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(Circulation. 1996;93:683-690.)
© 1996 American Heart Association, Inc.
Articles |
Absence of Focal Compensatory Enlargement or Constriction in Diseased Human Coronary Saphenous Vein Bypass Grafts
An Intravascular Ultrasound Study
Presented in part at the 67th Scientific Sessions of the American Heart Association, Dallas, Tex, November 14-17, 1994.
From the Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, Calif.
Correspondence to Robert J. Siegel, MD, Division of Cardiology, Room 5335, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, CA 90048.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Background No in vivo data are available on the occurrence of compensatory enlargement or vessel constriction in diseased human coronary saphenous vein bypass grafts (SVBGs). The aim of this intravascular ultrasound (IVUS) study was to examine to what extent lumen reduction is accompanied by (1) vessel wall thickening and (2) arterial wall constriction in SVBGs.
Methods and Results We used IVUS to examine 43 SVBGs from 42 patients (32 men, 10 women; mean age, 72±5 years) 8 to 23 (11±4) years after SVBG. IVUS images were obtained with a 3.5F monorail ultrasound catheter with a 30-MHz frequency and were analyzed at the lesion site, the reference site, and an intermediate site. The lumen area was significantly (P<.01) decreased; the vessel wall area (SVBG cross-sectional area minus lumen area) and the plaque area (area within the external elastic lamina minus lumen area) were significantly (P<.01) increased from the reference site through the lesion site. However, SVBG cross-sectional area was the same at these three sites (24.0±8.1 versus 24.4±8.6 versus 24.5±8.6 mm2, P=NS), and the external elastic lamina area was also quite constant in each vessel (17.8±6.0 versus 17.7±6.4 versus 17.6±6.2 mm2, P=NS).
Conclusions These in vivo IVUS data from human coronary SVBGs demonstrate that (1) no focal compensatory enlargement or vessel constriction occurred in stenotic segments compared with the reference segments and that (2) the absence of focal compensatory enlargement appears to be a potentially important factor in the progression of stenoses in coronary SVBGs.
Key Words: veins • bypass • grafting • ultrasonics • remodeling
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Compensatory enlargement of human atherosclerotic vessels was first described by Glagov et al1 in a postmortem histopathological study of left main coronary arteries. They showed that human coronary arteries enlarge during the development of arterial atherosclerotic plaque and that the lumen area is preserved until the plaque development exceeds the compensatory mechanisms of the blood vessel. This finding has been validated in vivo in studies of human coronary arteries by use of high-frequency epicardial echocardiography2 and IVUS imaging3 4 and reconfirmed by the pathological study of the left anterior descending coronary arteries from humans and nonhuman primates.5 Compensatory enlargement is also observed in human carotid arteries by high-resolution duplex scanning6 and in superficial femoral arteries studied by IVUS.7 These observations suggest that compensatory enlargement is a common phenomenon in all human atherosclerotic arteries. Moreover, a recent study8 of human femoral arteries using IVUS imaging and histopathological techniques demonstrated that arterial wall constriction or focal failure of compensatory enlargement may be a paradoxical mechanism for the development of severe arterial luminal narrowing. However, no data exist as to whether compensatory enlargement or vessel constriction occurs in stenotic SVBGs.
Accordingly, the aim of this IVUS study was to examine to what extent lumen reduction is accompanied by (1) vessel wall thickening and (2) failed or incomplete compensatory enlargement or constriction of the stenotic vessel segment in SVBG.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Patients and Vessels Studied
Forty-eight SVBGs from 47 consecutive patients (36 men, 11 women; mean age, 71±6 years) who had not undergone previous catheter intervention were studied by IVUS 8 to 23 years (mean, 12 years) after coronary SVBG. Informed consent was obtained from all patients before the IVUS procedure. Excluded from the study were 1 vessel in which we failed to introduce the imaging catheter into the SVBG and 4 vessels in which IVUS images were suboptimal for quantitative measurements because of heavy intimal calcification of the SVBGs or a technical problem with the IVUS system. In total, images from 43 SVBGs from 42 patients were included and analyzed in this study.
IVUS System and Imaging Procedure
To ensure reproducibility
of measurements, only one IVUS system
was used in this study. The IVUS imaging system consisted of an imaging
catheter (Sonicath, Boston Scientific Corp) and a SONOS Intravascular
System imaging console (Hewlett-Packard). The imaging catheter has a
30-MHz single piezoelectric crystal transducer mechanically rotating at
1800 rpm within a 3.5F monorail over-the-wire catheter
sheath.
