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Maher VMG et al. JAMA. 1995;274:1771-1774.
Stein JH, Rosenson RS.  Arch Intern Med. 1997;157:1170-1176.
Lp(a) in Atherogenesis: Another Culprit?
Identical to LDL particle except for addition of apo(a)
Plasma concentration predictive of atherosclerotic disease in many epidemiologic studies, although not all
Accumulates in atherosclerotic plaque
Binds apo B-containing lipoproteins and proteoglycans
Taken up by foam cell precursors
May interfere with thrombolysis
RR=relative risk; HT=hypertension; GI=glucose intolerance.
Bostom AG et al. JAMA. 1996;276:544-548.
1.9
1.8
1.8
1.2
2.7
3.6
RR
0.1
1
10
2
5
0.2
0.5
 Lp(a) TC HDL-C HT GI Smoking
Lp(a): An Independent CHD Risk Factor in
Men of the Framingham Offspring Cohort
Lp(a)=lipoprotein(a); CHD=coronary heart disease.
38.01
22.14
12.44
11.06
39.30
19.60
Total
57.31
23.06
18.99
13.41
45.39
22.22
5 (8.2-47.5)
36.97
20.53
12.18
 9.23
42.41
20.31
4 (5.6-8.1)
34.96
25.38
13.43
10.34
41.58
18.21
3 (3.1-5.5)
37.00
18.69
12.26
11.44
33.01
17.05
2 (1.3-3.0)
33.47
22.92
 6.33
11.38
36.15
19.87
1 (0.1-1.2)
Men
Women
Men
Women
Men
Women
Death
Stroke
CHD
Quintile (mg/dL)
No. of events/1,000 person-years
Adapted from Ariyo AA et al. N Engl J Med. 2003;349:2108-2115.
Lp(a): Vascular Events by Sex and Quintile
at Baseline (Cardiovascular Health Study)

McCully KS. Am J Pathol. 1969;56:111-128.
McCully KS. JAMA. 1998;279:392-393.
Rimm EB et al. JAMA. 1998;279:359-364.
Homocysteine: Role in Atherogenesis
Linked to pathophysiology of arteriosclerosis in 1969
CVD patients have elevated levels of plasma homocysteine
May cause vascular damage to intimal cells
Elevated levels linked to:
genetic defects
exposure to toxins
diet
Increased dietary intake of folate and vitamin B6 may reduce CVD morbidity and mortality
PDAY= Pathobiological Determinants of Atherosclerosis in Youth.
Fatty streaks
Raised lesions
White
15-19
20-24
25-29
30-34
0
10
20
30
Women
0
10
20
30
15-19
20-24
25-29
30-34
Black
Age (y)
0
10
20
30
White
15-19
20-24
25-29
30-34
Men
Black
15-19
20-24
25-29
30-34
0
10
20
30
Intimal surface (%)
Strong JP, et al. JAMA. 1999;281:727-735.
PDAY: Percentage of Right Coronary Artery
Intimal Surface Affected With Early
Atherosclerosis
McGill HC Jr, et al. Circulation. 2000;102:374-379.
20
0
40
60
80
100
15-19
Age (y) Prevalence (%)
30-34
25-29
60
60
40
40
20
20
0
0
0
1
2
3
4
5
0
20
40
60
20-24
0
1
2
3
4
5
AHA lesion grade
AHA lesion grade
Women
Men
Error bar=SE.
PDAY: Prevalence of Lesions in LAD
Post MI/Angina
Other Atherosclerotic
 Manifestations
Subclinical Atherosclerosis
Multiple Risk Factors
Low Risk
Secondary
Prevention
Primary Prevention
Courtesy of CD Furberg.
Continuum of Patients at Risk
for a CHD Event
Study
N
Patient type
Therapy
Duration
(yr)
% (Control-Treatment)
Progression
 
