risque d’IM et de mortalité CV
Points
10-year Risk 1 2 3 4 5 6 7 8 9 10 11 12 13 14 16 15 20 25
>17
>30
Low Risk: < 10%
Pour un homme 
Medium Risk: 10-20% 
High Risk: > 20%

12. OR (99% CI) adj for age, sex, smok All combined (extremes)
INTERHEART Risk of AMI associated with Risk Factors in the Overall Population ODDS RATIO
Risk factor
% Cont % Cases
OR (99% CI) adj for age, sex, smok
OR (99% CI) adj for all
ApoB/ApoA-1 (5 v 1)
20.0
33.5
3.87 (3.39, 4.42)
3.25 (2.81, 3.76)
Curr smoking
26.8
45.2
2.95 (2.72, 3.20)
2.87 (2.58, 3.19)
Diabetes
7.5
18.4
3.08 (2.77, 3.42)
2.37 (2.07, 2.71)
Hypertension
21.9
39.0
2.48 (2.30, 2.68)
1.91 (1.74, 2.10)
Abd Obesity (3 v 1)
33.3
46.3
2.22 (2.03, 2.42)
1.62 (1.45, 1.80)
Psychosocial -
2.51 (2.15, 2.93)
2.67 (2.21, 3.22)
Veg & fruits daily
42.4
35.8
0.70 (0.64, 0.77)
0.70 (0.62, 0.79)
Exercise
19.3
14.3
0.72 (0.65, 0.79)
0.86 (0.76, 0.97)
Alcohol Intake
24.5
24.0
0.79 (0.73, 0.86)
0.91 (0.82, 1.02)
All combined
129.2 (90.2, 185.0)
129.2(90.2, 185.0)
All combined (extremes)
333.7 (230.2, 483.9)
Yusuf S et al. Lancet 2004; 364:

13. INTERHEART Risk of AMI associated with Risk Factors in the Overall Population POPULATION ATTRIBUTABLE RISK
Risk factor
% Cont % Cases
PAR 1 (99% CI)
PAR 2 (99% CI)
ApoB/ApoA-1(5 v 1)
20.0
33.5
54.1 (49.6, 58.6)
49.2 (43.8, 54.5)
Curr smoking
26.8
45.2
36.4(33.9,39.0)
35.7,(32.5,39.1)
Diabetes
7.5
18.5
12.3 (11.2, 13.5)
9.9 (8.5, 11.5)
Hypertension
21.9
39.0
23.4 (21.7, 25.1)
17.9 (15.7, 20.4)
Abd Obesity (3 v 1)
33.3
46.3
33.7 (30.2, 37.4)
20.1 (15.3, 26.0)
Psychosocial -
28.8 (22.6, 35.8)
32.5 (25.1, 40.8)
Veg & fruits daily
42.4
35.8
12.9 (10.0, 16.6)
13.7 (9.9, 18.6)
Exercise
19.3
14.3
25.5 (20.1, 31.8)
12.2 (5.5, 25.1)
Alcohol
24.5
24.0
13.9 (9.3, 20.2)
6.7 (2.0, 20.2)
Combined
90.4 (88.1, 92.4)
Yusuf S et al. Lancet 2004; 364:

14. INTERHEART Risk of AMI with Multiple Risk Factors 1 2 4 8 16 32 64
128
256
512
OR (99% CI)
Salim Yusuf, Steven Hawken, Stephanie 埠npuu, Tony Dans, Alvaro Avezum, Fernando Lanas, Matthew McQueen, Andrzej Budaj, Prem Pais,John Varigos, Liu Lisheng, on behalf of the INTERHEART Study Investigators*SummaryBackground Although more than 80% of the global burden of cardiovascular disease occurs in low-income andmiddle-income countries, knowledge of the importance of risk factors is largely derived from developed countries.Therefore, the effect of such factors on risk of coronary heart disease in most regions of the world is unknown.Methods We established a standardised case-control study of acute myocardial infarction in 52 countries,representing every inhabited continent cases and controls were enrolled. The relation of smoking,history of hypertension or diabetes, waist/hip ratio, dietary patterns, physical activity, consumption of alcohol, bloodapolipoproteins (Apo), and psychosocial factors to myocardial infarction are reported here. Odds ratios and their99% CIs for the association of risk factors to myocardial infarction and their population attributable risks (PAR) werecalculated.Findings Smoking (odds ratio 2�87 for current vs never, PAR 35�7% for current and former vs never), raisedApoB/ApoA1 ratio (3�25 for top vs lowest quintile, PAR 49�2% for top four quintiles vs lowest quintile), history ofhypertension (1�91, PAR 17�9%), diabetes (2�37, PAR 9�9%), abdominal obesity (1�12 for top vs lowest tertile and1�62 for middle vs lowest tertile, PAR 20�1% for top two tertiles vs lowest tertile), psychosocial factors (2�67, PAR32�5%), daily consumption of fruits and vegetables (0�70, PAR 13�7% for lack of daily consumption), regular alcoholconsumption (0�91, PAR 6�7%), and regular physical activity (0�86, PAR 12�2%), were all significantly related toacute myocardial infarction (p<0�0001 for all risk factors and p=0�03 for alcohol). These associations were noted inmen and women, old and young, and in all regions of the world. Collectively, these nine risk factors accounted for90% of the PAR in men and 94% in women.Interpretation Abnormal lipids, smoking, hypertension, diabetes, abdominal obesity, psychosocial factors, consumptionof fruits, vegetables, and alcohol, and regular physical activity account for most of the risk of myocardial infarctionworldwide in both sexes and at all ages in all regions. This finding suggests that approaches to prevention can be basedon similar principles worldwide and have the potential to prevent most premature cases of myocardial infarction.
Smk DM
HTN
ApoB/A
1+2+3
All 4
+Ob
+PS
All RFs
Yusuf S et al. Lancet 2004; 364:

15. MCAS familiale précoce: RR = 1.7 à 2 ApoB, Lp(a), LDL dense, ApoA1
Notion « élargie » risque vasculaire Incluant le Consensus Canadien sur les Dyslipidémies Ajoutant les facteurs de risque « émergents »
MCAS familiale précoce: RR = 1.7 à 2
ApoB, Lp(a), LDL dense, ApoA1
Syndrome métabolique
Marqueurs sub-cliniques d'ASO:
ITH, ECG effort, Plaques et Intima-media
Facteurs de risque émergents
hsCRP, homocystéine
Diagnosis of asymptomatic atherosclerosisAtherosclerosis may be detected and the diagnosis of cardiovasculardisease confirmed using the following methods:･ Recommended: physical examination; ankleﾐbrachial index･ Possibly useful in subjects at moderate risk: carotid ultrasonography(may detect clinically unapparent atherosclerosis);electrocardiography; graded exercise testingin men over 40 years who have risk factors･ Not currently recommended, based on available evidence: flowmediatedvasodilatation, plethysmography, arterial compliance;electron beam CT scanning; MRI scanning; intravascularultrasonographyThe ankleﾐbrachial index is the ratio of systolic bloodpressure in the dorsalis pedis or posterior tibial artery tothe systolic blood pressure in the brachial artery. Requirementsinclude a blood pressure cuff and Doppler ultrasonicsensor. Measurement of the ankleﾐbrachial index canbe of particular utility in assessing asymptomatic vasculardisease in middle-aged or elderly patients with other riskfactors. An index of less than 0.90 in either leg is a reliableindicator of peripheral vascular disease, with a sensitivityof 90% and specificity of 98% for detecting stenosis ofgreater than 50%. Symptomatic peripheral vascular diseaseis associated with a marked increase in the risk of cardiovasculardisease.35Carotid B-mode ultrasonography can also be of use in assessingasymptomatic atherosclerosis. Most of the publishedliterature pertains to the measurement of intimalﾐmedialthickness. Measurements are obtained bilaterally on the distal1 cm of the common carotid, the carotid bifurcation andthe proximal 1 cm of the internal carotid. Among asymptomaticpeople over the age of 50, several studies have shownup to a 5-fold increase in the risk of cardiovascular diseasefor those with increased intimalﾐmedial thickness.36ﾐ38 Measurementof intimalﾐmedial thickness is a useful tool in cardiovascularrisk assessment but is not yet a standard measurein routine carotid ultrasonography. Although these measurementsare not routinely available, patients with evidenceof nonstenotic carotid lesions or sessile plaque on routinecarotid Doppler ultrasonography similarly are candidatesfor secondary prevention strategies. The degree of stenosisrequired for a high-risk approach has not been determinedin clinical trials.
Exercise stress testing in asymptomatic men over the ageof 40 years can also be useful in risk stratification. Gibbonsand coworkers39 studied healthy men with a meanage of 43 years. In this group of asymptomatic men, a positivestress test result was associated with a 21-fold increasedrelative risk of coronary artery disease among those with norisk factors and an 8- to 10-fold increase in relative riskamong those with risk factors. Earlier reports from theLipid Research Clinics Coronary Primary PreventionTrial40 and the Multiple Risk Factor Intervention Trial(MRFIT)41 also showed that a positive result of exercisestress testing strongly predicted risk of coronary artery disease.Thus, a positive exercise stress test result (1 mm ormore of ST-segment depression within 6 minutes on theBruce protocol) can move a middle-aged man from themoderate-risk to the high-risk secondary prevention category.In contrast, a negative stress test result and good exercisetolerance (greater than 8 metabolic equivalents) carriesa good prognosis in this group. Fewer data are availableto support exercise stress testing as part of risk assessmentfor women, although there may be a role for nuclear perfusionscanning in the presence of risk factors and possibleangina symptoms.

16. Risk factors: markers and / or activators
Atherosclerosis
Atherothrombosis
Stroke - MI - Death
IM   Plaque  Stenosis  Thrombosis
Triggering Factors
Smoking, Diabetes, LDL/oxLDL, HBP, AgII/AT1, Shear stress
Endothelial Factors
Inflammation Factors
Cells, Intercellular + intracellular signaling, proteins-enz. actions
Procoagulant Factors
TF, PAI-1 / tPA and TxA2 / Prostacycline imbalances

17. New insights: What has been improved’
1990’
2000’
Weight
BMI
Waist circumference
HBP > 160
HBP goal: 140
Ideal BP: 120
Chol + TG
LDL + HDL + TG
LDL + TC/HDL + ApoB
Diabetes
Diabetes + Met. Syndrome
Smoking
Sedentarism
Fitness
CAD
CAD + Stroke
CAD + Stroke + PAD

18. New insights: What has been added
Sub-clinical markers
Ankle-Brachial Index
Micro-albuminuria
Carotid intima-media thick.
Coronary calcification
Serological markers
hs-CRP
Lipoprotein(a)
Homocysteine
Insulinemia
sLp-PLA2 ++
+++
-/+ ++

19. CCS position statement 2006 Treatment of dyslipidemia and prevention of CVD
Niveau
de risque
Risque MCAS
en 10 ans
Recommendations
But du
traitement
Objectif
accessoire
LDL-C
mmol/L
CT/HDL
Baisse
de LDL-C
Apo B
Élevé
≥ 20 %
ou ASO
ou Diabète
Cible primaire
< 2.0
Cible secondaire
< 4.0
> 50%
< 0.85
Modéré %
Traiter si
≥ 3.5
≥ 5.0
> 40%
< 1.05
Bas
< 10%
≥ 6.0
< 1.2
Adapté de: Can J Cardiol 2006; 22 (11):

