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(Circulation. 1995;91:1389-1396.)
© 1995 American Heart Association, Inc.
Articles |
Angioscopic Prediction of Successful Dilatation and of Restenosis in Percutaneous Transluminal Coronary Angioplasty
Significance of Yellow Plaque
From the Division of Cardiology, National Cardiovascular Center, Suita, Osaka, Japan.
Correspondence to Akira Itoh, MD, Division of Cardiology, National Cardiovascular Center, 5-7-1 Fujishirodai, Suita, Osaka 565, Japan.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Background Coronary angiography has been used to assess the anatomy of coronary artery and intraluminal pathological changes. However, it has several limitations in its diagnostic quality and sensitivity in the detection of intraluminal details. Angioscopy has enabled coronary artery lumens to be visualized directly and fine intraluminal morphological changes to be detected. The information obtained by angioscopy is expected to provide new insights into the mechanisms and pathophysiology of transluminal coronary angioplasty.
Methods and Results Forty-seven patients (39 men and 8 women) with stable angina were enrolled in the present study. Angioscopy was performed before and after angioplasty with a 0.68-mm angioscope with a double–guiding catheter system. The patients who were successfully evaluated by angioscopy were divided into two groups according to the color of the lesion: group 1, mainly yellow; and group 2, white. Angiographic, angioscopic, and clinical parameters in the two groups were compared. Detailed angioscopic findings were obtained in 36 of the 47 patients (77%) before percutaneous transluminal coronary angioplasty (PTCA) and in 24 of the 47 (51%) after PTCA. Yellow plaque were found in 13 of 36 (36%). Age, sex, presence of coronary risk factors, serum cholesterol level, and duration of angina showed no correlation with plaque color. The incidence rates of dissection and thrombi after angioplasty also were not different. Successful dilatation was achieved in 13 of 13 patients (100%) in group 1 and in 21 of 23 (91%) in group 2. The restenosis rate of group 1 was significantly lower than that in group 2 (16.7% versus 57.9%, P<.05). Cox proportional hazards model revealed that plaque color was the independent variable associated with restenosis after PTCA (P=.03).
Conclusions The restenosis rate after successful balloon angioplasty differs, with the color of the target lesion being significantly higher in patients with solely white plaque. Therefore, angioscopic findings are highly predictive of restenosis.
Key Words: coronary disease • restenosis • angioscopy • angioplasty
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Coronary angiography is an established technique for the identification of coronary artery stenosis and the determination of its severity. However, it has several limitations of diagnostic quality. First, in many cases it is difficult to differentiate thrombus from atheromatous plaque, because angiography is able to show only the silhouette of the intraluminal pathological changes. Second, the severity of stenosis may be underestimated when compared with the postmortem pathological diagnosis.1 Novel diagnostic modalities for coronary artery lesions, such as coronary angioscopy and intravascular ultrasound, are expected to supplement coronary angiography. Angioscopy is superior in the investigation of vascular internal surface, ie, color, surface plaque morphology, and presence or absence of mural thrombi. This information may provide new insights into the mechanism of dilatation and restenosis in catheter-based coronary dilatation procedures. Recently, angioscopic findings of coronary arteries have been reported in patients with acute myocardial infarction,2 in patients with unstable angina pectoris,2 3 4 and in conjunction with other newly developed interventional therapeutic devices.5 6 7 8 However, the correlation of angioscopic findings with long-term results after coronary interventions has not been fully determined. The goal of the present study was to investigate with coronary angioscopy the color and shape of plaque in coronary arterial lesions of patients with stable angina and to clarify the correlation of the findings with the late outcome after percutaneous transluminal coronary angioplasty (PTCA).
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Patients
Forty-seven patients with stable angina pectoris (39 men and 8 women; age, 57±9 years) were enrolled in the present study. Eight had a prior myocardial infarction associated with the target vessel of PTCA. Four patients (patients 5 and 7 in group 1 and patients 8 and 14 in group 2) had had a prior PTCA in the same vessel. Their sites of stenosis were in the proximal portion of the major epicardial coronary arteries, and the section between coronary ostium and the target lesion was not tortuous, so they were considered suitable for coronary angioscopy. In five patients (patients 2 and 11 in group 1 and patients 7, 13, and 18 in group 2), holmium-YAG (Eclipse Inc) laser coronary angioplasty was applied as an initial dilatation procedure and then adjunctive balloon angioplasty was performed. Written informed consent was obtained from all patients.