 Regression
Lifestyle
28
CAD
Diet,
 exercise,
meditation
1
35
-40
STARS
90
CAD, high
 TC
Diet (including
-
 fiber)
3.2
35
-38
Heidelberg
113
CAD
Diet + exercise
1
25
-15
Superko HR, Krauss RM. Circulation. 1994;90:1056-1069.
Effect of Lifestyle Changes on Angiographic CAD
Pedersen TR et al. Am J Cardiol. 1998;81:333-335.
Fraction of patients
Fraction of patients
Fraction of patients
Fraction of patients
Months
Months
Months
Months
Simvastatin
Placebo
Intermittent Claudication
Carotid Bruit
Angina
Cerebrovascular Events
4S: Effects of Cholesterol Lowering on
Noncoronary Ischemic Symptoms and Angina
?2004 PPS?
% ?
Baseline lipid levels (mg/dL).
Fluvastatin: TC 222.3, LDL-C 146.4, HDL-C 43.6, TG 161.2.
Placebo: TC 221.0, LDL-C 144.7, HDL-C 44.7, TG 158.5.
-14.7
-23.9
8.5
-0.1
-0.7
-3.8
4
9.9
-13.5
-22.5
8.7
-0.1
-2.2
3.9
9.5
0.3
-30
-20
-10
0
10
20
All fluvastatin
All placebo
Fluvastatin only
Placebo only
TC
LDL-C
HDL-C
TG
Herd JA et al. Am J Cardiol. 1997;80:278-286.
LCAS: Effect on Lipids Between Baseline and End of Trial

MLD=minimum lumen diameter.
? MLD (mm)
-0.041
-0.024
-0.028
-0.117
-0.094
-0.1
-0.16
-0.14
-0.12
-0.10
-0.08
-0.06
-0.04
-0.02
0.00
Fluvastatin
Placebo
Monotherapy P=0.0161
Adjunctive cholestyramine
P=0.1389
All patients
P=0.0051
n=171
n=169
n=129
n=132
n=42
n=37
Herd JA et al. Am J Cardiol. 1997;80:278-286.
LCAS: Primary End Point Change in MLD Between Baseline and Angiogram

% of patients
*For difference between all fluvastatin and all placebo patients in the distribution among the three categories.
28.7
14.6
56.7
39.1
8.3
52.7
0
10
20
30
40
50
60
70
Definite progression
Definite regression
Mixed or no response
All fluvastatin
All placebo
P=0.0198*
Herd JA et al. Am J Cardiol. 1997;80:278-286.
LCAS: Effect of Treatment on Patients
Experiencing Progression or Regression

Herd JA et al. Am J Cardiol. 1997;80:278-286.
LCAS: Conclusions

? progression of atherosclerosis in patients with mild to moderate cholesterol elevations
Angiographic benefits: ? progression of coronary blockage measured by MLD (increases), % diameter stenosis (decreases), and new lesions
Fewer patients had progression, and more patients had regression
Similar changes in MLD seen in patients with LDL-C 3160 mg/dL, <160 mg/dL, and <130 mg/dL
In subset of patients undergoing PET, qualitative assessment at rest indicated improvement in myocardial perfusion
Although study was not designed to detect differences in clinical end points, favorable trends in event reduction were observed

Post-CABG Trial Investigators. N Engl J Med. 1997;336:153-162.
Post-CABG: Impact of Aggressive vs Moderate Lowering of LDL-C on Atherosclerosis
Study group characteristics
Sample size: 1,351 (M/F)
1 to 11 yr post-CABG
2 patent SVGs (1 in females)
LDL-C 130-174 mg/dL after diet
Treatment
Randomized, blinded to
lovastatin 40-80 mg/day + cholestyramine 8 g/day (if needed)
lovastatin 2.5-5 mg/day + cholestyramine  8 g/day (if needed)
aggressive LDL-C target: £85 mg/dL
moderate LDL-C target: 130-140 mg/dL
Monitoring
Quantitative coronary angiography
80
90
100
110
120
130
140
150
160
0
12
24
36
48
Follow-up (mo)
Aggressive Tx (93-96)*
Moderate Tx (134-136)*
6
Post-CABG Trial Investigators. N Engl J Med. 1997;336:153-162.
LDL-C
(mg/dL)
* Mean achieved.
Post-CABG Study: Aggressive vs Moderate Treatment
Post-CABG Trial Investigators. N Engl J Med. 1997;336:153-162.
Post-CABG: End Points, Results, Conclusions
Primary end point: Mean per-patient percentage of grafts with significant

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