20. Ultrasonographie carotidienne Évaluation de l’ASO et stratification de risque CV
Épaisseur Intima-Media
Intima-media thickness
“IMT”
Épaisseur de plaque
Surface de plaque
Volume de plaque
Sténose
Type de plaque:
Échogénicité
Homogénéité
Faible coût
Accessible
Non-invasive
Imagerie excellente
Quantitative
Reproductible
Mesure l’ASO intimale avant la sténose angiographique

21. Ultrasound Examination of the Carotid Artery
External carotid
Internal carotid
Skin
1.0 cm
Bifurcation cm
Common carotid
1.0 cm
Near Wall
Far Wall
B-mode ultrasound
Periadventitia-adventitia
Adventitia-media
Intima-lumen
Adventitia-periadventitia
Media-adventitia
Lumen-intima
Smilde TJ et al. Lancet 2001; 357:

22. Façons de déterminer la valeur d’un marqueur de risque Vasan R S
Façons de déterminer la valeur d’un marqueur de risque Vasan R S. Circ 2006; 113:

23. Considérations avant l’adoption d’un marqueur de risque CV Vasan R S
Considérations avant l’adoption d’un marqueur de risque CV Vasan R S. Circ 2006; 113:

24. Marqueurs structurels et fonctionnels de risque CV
Vasan R S. Circ 2006; 113:

25. 12 measurements in each patient Repeated at 1 month
Reproducibility of non-invasive ultrasonic measurement of carotid atherosclerosis The Asymptomatic Carotid Artery Plaque Study (ACAPS)
858 patients
12 measurements in each patient
Repeated at 1 month
Within and between sonographer variation
Mean IMT difference (exam 2-exam 1) 0.13 mm
90% of patients – mean difference < 0.2 mm
Result
Highly reproducible measurement
B-mode ultrasound can monitor small rates of lesion progression
Stroke 1992, Aug 23 (8),

26. Protocoles pour Épaisseur Intima-Media (IMT)
12 point manual measurement
Near and far wall of CCA, ICA, Bulb
Near and far wall of CCA, ICA
Far wall of CCA
Mean of maximal IMT measurement
Mean of mean IMT measurement
Manual VS automated edge detection
Plaque thickness summed
Plaque area summed
Plaque volume summed
Adapted from Weingert M SSVQ 2006

27. IMT Reproducibility of Measurement
Intra observer variability lower in studies limited to common carotid artery far wall (± 0.02 mm) VS multiple measurements at different carotid sites (± mm)
Studies using automated computerized IMT measurement rather than manual cursor placement have best reproducibility.
Adapted from Weingert M SSVQ 2006

28. IMT: quantitative vs caliper

29. IMT and ≥ 70% Coronary Stenosis Sensitivity vs Specificity
IMT of Sensitivity Specificity
0.6 mm % 20%
0.8 mm % 60%
1.0 mm % 90%
Aminbaklish A. et al. Clin. Invest. Med 1999; 22:

30. Evaluating Atherosclerosis by IMT measurement Anatomy
0.02 mm
0.80 mm
Courtesy E. Braunwald
Buithieu J /

31. Evaluating Atherosclerosis by IMT measurement Methodology
12 point manual measurement
Far wall of Common Carotid Artery
Near and far wall of CCA, ICA
Near and far wall of CCA, ICA, Bulb
Mean of maximal IMT measurement
Mean of mean IMT measurement
Manual / automated edge detection
Summation of plaque thickness
Summation of plaque area
Summation of plaque volume
ECA
ICA
ICA
10 mm
Bulb
10 mm
CCA
10 mm
CCA
Buithieu J /

32. Evaluating Atherosclerosis by computerized IMT measurement
Automated
Computerized
method
ECG gating
Diastole
distal CCA
Mean IMT over
100 pts along at least 1 cm
Avoids pulsatile deformation of wall thickness
Observer independent
Better precision/reproducibility : Intermeasurement Δ = 3 %
Buithieu J /

33. The Atherosclerosis Risk in Communities (ARIC) Study Predictive Value of CIMT: Methodology
Prospective, multicenter study
N = aged y (72.5 ± 5.5)
7289 women, 5552 men
No evidence of CV disease at enrollment
Median follow-up 5.2 years
Mean CIMT over 1 cm - far walls of Right & Left CCA-Bulb-ICA
ECA
ICA
10 mm
Bulb
10 mm
CCA
10 mm
Chambless LE & al. Am J Epidemiol :
Buithieu J /

34. Age and Gender adjusted CHD incidence/1000 patient-year
The Atherosclerosis Risk in Communities (ARIC) Study Predictive Value of CIMT for Myocardial Infarct / Death
Mean F-up 5.2 y
Age and Gender adjusted CHD incidence/1000 patient-year
CIMT (mm)
Chambless LE & al. Am J Epidemiol :
Buithieu J /

35. Age and Gender adjusted Stroke incidence/1000 patient-year
The Atherosclerosis Risk in Communities (ARIC) Study Predictive Value of CIMT for Stroke
Mean F-up 7.2 y
Age and Gender adjusted Stroke incidence/1000 patient-year
CIMT (mm)
Chambless LE & al. Am J Epidemiol :
Buithieu J /