Angioscopic Equipment
The system available for coronary
angioscopy at our institute
included the VFS-1400 endoscopic system and IF-783V fiberoptic
catheter (Nihon Kohden).8 The VFS-1400 endoscopic system
has a light source, 6-in color CRT monitor, and CCD camera head in a
small compact body. It is 27 cm wide, 52 cm long, and 37 cm high. The
IF-783V fiber-optic catheter is 0.68 mm in diameter and 1.5 m long. It
has 3000 pixels of imaging fiber with 50 bundles of lightening fiber.
The visual field angle is 55 degrees, and the depth of focus is 1 to 15
mm. The fiber-optic catheter was inserted into coronary arteries with a
double–guiding catheter system.9 We used an 8F Judkins
catheter (Schneider Inc) as an outer guiding catheter and a 4F probing
catheter (USCI Division, C.R. Bard Inc) as an inner guiding catheter.
For holmium-YAG laser coronary angioplasty, a 9F Superflow Judkins
catheter (Schneider Inc) was used for the outer guiding catheter to
provide an adequate lumen for the passage of the laser fiber catheter
and dye injection.
Angioscopic Procedure
After an 8F or a 9F sheath had been
placed in the femoral
artery, 5000 to 10 000 U of heparin and 500 mg of aspirin were
administered intravenously in the same manner as in our routine PTCA
procedure. An outer guiding catheter was inserted into the coronary
artery ostium, and baseline coronary angiography was performed. A
0.014-in guidewire was advanced to the lesion, beyond the lesion in
some cases, to assist in the advancement of the inner guiding catheter.
Then, the inner guiding catheter was advanced to just before the lesion
along with the guidewire. Before introduction of the fiber-optic
catheter into the inner guiding catheter, the white color balance and
sharpness were adjusted to match white sterile gauze. Brightness was
adjusted after introduction into the coronary artery to avoid halation.
After withdrawal of the guidewire and inner sheath of the probing
catheter, the fiberoptic catheter was inserted into the inner
guiding catheter until the distal marker of the catheter was visible.
Visualization of the inside of the coronary artery lumen was achieved
after the inner guiding catheter had been flushed with heparinized
saline (warmed to 37°C) by manual injection (3 to 4 mL/s) or with the
use of a compression bag. It was necessary to rotate or withdraw the
inner guiding catheter to keep the fiber-optic catheter coaxial with
the vessel for adequate visualization. Concerning the site of
angioscopic observation, we carefully maintained the angioscope at just
before the lesion using fluoroscopic and angiographic guidance.
Side branches were useful markers with which to determine the position.
The inner guiding catheter has a radiopaque marker on the distal tip,
and the fiber-optic catheter can be seen by fluoroscopy. After the
angioscopic procedure, PTCA was performed in the usual manner, and
angioscopy was repeated to examine the results of balloon dilatation.
Angioscopic images before and after PTCA were recorded on S-VHS
videotape and on 35-mm film for later review and analysis. All
angioscopic recordings were reviewed by three or more experienced
cardiologists, and the angioscopic findings were determined by a
discussion among them.
Definition of Angioscopic Findings
The angioscopic procedure
was defined as success when it was
possible to deliver the fiber-optic catheter to the lesion and to
obtain coaxial circumferential images of the coronary artery lumen. The
color of the lesion was defined as yellow when there was a yellow
plaque at the stenosis and as white when there was no yellow. White
lesions usually presented a uniform white appearance. The
brownish-yellow plaque were placed in the yellow plaque category.
Thrombi were defined as protruding or flat masses colored red or a
combination of red and white. They were not flushed out by saline
injection. Endothelial exfoliation was defined as thin, friable,
mobile, and translucent tissue that appeared to be loosely adherent to
the wall. Dissection was diagnosed when there was a disruption of
atheroma or adjacent vessel wall, ie, when the tear was recognized. The
color of the lesion (yellow or white), the surface plaque morphology
(regular or irregular), and the presence or absence of thrombi were
determined by angioscopy before PTCA. As for a decision on lesion
color, the intraobserver agreement was 97% in the present study as
reanalyzed by the same observer, and the interobserver agreement was
92%. When there was a disagreement on the results, a third observer
reviewed the study and formed a final judgment. The occurrence of
dissection or endothelial exfoliation, the presence or absence of
thrombi, and the change of the plaque shape and size were examined
after PTCA.