The right or left femoral artery was punctured by use of the Seldinger technique, an 8F or 9F arterial introducer sheath was advanced retrogradely over a guide wire, and the sheath was placed in the femoral artery. After the completion of angiography of native coronary arteries and SVBGs, the imaging catheter was introduced into the SVBG through an 8F to 9F coronary guiding catheter over a 0.014- or 0.018-in guide wire. To obtain maximum vasodilation, 100 to 200 µg of nitroglycerin was administered into the SVBG before or during the IVUS catheter imaging. After the imaging catheter was advanced across the lesion to the distal portion of the vessel under fluoroscopic guidance, IVUS imaging was performed during the slow pullback (1 mm/s) of the imaging catheter. The two-dimensional images of the SVBG were displayed on a SONOS Intravascular System imaging console and recorded on a 0.5-in Super-VHS videotape for subsequent playback, review, and quantitative analysis.
Image Analysis
IVUS images were analyzed off-line with a
SONOS
Intravascular System. In the SVBG examined, the ostial portion and the
site of anastomosis to the native coronary artery were excluded
from the measurements to eliminate any distortion due to sutures at
these sites.
In each SVBG, with digital angiographic images as a road map, three sites were selected by IVUS for quantitative analysis: the lesion site with the smallest lumen area, the reference site with the largest lumen area, and an intermediate site with a lumen area of intermediate size between the lesion and reference sites.
For these three sites in each SVBG, vessel lumen area was measured by planimetry. To assess the vessel lumen area (in square millimeters), the lumen-intimal border was traced and the area within this border was measured with a planimeter. Contrast medium was injected to enhance the ultrasound definition of the lumen in cases in which the lumen-intimal border was ambiguous.
In 36 vessels of 43 SVBGs, the
entire vessel cross-sectional area
(in square millimeters) was clearly delineated and measured by tracing
the outer border of the whole vessel, as shown in Fig 1
.
The vessel wall area (in square millimeters) was calculated by
subtracting the lumen area from the vessel cross-sectional area.
Lumen area ratio, vessel wall area ratio, and vessel
cross-sectional area ratio were also defined and calculated
according to the following formulas numbered (1), (2), and (3) compared
with the vessel cross-sectional area at the reference site: (1)
lumen area ratio=lumen area at the lesion, intermediate, or reference
site/vessel cross-sectional area at the reference site; (2) vessel
wall area ratio=vessel wall area at the lesion, intermediate, or
reference site/vessel cross-sectional area at the reference site;
and (3) vessel cross-sectional area ratio=vessel
cross-sectional area at the lesion, intermediate, or reference
site/vessel cross-sectional area at the reference site.
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In 25 vessels
of 43 SVBGs, a sonolucent zone that has been reported to
represent media9 10 was clearly visualized by
IVUS, as shown in Fig 2. The EEL of the vessel was
defined as the outer border of the sonolucent zone, and the area within
the EEL (the EEL area) was measured by planimetry. The plaque area (in
square millimeters) was defined and calculated by subtracting the lumen
area from the EEL area. Lumen area ratio, plaque area ratio, and EEL
area ratio were defined and calculated according to the following
formulas numbered (4), (5), and (6) compared with the EEL area at the
reference site: (4) lumen area ratio=lumen area at the lesion,
intermediate, or reference site/EEL area at the reference site; (5)
plaque area ratio=plaque area at the lesion, intermediate, or reference
site/EEL area at the reference site; and (6) EEL area ratio=EEL area at
the lesion, intermediate, or reference site/EEL area at the reference
site.
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In Vitro Saphenous Vein Study
In 18 SVBGs in which only
vessel cross-sectional area was
used as a marker of vessel remodeling, the plaque area could not be
calculated, and consequently the disease severity at the reference site
of SVBG was uncertain. Therefore, 7 fresh saphenous veins were
harvested from 5 patients undergoing CABG, imaged by IVUS under
physiological pressures, and compared with the
measurements at the reference sites of SVBGs. The extra saphenous vein
segments that were prepared for CABG with all their side branches tied
were obtained and stored in normal saline solution at 3°C. The IVUS
images were obtained within 6 hours of harvesting. A three-way
stopcock was attached to one end of the vessel to close the lumen, and
a Touey-Borst connector was attached to the other end. The saline
solution, attached to a pressure bag, was connected to a Touey-Borst
connector. The vessel was distended with a nonpulsatile pressure of 100
mm Hg.11 All in vitro IVUS imaging was performed in a
saline bath. The IVUS system used in this in vitro study was exactly
the same system as used for the in vivo study. The IVUS catheter was
introduced through the Touey-Borst connector, and two-dimensional
cross-sectional images of the vessel were recorded on videotape
during the slow pullback (1 mm/s) of the imaging catheter. The IVUS
images were analyzed with the same imaging console as the in
vivo study, and the same kinds of measurements and calculated
variables were derived for 35 segments selected from 7 veins in
random fashion.