36. The Atherosclerosis Risk in Communities (ARIC) Study Predictive Value of CIMT by incremental value
CIMT (mean of CCA-Bulb-ICA) increment is associated with increased hazard rate ratio (HRR)
Increment
CHD
Stroke
Men
Women
0.19 mm
1.17
1.38
0.18 mm
1.21
1.36
Chambless LE & al. Am J Epidemiol :
Chambless LE & al. Am J Epidemiol :
Buithieu J /

37. The Atherosclerosis Risk in Communities (ARIC) Study Predictive Value of CIMT by strata
Hypertension
2.1
Diabetes
2.5
Current smoking
1.3
CIMT (mean of CCA-Bulb-ICA) increased hazard rate ratio (HRR) vs CIMT < 0.6 mm
CIMT
CHD
Stroke
Men
Women
> 1.0 mm (Yes/No)
1.20
2.62
1.78
2.02
> 1.0 mm
2.15
7.40
2.59
4.32 mm
2.44
3.35
2.08
3.14 mm
1.56
3.56
1.26
1.73 mm
1.21
2.53
0.79
2.07
Chambless LE & al. Am J Epidemiol :
Chambless LE & al. Am J Epidemiol :
Buithieu J /

38. Age, sex, race, center, BMI, waist-hip ratio, sporting activity
The Atherosclerosis Risk in Communities (ARIC) Study Predictive Value of CIMT: Conclusions
N = patients
CIMT measurements
Reproducible
Independent predictor of adverse cardiovascular events after adjustment for:
Age, sex, race, center, BMI, waist-hip ratio, sporting activity
Diabetes, LDL, HDL, hypertension, smoking
Fibrinogen, WBC, LVH
Chambless LE & al. Am J Epidemiol :
Chambless LE & al. Am J Epidemiol :

39. Predicting clinical coronary events: role of Carotid IMT CLAS Sub-Study
133 patients: 8.8 year follow-up
Close correlation between far wall CCA-IMT and changes in catheterization
Progression of IMT correlated with:
Progression of CAD
Increased coronary events
Absolute IMT thickness and progression of IMT more strongly correlated with coronary events than
Changes in lipid levels
Lesion changes on coronary catheterization
Result: every 0.03 mm increase in IMT increases risk of coronary event 3.1 %
Hodis H.N. et al Ann Int Med 1998; 128:

40. Non fatal MI, Coronary Death, Revascularization
Predicting clinical coronary events: role of Carotid IMT CLAS Sub-Study
CIMT directly associated with higher risk for future MI and CHD death
N = 146 CABG
p < 0.001
Non fatal MI, Coronary Death, Revascularization
CHD Risk
8.8 y follow=up
CIMT & coronary angiography
Carotid Intima-Media Thickness (mm)
Hodis HN & al. Ann Intern Med :
Buithieu J /

41. Non fatal MI, Coronary Death, Revascularization
Predicting clinical coronary events: role of Carotid IMT progression CLAS Sub-Study
CIMT progression directly associated with higher risk for future MI and CHD death
N = 146 CABG
p < 0.001
Non fatal MI, Coronary Death, Revascularization
CHD Risk
CIMT progression rate: marker of increased risk for events
CIMT measurement is tracked across time to assess for changes in atherosclerosis extent during pharmacotherapy; slower rates of progression have been associated with lower risk from CHD in the Cholesterol Lowering Atherosclerosis Study (CLAS). In CLAS, there was a direct relationship between CIMT progression and clinical events; a 3-fold greater CIMT progression rate was associated with a 3-fold higher risk for events. These data helped establish CIMT as a valid surrogate endpoint for clinical events.
Every 0.03 mm CIMT increase augment the risk of coronary event by 3.1 %
Reference:
Hodis HN, Mack WJ, LaBree L, et al. The role of carotid arterial intima-media thickness in predicting clinical coronary events. Ann Intern Med 1998;128:
CIMT progression (mm/y)
Hodis HN & al. Ann Intern Med :
Buithieu J /

42. Cardiovascular Health Study (NHLBI) Predictive Value of CIMT: methodology
Prospective, multicenter study
N = aged > 65 y (72.5 ± 5.5)
Male 38.8 %, Caucasian 84.8 %
No evidence of CV disease at enrollment
Median follow-up 6.2 years
Maximal CIMT mean of near & far walls of R + L CCA
Maximal CIMT mean of near & far walls of R + L ICA
O’Leary D & al N Eng J Med 1999;.340: 14-22
Buithieu J /

43. Cumulative Event-free Rate (%)
Cardiovascular Health Study (NHLBI) Predictive Value of CIMT for Myocardial Infarction & Stroke
Cumulative Event-free Rate (%)
100 95 90 85 80 75 2 1 3 7 6 5 4
Years
1st Quintile
2nd Quintile
3rd Quintile
4th Quintile
5th Quintile
5 %
25 %
O’Leary D & al N Eng J Med 1999;.340: 14-22
Buithieu J /

44. Myocardial Infarction or Stroke (Rate per 1000 Person-Years)
Cardiovascular Health Study (NHLBI) Predictive Value of CIMT for Myocardial Infarction & Stroke
Myocardial Infarction or Stroke
(Rate per 1000 Person-Years)
Quintiles
O’Leary D & al N Eng J Med 1999;.340: 14-22
Buithieu J /

45. Adjusted Relative Risk *
Cardiovascular Health Study (NHLBI) Predictive Value of CIMT for Myocardial Infarction & Stroke
CIMT - CCA
Quintile
Thickness (mm)
MI-CVA Rate (%)
at 7 y
Adjusted Relative Risk *
MI - CVA MI
CVA 1
< 0.87
5.2
1.00 2
9.3
1.49
1.79
1.33 3
9.0
1.29
1.40
1.21 4
13.2
1.76
2.07
1.39 5
> 1.18
18.7
2.22
2.46
2.13
* Relative Risk adjusted for age, sex, sBP, HTN, Atrial fibrillation, Diabetes
O’Leary D & al N Eng J Med 1999;.340: 14-22
Buithieu J /