Angiographic Findings
The percent diameter stenosis before
and after PTCA was measured
by automatic edge detection. The presence or absence of contrast
haziness and occurrence of dissection were judged by angiography after
PTCA. The angiographic criterion for identification of thrombi was a
filling defect outlined circumferentially by contrast material seen in
multiple projections.10 The criterion for diagnosis of
dissection by angiography was the presence of a small radiolucent area
within the lumen or an extravasation of the temporary or persistent
contrast material.11
Clinical and Laboratory Data
Lipidemia and Other
Coronary Risk Factors
Before PTCA, serum levels of total cholesterol,
LDL cholesterol,
HDL cholesterol, and triglycerides were measured with participants in a
fasting state. A positive history of hypercholesterolemia (total
cholesterol, >250 mg/dL) requiring lipid-lowering drugs, diabetes
mellitus, and hypertension were also recorded from medical
records.
Duration of Angina and Angioscopic Findings
In patients with one-vessel disease and no history of myocardial
infarction or prior PTCA, the time interval between the onset of angina
and PTCA was recorded from medical records and expressed in months.
These data may be correlated with the changes of angioscopic findings
in coronary atherosclerotic lesions since the onset of angina.
Patient Follow-up
In all patients, clinical symptoms were
followed and exercise
201Tl scintigraphy was performed 3 months after PTCA.
Coronary angiography was performed in all patients except three who
refused follow-up angiography 6 months (average, 10.6 months) after
PTCA (angiographic follow-up rate was 92%). Angiographic evidence of
restenosis was defined as 50% diameter stenosis at the site of the
previous dilatation. The degree of stenosis was evaluated by
quantitative coronary angiography with automatic edge
detection.12 Calibration of the diameter of the vessels in
absolute values (in millimeters) was achieved with the diagnostic or
guiding catheter used as a reference. Measurements were repeated three
times, and the mean values were recorded.
Statistical Analysis
Data were expressed as mean±SD.
The two groups were compared
for continuous variables by the unpaired t test. Differences
of proportions were assessed by the 
2 test or
Fisher's exact probability test where appropriate. Regression
analysis was performed using Cox proportional hazards model to
identify variables independently predictive of restenosis. Values of
P<.05 were considered to be significant.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Success Rates of Angioscopic Observation
Angiograms of a representative patient with lesions successfully evaluated by angioscopy are shown in Figs 1
and
2 (group 1, patient 8). Luminal enlargement by PTCA
was achieved mainly by disruption and compression of a large yellow
plaque.
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The success rates for angioscopic observation before and after
PTCA are
listed in Table 1. The overall angioscopic success rates
before and after PTCA were 77% and 51%, respectively. The success
rate for the left anterior descending coronary artery was higher than
that for any other vessel. In 12 patients, adequate visualization of
the lesion was achieved only before PTCA. In 6 patients, failure of the
angioscopic procedure after PTCA was due to the inability to deliver
the inner guiding or fiber-optic catheters to the lesion because of
bending in the proximal portion of the vessel. In 4 patients, although
it was possible to deliver the fiber-optic catheter to the lesion, a
circumferential view of the target lesion was not obtained because of
the malalignment of the fiber-optic catheter with the vessel. In the
remaining 2 patients, the main reason for failure was incomplete
removal of blood from the visual field because the blood flow increased
after vessel dilatation.
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Patient Background Data
The clinical and angiographic data
and the angioscopic findings of
36 patients who were successfully evaluated by angioscopy before and/or
after PTCA are listed in Tables 2 and 3;
there were 29 men and 7 women with a mean age of 58±9 years. The
average age of group 1 patients was somewhat higher than that of group
2 patients, although the difference was not statistically significant
(P=.06). The mean percentage of diameter stenosis before and
after successful PTCA was 76.3% and 28.0%, respectively. Neither a
history of prior myocardial infarction nor the duration of angina was
related to the plaque color. There were no differences between the two
groups in total cholesterol, LDL cholesterol, HDL cholesterol, or
triglyceride levels. Smoking habits, diabetes mellitus, hypertension,
and medical treatment after PTCA also did not differ between the two
groups.
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Angiographic and Angioscopic Findings
Typical examples of
yellow and white lesions are shown in Fig 3 (group 1, patient
9, and group 2, patient 12).
Although the location of the stenosis was almost the same (midportion
of a large obtuse marginal branch), the appearances as assessed by
angioscopy were quite different. The findings of angiography and
angioscopy are summarized in Table 2
. Mean diameter stenosis
before and
after PTCA was not different in the two groups. The target lesions for
PTCA were located in the proximal left anterior descending coronary
artery in 23 patients, left circumflex artery in 6 patients, right
coronary artery in 5 patients, and saphenous vein graft in 2 patients.