In fresh saphenous veins, the lumen area and the entire vessel cross-sectional area were measured without difficulty in every case, and these measurements and the calculated data of fresh saphenous veins were compared with those of 36 SVBGs in which the vessel cross-sectional area was measured.
Reproducibility Study
Intraobserver and interobserver
variabilities of the
measurements of the lumen area and the vessel cross-sectional area
were calculated on 10 segments of SVBG selected at random from 36 SVBGs
in which the vessel cross-sectional area was measured.
Intraobserver and interobserver variabilities of the EEL area were
calculated on 10 segments of SVBG selected at random from 25 SVBGs in
which the EEL area was measured. Two independent observers measured the
lumen area, the vessel cross-sectional area, and the EEL area of
these segments on two occasions separated by a minimum of 7 days. These
data were analyzed, and the mean difference between two
observations and the range of the differences were derived.
Statistical Analysis
All data were expressed as
mean±SD. Measured and calculated
areas at the lesion site, the reference site, and the intermediate site
were compared by repeated-measures ANOVA with the
Student-Newman-Keuls test as the post hoc test. For comparison of data
between the reference segments in SVBGs and the fresh saphenous veins,
an unpaired Student's t test was performed. A value of
P<.05 was considered statistically significant.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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The IVUS studies of in vivo SVBGs were completed without any vascular complications. Of 43 SVBGs in which quantitative analysis was performed, reproducible measurements could be made for the vessel cross-sectional area in 36 SVBGs, for the EEL area in 25 SVBGs, and for both the vessel cross-sectional area and the EEL area in 18 SVBGs.
Reproducibility
For the measurement of the lumen area, the
mean difference between
two observations by the same observer was 3.1%, with a range of 0% to
9.0%. Between two observers, the mean difference was 3.8%, with a
range of 1.0% to 5.6%.
For the measurement of the vessel cross-sectional area, intraobserver variability was calculated, with a mean difference of 1.6% and a range of 0% to 2.7%. Interobserver variability was also determined, with a mean difference of 2.7% and a range of 0.4% to 5.7%.
For the measurement of the EEL area, the mean difference between two observations by the same observer was 1.7%, with a range of 0% to 3.2%. Between two observers, the mean difference was 2.7%, with a range of 0.8% to 4.5%.
Fresh Saphenous Veins and SVBGs in Which the Vessel
Cross-sectional Area Was Measured
The measured and calculated data of
in vitro fresh saphenous veins
are summarized in Table 1 and Fig 3. The
lumen-intimal border and the outer border of the entire vessel were
clearly delineated without difficulty in every case, but the sonolucent
zone was not observed or was ambiguous in most cases. Consequently,
only lumen area and vessel cross-sectional area were measured, and
lumen area ratio, vessel wall area ratio, and vessel
cross-sectional area ratio were calculated. Even fresh saphenous
veins had a substantial vessel wall area of 7.4±2.1
mm2, which occupied 
30% of the total vessel
cross-sectional area.
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Fig 1
shows IVUS images of one of
the 36 SVBGs in which the outer
border of the entire vessel was clearly visualized. In 53% (19/36) of
SVBGs, as shown in Fig 1, the vessel was surrounded by minimal
tissue
or separated from the surrounding tissue, and the outer border of the
entire vessel was traced without difficulty. Even when the whole
circumference of the SVBG was surrounded by connective tissue, the
outer border was differentiated from the adjacent tissue under careful
observation of the different movements and the different echo
intensities of the vessel itself and the surrounding tissue. Despite
the disease progression from Fig 1A through 1C, the vessel
cross-sectional areas were almost identical.
The measured and
calculated data of in vivo SVBGs in which the vessel
cross-sectional area was measured are summarized with those of
fresh saphenous veins in Table 1 and Fig 3. All
values at the reference
sites of the SVBGs were similar to those of the fresh saphenous veins.