46. The Rotterdam Study Comparative Predictive Value for Incident Myocardial Infarction
Population-based cohort
N = 6389 aged > 55 (69.3 ± 9.2)
Male 38.1 %, Caucasian 100 %
No prior MI or revascularization
Mean Follow-up 4.2 years
Background and PurposeﾑWe determined the contribution of common carotid intima-media thickness (IMT) in theprediction of future coronary heart disease and cerebrovascular disease when added to established risk factors.MethodsﾑWe used data from a nested case-control study comprising 374 subjects with either an incident stroke or amyocardial infarction and 1496 controls. All subjects were aged 55 years and older and participated in the RotterdamStudy. Mean follow-up was 4.2 years (range, 0.1 to 6.5 years). We evaluated which correlates of coronary heart diseaseand cerebrovascular disease contribute to the prediction of either a new incident myocardial infarction or a stroke.Logistic regression modeling and the area under the receiver operating characteristic curve (ROC area) were used toquantify the predictive value of the established risk factors and the added value of IMT.ResultsﾑThe ROC area of a model with age and sex only was 0.65 (95% CI, 0.62 to 0.69). Independent risk factors wereprevious myocardial infarction and stroke, diabetes mellitus, smoking, systolic blood pressure, diastolic blood pressure,and total and HDL cholesterol levels. These risk factors increased the ROC area from 0.65 to 0.72 (95% CI, 0.69 to0.75). This model correctly predicted 17% of all subjects with coronary heart disease and cerebrovascular disease. Whencommon carotid IMT was added to the previous model, the ROC area increased to 0.75 (95% CI, 0.72 to 0.78). Whenonly the IMT measurement was used, the ROC area was 0.71 (95% CI, 0.68 to 0.74), and 14% of all subjects werecorrectly predicted. There was no difference in ROC area when different measurement sites were used.ConclusionsﾑAdding IMT to a risk function for coronary heart disease and cerebrovascular disease does not result in asubstantial increase in the predictive value when used as a screening tool. (Stroke. 2001;32: )
In several studies a high carotid IMT was related to futurecoronary heart and cerebrovascular events.4,5,7 Despite thedifferent ultrasound protocols used in these studies, theresults for the CCA IMT are remarkably similar. The OR perSD increase in the Atherosclerosis Risk in Communities(ARIC) Study for coronary heart disease was 1.92 (95% CI,1.66 to 2.22) for women and 1.32 (95% CI, 1.13 to 1.54) formen. In the Cardiovascular Health Study, the relative risk forcoronary heart disease and stroke as a combined outcome was1.35 (95% CI, 1.25 to 1.45). In the Rotterdam Study, the ORswere1.41 (95% CI, 1.25 to 1.82) for stroke and 1.43 (95% CI,1.16 to 1.78) for myocardial infarction. Recently, Touboul etal21 found, in cross-sectional analyses on data from the フudedu Profil G始師ique de lﾕInfarctus C屍暫ral (GクIC) study,that an increased CCA IMT was associated with braininfarctions, both overall and in the main subtypes. In allstudies, including the present one, the association remainedwhen coronary heart disease and cerebrovascular disease riskfactors were accounted for.In conclusion, the present study indicates that a singlecarotid IMT measurement is of the same importance ascommonly used risk factors in the prediction of coronaryheart disease and cerebrovascular disease. Relative to theother easily obtainable and established risk factors, it does notadd substantially when used as a screening tool to discriminatesubjects with high and low risk of coronary heart diseaseand cerebrovascular disease.
van der Meer IM & al. Circ :

47. The Rotterdam Study Comparative Predictive Value for Incident Myocardial Infarction
Carotid - Ultrasonography
Maximal CIMT mean of near and far wall of left & right CCA
Carotid plaque - weighted score
Aorta - Lateral abdominal X-ray
Calcifications - length of affected area
0cm, <1.0, , , , ≥10.0cm
Lower extremities - Ankle-Brachial Index (ABI)
, , ,
Composite atherosclerosis score
Background and PurposeﾑWe determined the contribution of common carotid intima-media thickness (IMT) in theprediction of future coronary heart disease and cerebrovascular disease when added to established risk factors.MethodsﾑWe used data from a nested case-control study comprising 374 subjects with either an incident stroke or amyocardial infarction and 1496 controls. All subjects were aged 55 years and older and participated in the RotterdamStudy. Mean follow-up was 4.2 years (range, 0.1 to 6.5 years). We evaluated which correlates of coronary heart diseaseand cerebrovascular disease contribute to the prediction of either a new incident myocardial infarction or a stroke.Logistic regression modeling and the area under the receiver operating characteristic curve (ROC area) were used toquantify the predictive value of the established risk factors and the added value of IMT.ResultsﾑThe ROC area of a model with age and sex only was 0.65 (95% CI, 0.62 to 0.69). Independent risk factors wereprevious myocardial infarction and stroke, diabetes mellitus, smoking, systolic blood pressure, diastolic blood pressure,and total and HDL cholesterol levels. These risk factors increased the ROC area from 0.65 to 0.72 (95% CI, 0.69 to0.75). This model correctly predicted 17% of all subjects with coronary heart disease and cerebrovascular disease. Whencommon carotid IMT was added to the previous model, the ROC area increased to 0.75 (95% CI, 0.72 to 0.78). Whenonly the IMT measurement was used, the ROC area was 0.71 (95% CI, 0.68 to 0.74), and 14% of all subjects werecorrectly predicted. There was no difference in ROC area when different measurement sites were used.ConclusionsﾑAdding IMT to a risk function for coronary heart disease and cerebrovascular disease does not result in asubstantial increase in the predictive value when used as a screening tool. (Stroke. 2001;32: )
In several studies a high carotid IMT was related to futurecoronary heart and cerebrovascular events.4,5,7 Despite thedifferent ultrasound protocols used in these studies, theresults for the CCA IMT are remarkably similar. The OR perSD increase in the Atherosclerosis Risk in Communities(ARIC) Study for coronary heart disease was 1.92 (95% CI,1.66 to 2.22) for women and 1.32 (95% CI, 1.13 to 1.54) formen. In the Cardiovascular Health Study, the relative risk forcoronary heart disease and stroke as a combined outcome was1.35 (95% CI, 1.25 to 1.45). In the Rotterdam Study, the ORswere1.41 (95% CI, 1.25 to 1.82) for stroke and 1.43 (95% CI,1.16 to 1.78) for myocardial infarction. Recently, Touboul etal21 found, in cross-sectional analyses on data from the フudedu Profil G始師ique de lﾕInfarctus C屍暫ral (GクIC) study,that an increased CCA IMT was associated with braininfarctions, both overall and in the main subtypes. In allstudies, including the present one, the association remainedwhen coronary heart disease and cerebrovascular disease riskfactors were accounted for.In conclusion, the present study indicates that a singlecarotid IMT measurement is of the same importance ascommonly used risk factors in the prediction of coronaryheart disease and cerebrovascular disease. Relative to theother easily obtainable and established risk factors, it does notadd substantially when used as a screening tool to discriminatesubjects with high and low risk of coronary heart diseaseand cerebrovascular disease. ?
van der Meer IM & al. Circ :