Successful dilatation was achieved in 13 of 13 patients (100%) in
group 1 and 21 of 23 patients (91%) in group 2. The difference between
these success rates was not statistically significant. In 2 patients
from group 2 (patients 21 and 22) for whom PTCA failed, acute occlusion
of the vessel occurred. Although one artery (in patient 21) was
reopened by a second balloon dilatation, both patients had small
non–Q-wave myocardial infarctions. There were no patients for whom
PTCA failed in group 1. Mural thrombi were observed angioscopically in
7 patients (22%) before PTCA; none of them were detected by
angiography. The presence of mural thrombi before PTCA was not
different between the two groups (23% versus 17%). Coronary artery
dissection or endothelial exfoliation after PTCA was found in 55% (6
of 11) of group 1 patients and in 54% (7 of 13) of group 2 patients.
In 4 patients, dissection was detected by angiography, but angioscopy
showed no evidence of it. The incidence of haziness and dissection
after PTCA as detected by angiography also did not differ between the
two groups. Serial changes in percent diameter stenosis and minimal
luminal diameter are shown in Figs 4 and 5.
Follow-up coronary angiography showed that the mean
percent diameter stenosis in group 2 was significantly higher than that
in group 1. Restenosis rates after successful PTCA are shown in Fig
6. The overall restenosis rate was 41.9% (13 of 31).
The restenosis rate for group 1 patients was significantly lower than
that for group 2 patients (16.7% versus 57.9%, P<.05). In
a univariate Cox proportional hazards model (Table 4),
plaque color and percent diameter stenosis after PTCA were related to
restenosis, although the latter did not reach strict statistical
significance (P=.052). Multivariate relations between
variables and restenosis according to a Cox proportional hazards model
are shown in Table 5. Plaque color was the independent
variable associated with restenosis.
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Complications
During the angioscopic procedure, acute closure
of the vessel
occurred in 3 patients; in 2 of them, the vessel was reopened by
intracoronary injection of nitroglycerin, and in 1, there was no
response to nitroglycerin but the vessel was reopened by repeat PTCA.
One patient had polymorphic ventricular tachycardia during saline
flushing that ended after the cessation of flushing.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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We have demonstrated that the restenosis rate for yellow plaque is lower than that for white plaque. Angioscopic findings appear to be highly predictive of the prognosis after successful angioplasty.
Methodological Considerations for Coronary Angioscopy
Several
guiding systems for coronary angioscopy have been
reported. Over-the-guidewire type,5 7 13
the monorail
type,5 and the double–guiding catheter
system9 used in the present study have been described.
The advantage of the double–guiding catheter system is that flushing
can be performed easily through the inner guiding catheter, so
angioscopic images are clear. Especially when a balloon-tipped inner
guiding catheter is used, flushing can be performed more completely.
Moreover, a fiber-optic catheter can be inserted into a coronary artery
without damaging the inner surface of the vessel wall, since the
relatively hard fiber-optic catheter is never in direct contact with
the vessel wall. The disadvantage is that it is sometimes difficult to
get a coaxial image of the lumen, especially in a bending portion,
because the guidewire, which serves to straighten the vessel, must be
withdrawn before insertion of the fiber-optic catheter. Moreover, it is
not desirable to retract the guidewire, because abrupt closure may
occur during the procedure. Franzen et al14 compared
several types of guiding systems for angioscopy and concluded that the
over-the-wire angioscope was superior with respect to guiding,
alignment capability, and safety. However, they did not compare it with
the double–guiding catheter system.
Significance of Yellow Plaque
Mizuno et
al2 4 reported that yellow plaque is common
in the culprit lesions of acute myocardial infarction and unstable
angina and that they have a thin fibrous cap and are prone to rupture.
They found yellow plaque in 50% of patients with acute coronary
disorders and 15% of those with stable angina.2 All of
the patients in the present study had stable angina, 8 of them had
had a prior myocardial infarction, and 33% had yellow plaque. We
separated the patients according to plaque color, because the color of
the plaque is an obvious identifying characteristic even when
angioscopic images are not clear. It was found in intravascular
ultrasound studies that lipid-rich plaque is echolucent and hard
fibrous plaque is echogenic.15 16 17 In a
patient examined
simultaneously with angioscopy and intravascular ultrasound, we found
that white plaque lesions showed an echogenic pattern.8
Thus, yellow plaque appears to be soft and lipid rich, and white plaque
appears to be hard and fibrous.
