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HATA ET AL
AGGRESSIVE LIPID CONTROL FOR SVG DISEASE
Group I
Group II
13.6 1.6
Study duration (month) 13.7 1.3
LDL (mg/dL)
64.1 11.9 130.2 66.1
HDL (mg/dL)
50.3 17.3
48.7 8.2
LDL/HDL ratio
1.36 0.34
2.64 1.25
TG (mg/dL)
160.2 81.0 125.8 61.1
HbA1c (mg/dL)
6.0 0.9
6.3 1.4
hsCRP (mg/dL)
0.045 0.100 0.116 0.020
a
Age
Male/female
Hypertension (%)
Diabetes (%)
Smoking (%)
Numbers of grafts
Target vessel for SVGs
LAD
CX
RCA
Group I
Group II
p Value
62.3 11.8
9/1
80
50
40
3.30 0.48
63.7 6.9
8/3
63.6
45.5
45.5
3.27 0.47
0.5624
0.3141
0.4071
0.835
0.8008
0.1315
0.7887
1
4
8
2
5
7
CX circumflex artery;
LAD left anterior descending artery;
RCA right coronary artery;
SVG saphenous vein graft.
p Value
0.5345
0.0038
0.3463
0.0036
0.2018
0.2007
0.0125
Statistical Examination
Results were expressed as the mean SD. Statistical
calculations were conducted using StatView (SAS Inc, Cary,
NC). Using parametric and nonparametric data, statistically
significant differences were determined using the Student t
test and Fisher exact test, respectively. A p value of less than
0.05 was considered statistically significant.
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ADULT CARDIAC
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ADULT CARDIAC
HATA ET AL
AGGRESSIVE LIPID CONTROL FOR SVG DISEASE
Results
There was no difference between the groups in terms of
average age, sex, prevalence of hypertension, diabetes,
smoking, and target vessels of SVGs (Table 1). Average
postoperative study duration was approximately 14
months in both groups (Table 2). The serum LDL-C level
was significantly lower in group I (64.1 11.9 mg/dL)
compared with group II (130.2 66.1 mg/dL) (p 0.0038;
Table 2). The LDL/HDL ratio was significantly lower in
Fig 3. Entire clear white intima without any yellow plaque and
thrombi detected by angioscopy. Around the distal anastomosis site.
Group I
Group II
p Value
5 SVGs (35.7%)
0.032
11 SVGs (78.6%)
0.0001
0
0
14 SVGs (100%)
11 SVGs (78.6%)
0.0001
0.0001
diseases such as yellow plaque and thrombi was significantly higher in group II than in group I (p 0.0001;
Table 3). During follow-up periods, there was no coronary event in either group.
Comment
It is evident from this angioscopic study that the major
features of SVG diseases are the presence of unstable
atherosclerotic plaques and thrombi. Especially, SVG
atherosclerosis predisposes to thrombosis because of the
high content of lipids and tissue factor, chronic flow
disturbances, and associated impairment of vasodilatation. The SVG atheromas are more diffuse and vulnerable to rupture, and the major consequences of plaque
rupture in SVGs seem to be rapid platelet aggregation
and certain thrombotic occlusion [12]. Therefore, antiplatelet agents and cholesterol lowering therapy are
theoretically attractive options for the prevention of such
consequences.
In the present study, all patients received ticlopidine as
well as aspirin. Our previous study [9] showed that
ticlopidine reduced the development of SVG thrombi
caused by nonlaminar or sluggish flow within the SVG.
Several investigators have also reported that the addition
of ticlopidine to aspirin significantly inhibited high shear
stress which induced platelet aggregation [13]. In the
present study, although the patients in both groups have
received the same antiplatelet therapy, more than 70% of
SVGs in group II still had thrombi; no thrombi, on the
other hand, was detected in all group I SVGs. It should be
demonstrated that thrombi on the yellow plaques were
not only caused by platelet aggregation due to sluggish
blood flow, but also by multiple plaque rupture of vulnerable plaques [14, 15]. The predominant mechanisms
for SVG disease are intimal hyperplasia appearing from
postoperative early phase and accelerated atherosclerosis. Saphenous vein graft atherosclerosis is especially
prone to thrombi because of the high content of lipids
and tissue factor, chronic flow disturbance, and impaired
vasodilation. These SVG atheroma are more diffuse and
vulnerable to rupture, and the consequences of plaque
rupture in SVGs seem to be associated with almost
certain thrombotic occlusion [12]. Therefore, regular antiplatelet therapy is not enough to avoid SVG thrombi; it
may be more important and essential to interrupt the
development of vulnerable yellow plaques.
A post-CABG trial with angiographic assessment has
shown that aggressive lowering and maintenance of the
LDL-C level below 100 mg/dL was more effective than
moderate lowering of LDL-C in reducing the progression
of atherosclerosis in SVGs. It defined the prognostic
factors for risk of atherosclerotic progression in SVGs in
the large and well-characterized post-CABG patient population [10]. In the present study, the LDL-C level of
group I was maintained below 80 mg/dL. However, the
National Cholesterol Education Program (NCEP) Adult
Treatment Panel III guidelines now recommend achieving more aggressive target levels (an LDL-C level 70
mg/dL) in certain very high-risk secondary prevention
HATA ET AL
AGGRESSIVE LIPID CONTROL FOR SVG DISEASE
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Study Limitation
This study has several limitations. It is a case control
analysis of a single institution. Therefore, the sample size
was slightly small, quantitative coronary analysis in angiography has not been conducted, and we have no data
of coagulation factors in each patient. In the aggressive
lipid controlling therapy, however, serum LDL-C and the
LDL/HDL ratio were quite strictly controlled lower than
80 mg and 1.5, respectively. These lipid controls were
much more aggressive than those of a previous report
[10]. Furthermore, as far as we know, the data from SVG
endoscopy in very high-intensity statin therapy is quite
unique and results were obviously better than regular
treatment. We have to keep observing the patients and
ADULT CARDIAC
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HATA ET AL
AGGRESSIVE LIPID CONTROL FOR SVG DISEASE
12.
Conclusion
Prophylactic treatment for yellow plaque and thrombus
formation are extremely important in the development of
early and late SVG disease. Use of more effective new
generation statins is vitally important to achieve a LDL/
HDL ratio below 1.5. Aggressive lipid controlling therapy
is quite attractive to avoid post-CABG SVG disease and
the study indicated that it may be effective to maintain
the long-term graft patency.
13.
References
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