48. Severity of Atherosclerosis
The Rotterdam Study Comparative Predictive Value for Incident Myocardial Infarction
Incident MI : 258 / = 4.0 %
Adjusted HR
Severity of Atherosclerosis
None
Mild
Moderate
Severe
Carotid plaques
1.00
1.19
1.28
1.83
CIMT
1.56
1.63
1.95
Aortic Calcification
1.06
1.81
1.94
ABI
1.12
1.55
1.59
Composite Score
1.52
2.28
4.35
Hazard ratios Adjusted Age, gender, smoking, BMI, TC, HDL, sBP, dBP, DM, ASA, anti-HTA Rx, lipid-lowering Rx
The predictive value for MI of each of the individual measures of atherosclerosis was independent of a wide variety of traditional cardiovascular risk factors and of medication use.
the hazard ratios for MI associated with lower-extremity atherosclerosis were slightly lower in the present study than those associated with the other measures of atherosclerosis,
The relatively crude measures directly assessing plaques in the carotid artery and abdominal aorta predict MI equally well as the more precisely measured carotid IMT.
van der Meer IM & al. Circ :

49. Carotid Plaque Predictive value
76 asymptomatic patients
Aged 35-65
TC > 6.5
Stress test, cath, carotid ultrasound
≥ 1 Plaque: 64%
57% had critical CAD
Positive predictive value for coronary atherosclerosis: 76%
No Plaque
Women: none had CAD
Men: - with positive stress test – 21% significant CAD
Giral P. et al. Am J Card 1999; 84: 14-17

50. PLAQUE AREA CAD rather than Stroke prediction
Carotid IMT, which predicts stroke more strongly than
myocardial infarction,22 is an indirect method of assessing
atherosclerosis, which is mainly an intimal process. Because
IMT represents largely medial hypertrophy related to hypertension23,24
and a substantial proportion of strokes are due to
hypertensive small-vessel disease, it is not surprising that
IMT predicts stroke more strongly than myocardial infarction,
whereas we found the opposite for plaque area, as shown
in Table 3.
CIMT-LVH-CAD: Kromm R. A. et al. Am. J. Card. 1996; 77:
Plaque Carotid-Coronary: Megnien, I. L. et al. J Hypertens. 1998; 16:
Total carotid plaque area (the sum of cross-sectional areas of all plaques in the carotid
arteries, measured in longitudinal views of each plaque) is a
strong predictor of stroke, death, and myocardial infarction.12
Patients in the top quartile of baseline plaque area have, after
adjustment for age, sex, blood pressure, cholesterol, pack
years of smoking, homocysteine, diabetes, and treatment of
lipids and blood pressure, a relative risk of 3.4 for stroke,
death, and myocardial infarction compared with patients in
the lowest quartile of baseline plaque area. Patients with
progression ( 45% of cases) had twice the risk of those with
regression (35% of cases) or stable plaque (20% of cases).12
Plaque volume and plaque area are closely related
(R 0.93);21 therefore, it is expected that plaque volume will
also be a strong predictor of outcomes; long-term studies will
be needed to confirm that.
Spence JD & al. Stroke (12):
Buithieu J /