In the SVBGs, the lumen area was greatest at the reference site
(15.8±5.0 mm2), moderate at the intermediate site
(9.4±3.4 mm2), and least at the lesion site (5.5±2.2
mm2), as expected from the definition of these three sites.
The vessel wall area was greatest at the lesion site (19.0±7.4
mm2), moderate at the intermediate site (15.0±6.2
mm2), and least at the reference site (8.4±3.9
mm2). All differences of measurements among these sites
were statistically significant (P<.01). However, the SVBG
cross-sectional areas were quite constant in each vessel, measuring
24.0±8.1 mm2 at the reference site, 24.4±8.6
mm2 at the intermediate site, and 24.5±8.6 mm2
at the lesion site.
Fig 4A and 4B
demonstrates the relation between lumen
area ratio and vessel cross-sectional area ratio (A) and between
lumen area ratio and vessel wall area ratio (B). In Fig 4A, if
focal
compensatory enlargement of SVBG occurs at the stenotic
segments, the vessel cross-sectional area ratio should become
larger as the vessel lumen area ratio decreases, and if failed or
incomplete compensatory enlargement, or constriction of the
stenotic vessel segment occurs, the vessel cross-sectional
area ratio should decrease, accompanying the lumen area ratio
reduction. However, the vessel cross-sectional area ratio was near
one and constant for the intermediate and stenotic lesion sites
compared with the reference sites. Moreover, the variability of the
SVBG cross-sectional area (mean±SD, 1.009±0.052; range, 0.825 to
1.136) shown in this graph was almost identical to that of the fresh
saphenous veins (mean±SD, 1.013±0.076; range, 0.868 to 1.240).
In Fig 4B, the plotted points of the vessel wall area ratios of
the
stenotic vessel segments (intermediate and lesion sites)
indicate that lumen area reduction is due to the increase in vessel
wall area.
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SVBGs in Which the EEL Area Was Measured
Fig 2
shows IVUS images of one of the 25 SVBGs in which the EEL
area was measured. No focal compensatory enlargement was observed at
the intermediate site and the stenotic lesion site compared
with the reference site, despite the disease progression from Fig
2A
through 2C.
Table 2 and Fig 5 summarize
the measured
and calculated data of SVBGs in which the EEL area was measured. The
lumen area significantly (P<.001) decreased and the plaque
area significantly (P<.01) increased from the reference
site through the lesion site. However, the EEL areas were quite
constant in each vessel, measuring 17.8±6.0 mm2 at the
reference site, 17.7±6.4 mm2 at the intermediate site, and
17.6±6.2 mm2 at the lesion site.
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Fig
6A and 6B demonstrates the relation between
lumen
area ratio and EEL area ratio (A) and between lumen area ratio and
plaque area ratio (B). In Fig 6A, the EEL area ratio was near
one and
constant (mean±SD, 1.014±0.075; range, 0.863 to 1.194) for the
intermediate and stenotic lesion sites compared with the
reference sites. In Fig 6B, the plotted points of plaque area
ratios of
the stenotic vessel segments (intermediate and lesion sites)
indicate that lumen area reduction is due to the increase in plaque
area.
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SVBGs in Which Both the EEL Area and the Vessel Cross-sectional
Area Were Measured
The measured and calculated data of 18 SVBGs in
which both the EEL
area and the vessel cross-sectional area were measured are
summarized in Table 3. The lumen area was significantly
(P<.001) decreased and the plaque area and the EEL area
were significantly (P<.01) increased from the reference
site through the lesion site. However, the EEL areas and the vessel
cross-sectional areas were quite constant, and the EEL area ratio
and the vessel cross-sectional area ratio were near one.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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This is the first study to demonstrate an absence of focal compensatory enlargement or vessel constriction (shrinkage) in diseased human coronary SVBGs. Our in vivo IVUS study of three different segments in SVBGs using the total vessel cross-sectional area or the area within the EEL as an index of vessel remodeling found that no focal compensatory enlargement or vessel constriction occurs in the stenotic segments compared with the reference segments with minimal disease. The SVBG behaves like a prosthetic conduit without any difference in the vessel cross-sectional area and the EEL area among the lesion site, intermediate site, and reference site. These unique findings in SVBGs are different from previous reports demonstrating the presence of compensatory enlargement in native coronary arteries by postmortem histopathological examination,1 5 epicardial echocardiography,2 and IVUS imaging3 4 or from the paradoxical constriction or the focal failure of compensatory enlargement reported by Pasterkamp et al8 in femoral arteries using IVUS imaging and histopathological examination. The absence of focal compensatory enlargement in stenotic SVBGs appears to be a potentially important contributing factor associated with the progression of stenoses in coronary SVBGs.