51. PLAQUE AREA Stoke and MI risk
(cm2)
Stroke alone
Stroke and MI
5 y Risk (%) RR
1.6
1.0
4.8
2.3
1.4
9.3
1.9
3.9
2.4
12.3
2.5
4.0
14.0
2.9
Carotid IMT, which predicts stroke more strongly than
myocardial infarction,22 is an indirect method of assessing
atherosclerosis, which is mainly an intimal process. Because
IMT represents largely medial hypertrophy related to hypertension23,24
and a substantial proportion of strokes are due to
hypertensive small-vessel disease, it is not surprising that
IMT predicts stroke more strongly than myocardial infarction,
whereas we found the opposite for plaque area, as shown
in Table 3.
CIMT-LVH-CAD: Kromm R. A. et al. Am. J. Card. 1996; 77:
Plaque Carotid-Coronary: Megnien, I. L. et al. J Hypertens. 1998; 16:
Total carotid plaque area (the sum of cross-sectional areas of all plaques in the carotid
arteries, measured in longitudinal views of each plaque) is a
strong predictor of stroke, death, and myocardial infarction.12
Patients in the top quartile of baseline plaque area have, after
adjustment for age, sex, blood pressure, cholesterol, pack
years of smoking, homocysteine, diabetes, and treatment of
lipids and blood pressure, a relative risk of 3.4 for stroke,
death, and myocardial infarction compared with patients in
the lowest quartile of baseline plaque area. Patients with
progression ( 45% of cases) had twice the risk of those with
regression (35% of cases) or stable plaque (20% of cases).12
Plaque volume and plaque area are closely related
(R 0.93);21 therefore, it is expected that plaque volume will
also be a strong predictor of outcomes; long-term studies will
be needed to confirm that.
Spence JD & al. Stroke (12):
Buithieu J /

52. PLAQUE AREA Regression vs Progression
Spence JD & al. Stroke (12):
Buithieu J /

53. PLAQUE AREA Progression
Spence JD & al. Stroke (12):
Buithieu J /

54. PLAQUE AREA Predictor for MI and CVA
CIMT : mostly medial thickness Medial hypertrophy related to HTN Correlation w LVH > CAD predicts CVA > MI
Plaque area : intimal process related to ASO High associated with coronary plaque predicts MI more strongly
Carotid IMT, which predicts stroke more strongly than
myocardial infarction,22 is an indirect method of assessing
atherosclerosis, which is mainly an intimal process. Because
IMT represents largely medial hypertrophy related to hypertension23,24
and a substantial proportion of strokes are due to
hypertensive small-vessel disease, it is not surprising that
IMT predicts stroke more strongly than myocardial infarction,
whereas we found the opposite for plaque area, as shown
in Table 3.
CIMT-LVH-CAD: Kromm R. A. et al. Am. J. Card. 1996; 77:
Plaque Carotid-Coronary: Megnien, I. L. et al. J Hypertens. 1998; 16:
Total carotid plaque area (the sum of cross-sectional areas of all plaques in the carotid
arteries, measured in longitudinal views of each plaque) is a
strong predictor of stroke, death, and myocardial infarction.12
Patients in the top quartile of baseline plaque area have, after
adjustment for age, sex, blood pressure, cholesterol, pack
years of smoking, homocysteine, diabetes, and treatment of
lipids and blood pressure, a relative risk of 3.4 for stroke,
death, and myocardial infarction compared with patients in
the lowest quartile of baseline plaque area. Patients with
progression ( 45% of cases) had twice the risk of those with
regression (35% of cases) or stable plaque (20% of cases).12
Plaque volume and plaque area are closely related
(R 0.93);21 therefore, it is expected that plaque volume will
also be a strong predictor of outcomes; long-term studies will
be needed to confirm that.
Spence JD & al. Stroke (12):

55. PLAQUE VOLUME
N = 21
N = 17
We found that 3D US measurement of plaque progression
demonstrated statistically significant effects of a highly efficacious
therapy in a small sample over 3 months. This
methodology promises to be extremely useful in evaluation of
new therapies. A major advantage of 3D plaque measurement
relates to the way that plaques grow. Plaque progresses along
the vessel (in the axis of flow) 2.4 faster than it thickens22
and also grows circumferentially. Therefore, methods that
capture longitudinal and circumferential growth and regression
of plaque are inherently more sensitive to change in
plaque over time and with therapy than methods limited to
measurement of change in thickness.
Table 2 shows sample size estimates for treatments with
effect sizes compared with that of atorvastatin. Assuming that
progression on placebo and regression on atorvastatin continue
in a linear fashion, with equal variances (an SD of
80 mm3, ie, slightly more than the average variance of the 2
groups), a treatment 25% as effective as atorvastatin would
require 86 patients per group treated over 3 months, or 22 per
group treated over 6 months to give a power of 90% to show
a 2-tailed difference significant at the 0.05 level. Sample sizes
using the results from the analysis of covariance were
somewhat smaller.
By comparison, measurement of IMT requires much larger
sample sizes for much longer times. Bots et al23 reported that
a treatment with an effect size of 30% would require 468
patients followed for 2 years to give a power of 80% to show
an effect significant at the 0.05 level. A similar sample size
(366 per group over 2 years) was calculated for the Study to
Evaluate Carotid Ultrasound Changes in Patients Treated
with Ramipril and Vitamin E (SECURE) trial comparing
effects of ramipril and vitamin E on progression of IMT.24
Newer methods of IMT measurement using automated edge
detection25 may reduce sample sizes by reducing variability
of measurement25 to as low as 68 per group followed for 1
year to give a 90% power of showing a 30% treatment effect
Ainsworth CD & al. Stroke
Buithieu J /

56. IMT vs Plaque area vs Plaque volume
CIMT
Hypertension
Total Plaque Area
Smoking
Plasma cholesterol
Total Plaque Volume
Diabetes
Ultrasound measurements are both surrogate markers and risk factors for atherosclerosis end points. Carotid intima-media thickness (IMT)
is most commonly used, but ultrasound can also define structures in higher spatial dimensions, such as total plaque area (TPA) and total plaque
volume (TPV). Because there are minimal data regarding the relationship between IMT, TPA and TPV, we measured these variables in 272
Oji-Cree subjects.We found pairwise correlations for IMT:TPA, IMT:TPV and TPA:TPV of 0.507, and 0.846, respectively (transformed
variables, all P < ).
In a subset of 168 subjects (100 females - 68 males) with complete cardiovascular risk factor data, we performed multivariate regression
analysis to identify sources of variation for IMT, TPAand TPV.We found that the ultrasound traits showed different correlations with individual
cardiovascular risk factors. In particular, IMT was significantly associated with hypertension, TPA with smoking and plasma cholesterol, and
TPV with diabetes. Therefore, these ultrasound measures of carotid artery morphology, while somewhat correlated, likely represent distinctive
quantitative traits with different biological determinants, as underscored by different risk factor associations in the multivariate regression
analysis. Because the measurements have different implications and determinants, investigators might need to be selective about the particular
measurements they choose for specific applications.
Al-Shali & al. Atherosclerosis :
Buithieu J /

57. Plaque roughness IMT roughness
Imaging Research laboratories
Stroke Prevention and Atherosclerosis Research Centre
Robarts Research Institute, London , Ontario, Canada
IMT roughness
N = 15 healthy (24.9 ± 2.3) N = 22 healthy (62.9 ± 3.5) N = 46 CAD (62.0 ± 9.2)
AUC SE
p level
CIMT mean
0.66
0.07
0.03
CIMT max
0.71
0.01
IMT roughness
0.80
0.00
Young
healthy
Older
CAD
CIMT mean
0.55
0.77**
0.88
CIMT max
0.65
0.87**
1.01
IMT roughness
0.035
0.040*
0.075**
* p < ** p < 0.01
Schmidt-Trucksass A & al. Atherosclerosis :57-65
Buithieu J /

58. Reference Values for CIMT (75th percentile)
1.2
1.0
0.8
0.6
CIMT (mm)
0.4
0.2
0.0
Age (years)
Redberg R & al. JACC Task Force #3. J Am Coll Cardiol :
Buithieu J /

59. IMT selon l’âge
Age IMT (years) (mm)
Familial HC
Normal controls
Figure 4. Arterial wall thickness progression estimates in personsheterozygous for familial hypercholesterolemia (FH; LDL-C7.2$2.0 mmol/L; IMT 0.79$0.20 [range, 0.45 to 1.53] mm; reddots) and healthy controls (LDL-C 3.4$0.8 mmol/L; IMT0.63$0.14 [0.48 to 1.14] mm; blue dots). For the pooled FH (redline) and the pooled control data (blue line), IMT increase wasestimated by linear regression (with respective 95% confidenceintervals depicted in gray lines). On average, healthy controlsreach an IMT of approximately 0.8 mm at age 80, whereas FHsubjects reach this value (and, if untreated, often their first cardiovascularsymptoms) around the age of 40 years.
From Weingert M, SSVQ 2006
De Groot Circ. 2004; 109 (suppl): 111:33-38

60. IMT conclusion 1 Atherosclerosis is a diffuse disease
Detection in one vascular bed highly associated with atherosclerosis in other beds
Carotid atheroma associated with increased risk of vascular events in direct relationship to extent of atherosclerosis
IMT ≥ 1 mm vs. < 1 mm, associated with 5-fold increased risk of CAD
Risk for CVA and MI correlate with carotid IMT independent of standard risk factors (ARIC)
Adapted from Weingert M SSVQ 2006

61. IMT conclusion 2 Progression and relations
Normal progression is mm/year
Direct relationship between number of risk factors and IMT
Direct relationship between IMT and CAD and cardiac events as well as stroke
Burk, G.I. et al Stroke 1995; 26:
O’Leary, D.H. et al NEJM, 1999; 340:14-25
Mannami, T. et al Arch.-Int. Med 2000; 160:
Hodes, H.N. et al Ann Int Med 1998; 128:

62. IMT conclusion 3 ↑ Carotid IMT: Associations
IMT augmentation is associated with:
White matter lesions on MRI
Coronary disease on catheterization
EBCT coronary artery calcification
LVH on echocardiogram
Microalbuminuria in diabetics
Peripheral Vascular Disease
Adapted from Weingert M SSVQ 2006

63. IMT conclusion 4 Carotid IMT: Usefulness
Reflects impact of multiple risk factors
Mirrors atherosclerotic burden
Predictor of cardiovascular and neurological events
Can reclassify patient to higher risk category, worthy of more aggressive treatment

64. Diagnosis of Asymptomatic Atherosclerosis
Recommendations for the Management of Dyslipidemia and the Prevention of Cardiovascular Disease: 2003 Update
Diagnosis of Asymptomatic Atherosclerosis
Recommended
Physical examination
Ankle-brachial index
Possibly useful in subjects at moderate risk
Carotid ultrasonography
Electrocardiography
Graded exercise testing in Men > 40 with risk factors
Genest JG & al. Can Med Assoc J (9):

65. Diagnosis of Asymptomatic Atherosclerosis
Recommendations for the Management of Dyslipidemia and the Prevention of Cardiovascular Disease: 2003 Update
Diagnosis of Asymptomatic Atherosclerosis
Not currently recommended based on available evidence
Flow-mediated vasodilatation
Plethysmography
Arterial compliance
Electron beam CT scanning
MRI scanning
Intravascular ultrasonography
Genest JG & al. Can Med Assoc J (9):

66. Class IIa, Level of evidence C Class IIb, Level of evidence C
2006 Position Statement Recommendations for the Diagnosis and Treatment of Dyslipidemia and Prevention of Cardiovascular Disease
Useful non-invasive investigations in the intermediate risk category to detect subclinical atherosclerosis and/or to further define future CAD risk
Ankle-Brachial Index (ABI)
Carotid ultrasound
Graded exercise testing (GXT)
Electrocardiogram (ECG)
Class IIa, Level of evidence C
Class IIb, Level of evidence C
MacPherson R & al. Can J Cardiol October In Press