Technical Concerns
To investigate the vascular remodeling in
human coronary
arteries, three conventional quantitative techniques are used:
pathological study, epicardial ultrasound imaging during cardiac
surgery, and IVUS imaging during coronary
catheterization. In pathological studies, perfusion
fixation is needed to prevent shrinkage of the specimen. However, even
this fixation method and pathological preparation alter quantitative
measurements and thus are not ideal compared with in vivo
studies.12 Epicardial ultrasound imaging is performed
under general anesthesia, in an open-chest state, and
the ultrasound probe is placed directly on the exposed epicardial
coronary artery; thus, measurement of dimension and area of the
vessel may not represent the normal
physiological state. The accuracy of IVUS
measurements has been validated.13 14 However, IVUS
imaging, which requires selective SVBG catheterization
and insertion of the imaging catheter into the vessel, has the
potential to cause vasospasm in up to 3% of
patients.15 16 To prevent this potential side effect,
100
to 200 µg of nitroglycerin was injected directly into
the SVBG before or during the imaging with the IVUS catheter. No
clinically or angiographically apparent vasospasm was detected in this
study.
In studies of native coronary arteries using IVUS, lumen area and area within the internal elastic lamina or EEL are usually measured because the sonolucent zone reported to represent the media9 10 is often relatively clear and the border between the adventitia and surrounding connective tissue is usually difficult to differentiate. However, in the study of SVBGs, it is unclear which portion of the vessel wall, intima, media, or adventitia results in remodeling of the whole vessel. Therefore, in this study, we used both the EEL area and the vessel cross-sectional area to examine the focal compensatory enlargement or vessel constriction in SVBGs. We found that of 43 SVBGs, the outer border of the whole vessel was clearly demonstrated in 36 vessels (84%) and a circumferential sonolucent zone was identified in 25 vessels (58%). The difference between SVBGs and native coronary arteries in the ability to measure the vessel cross-sectional area and the EEL area may reflect the pathological changes that occur in SVBGs after implantation as arterial conduits. The media and the adventitia are reported to be replaced with fibrous tissue, and the internal and external elastic laminae may become obscure even under microscopic examination.17
In cases in which the sonolucent zone of the SVBG was not identified and only the outer border of the vessel was delineated, the plaque area could not be calculated, and therefore, the disease severity at the reference site in SVBG was uncertain. Therefore, to compare the disease severity between the reference site in SVBGs and that of fresh saphenous veins, we measured in vitro the lumen area and the vessel cross-sectional area of fresh saphenous veins that were prepared for CABG but not used. The measured and calculated variables of the reference sites in SVBGs were very similar to those of fresh saphenous veins. These data suggest that the reference sites of the SVBGs are minimally diseased and can be used as true references in this study.
Intraobserver and interobserver variabilities for measurements of lumen area, vessel cross-sectional area, and EEL area in SVBGs were quite small, with mean differences of <4%. Thus, the measurements are considered to be reproducible and reliable.
Compensatory Enlargement in Native Coronary Arteries and
Other Arteries
Compensatory arterial enlargement in response to
plaque formation was first described in coronary
arteries18 and peripheral
arteries19 of monkeys and was illustrated in human left
main coronary arteries by postmortem
histological examination.1 Glagov et
al1 showed that human left main coronary arteries
enlarge in relation to the development of atherosclerotic plaque and
that the lumen area is preserved until the plaque development exceeds
the compensatory mechanisms of the vessel, usually when plaque size is
40% of the arterial cross-sectional area. Although
the mechanisms of compensatory arterial enlargement have
not been clarified, some hypotheses have been proposed20 :
(1) The local increase in wall shear stress caused by plaque
development may stimulate endothelium-dependent
arterial dilatation or (2) the development of plaque may
lead to degradation of the media and adventitia, resulting in passive
bulging of the plaque. This concept of compensatory enlargement
suggests and is consistent with the findings that
angiographically normal or nearly normal segments of the artery have
substantial plaque, and further, that the lesion severity can
frequently be underestimated by angiography, which visualizes only the
lumen of the vessel. This finding has been validated in in vivo human
coronary arteries by IVUS imaging3 4 and also
confirmed by the pathological study of the left anterior descending
coronary arteries from humans and nonhuman
primates.5
As noted by Losordo et al,7 however, many of the conclusions of pathological and IVUS studies1 3 4 5 are based on the correlation between plaque area size and vessel area size pooled from single measurements of different vessels of different individuals, and no comparison was made within the same vessel. If lumen area size, plaque area size, and vessel area size of different individuals are analyzed together, the interpretation of the data becomes very complex because the vessel size is reported to vary according to age, body weight, height, heart size, sex, blood pressure level, and plasma lipid concentrations.1 5 21 In studies of native human coronary arteries, only McPherson et al2 have previously compared coronary arterial size at proximal and distal coronary segments by epicardial echocardiography. They showed that in patients with coronary arterial lesions, total arterial area increased from the proximal reference site to the lesion site of the artery, confirming the concept of compensatory enlargement in native coronary arteries. In our study, the factors that make the measurements at the lesion site, intermediate site, and reference site comparable are that each of the segments are a part of the same vessel, that each segment of the SVBG was exposed to the same systemic factors over time, and that the SVBGs have no side branches, which have been reported to affect vessel size.22
Our findings do not exclude the possibility that uniform vessel enlargement or constriction was occurring in the whole SVBGs, because no control measurements were made just after the implantation of the SVBGs. There are inherent limitations to using in vitro fresh saphenous veins as a reference standard, even when imaged, as in this study, under physiological pressures. Namely, the size of the vein graft itself and the lack of physiological conditions all may create some degree of artifact. Although the vessel cross-sectional area of in vitro fresh saphenous vein was identical to that demonstrated in patients, it is still possible that this is artifactual and that the SVBG either dilated or constricted in its entirety from its condition immediately after implantation at the time of surgery. Nonetheless, it is clear from our data that there was no difference in the degree of vessel remodeling among the three different sites (reference, intermediate, and lesion site), and we believe it is unlikely that the same degree of vessel remodeling would occur at each site with different disease severity.
Development of Stenosis and Vessel Remodeling in
SVBG
The long-term patency of SVBGs is reported to be 40% to 60%
for grafts 
10 years old after CABG.23 However, in most
patients who need multiple CABGs, the two internal mammary arteries are
not sufficient, and SVBGs are needed for complete
revascularization. Thus, the autologous saphenous
vein still remains the most commonly used coronary artery
bypass conduit.
The closure of SVBGs soon after surgery is reported to
be caused by
thrombosis, whereas late closure of SVBG is due to fibromuscular
intimal hyperplasia and/or atherosclerosis, with some
contribution from mural thrombi.24 Many mechanisms
resulting in development of stenosis in SVBG are postulated,
including functional differences in venous and arterial
endothelium, mechanical and functional
endothelial damage, secondary activation of
platelet and vasoactive substances, and vessel wall
ischemia caused by the loss of vasa vasorum.17 24
In addition to these possible mechanisms, our data suggest that the
absence of focal compensatory enlargement could be one of the
mechanisms resulting in the development of stenoses in SVBGs
that have been implanted for 8 years. One possible explanation for
the absence of focal compensatory enlargement in SVBGs may be related
to fibrous tissue proliferation secondary to intimal damage and vessel
wall ischemia. Besides fibromuscular intimal hyperplasia, it
has been reported that the smooth muscle fibers of the media are
replaced, in part or in whole, by fibrous tissue and collagen, and in
the adventitia there is a marked increase in fibrous tissue, with
severe disruption or complete replacement of elastic
fibers.17 The previously described mechanisms of
compensatory arterial enlargement may not be operant under
the circumstances in which much of the normal vessel wall has been
replaced by fibrous tissue.
Conclusions
These in vivo IVUS data from human coronary SVBGs
8 to 23
years after implantation demonstrate (1) that no focal compensatory
enlargement or vessel constriction occurred in stenotic
segments compared with the reference segments and (2) that the absence
of compensatory enlargement appears to be a potentially important
factor in the progression of stenoses in coronary
SVBGs.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This work was supported in part by the Self Defense Forces Central Hospital, Japan; the Swedish Medical Association; St Paul's Hospital, South Korea; the Lee E. Siegel, MD, Memorial Fund; and the Herbert Stein, MD, Research Fund. The authors thank Dr Michael C. Fishbein for his critical review of this manuscript.
Received June 20, 1995; revision received August 23, 1995; accepted September 25, 1995.
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References |
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TopAbstractIntroductionMethods Results Discussion References |
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