The restenosis rate of yellow plaque lesions was significantly lower than that of white plaque lesions. The exact reason why yellow plaque lesions had a low restenosis rate is unclear. Several studies have examined retrospectively the influence of clinical and anatomic variables on the incidence of restenosis. These include clinical variables such as unstable angina,18 vasospastic angina,19 the presence of diabetes mellitus,20 21 22 and the presence of hyperlipidemia.21 Anatomic variables such as a dilatation of proximal left anterior descending coronary artery stenosis,18 22 a totally occluded vessel,23 and the presence of collateral vessels24 are also reported. Several studies of detailed morphological variables of a relatively small number of patients have shown that the incidence of restenosis was higher in patients whose coronary artery stenoses are eccentric, calcified, or long.22 25 26 However, other studies of a large number of patients failed to show that these factors had an influence on restenosis.18 20 In the present study, none of these clinical and coronary anatomic variables differed between the two groups. The most frequently identified risk factor for restenosis has been a variable directly related to a poor angioplasty result, such as a residual stenosis or a residual pressure gradient.18 20 25 26 The residual stenosis after PTCA also was not different between the two groups in the present study. Therefore, the presence of yellow plaque is believed to be a new independent predictor of restenosis. The intimal hyperplasia or proliferation of medial smooth muscle cells triggered by vessel injury is considered a fundamental process of restenosis. It is reasonable to think that the more extensive is the injury, the more intense will be the reparative response and restenosis. Schwartz et al27 reported in an experimental study using a porcine model of coronary stenosis that restenosis depends on the degree of vessel injury sustained during angioplasty. The elements that constitute the fibrous tissue in white plaque are collagen, elastin, and proteoglycans, and elastin fibers are reported to contribute to hard calcification of the plaque.28 Farb et al29 and De Morais et al30 found in postmortem studies that stenoses that contained lipid-rich plaque, ie, yellow plaque, were more likely to be disrupted by balloon inflation than was predominantly fibrous plaque. Fitzgerald et al31 reported, using intravascular ultrasound, that if calcium is present within a plaque, balloon expansion will result in nonuniform energy distribution and lead to the formation of deeper cracks and tears. Therefore, it is postulated that in diseased vessels with hard plaque (white plaque), the more intense injury in deep layer of vessel wall may occur. Because it is difficult to assess the depth of vessel wall injury by angioscopy, simultaneous angioscopy and intravascular ultrasound examinations are needed to confirm this hypothesis.
Yellow plaque is believed to contain much more cholesterol ester than white plaque. The plaque color may be correlated with the serum cholesterol level to some extent, but we could not demonstrate any relation between plaque color and serum cholesterol level. A history of hypercholesterolemia also was not related to plaque color. Because coronary atherosclerosis is a complicated and multifactorial process formed over a long period, the formation of yellow plaque cannot be explained solely by a serum lipid abnormality.
Study Limitations
Angioscopy cannot show the intraluminal
pathological changes that
lie beyond its view, and it is possible to observe only the proximal
portion of the stenosis. Four patients in the present study showed
angiographic evidence of local dissection after PTCA, although
angioscopy could not detect the tears, presumably because of their
size and location.
The results of the present study were derived from the observations of lesions believed to be suitable for angioscopic evaluation, so they may not be representative of all types of coronary artery stenosis. Also, the number of patients studied was small. However, it is noteworthy that the restenosis rate differs depending on the plaque color or content. Therefore, the angioscopic findings are highly predictive of the results of PTCA.
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Acknowledgments |
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We thank all the members of catheterization laboratory. We are also grateful to A.S. Cary, MD, for reading the manuscript.
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Footnotes |
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Present address of Dr Haze is Department of Cardiology, Osaka City General Hospital, 2-13-22 Miyakojima Hondori, Miyakojimaku, Osaka, Osaka 534, Japan.
Received August 9, 1994; revision received September 27, 1994; accepted October 24, 1994.
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References |
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|
TopAbstractIntroductionMethods Results Discussion References |
|---|
1. Arnett EN, Isner JM, Redwood DR, Kent KM, Baker WP, Ackerstein H, Roberts WC. Coronary artery narrowing in coronary heart disease: comparison of cineangiographic and necropsy findings. Ann Intern Med. 1979;91:350-356.
2. Mizuno K, Miyamoto A, Satomura K, Kurita A, Arai T, Sakurada M, Yanagida S, Nakamura H. Angioscopic coronary macromorphology in patients with acute coronary disorders. Lancet. 1991;337:809-812. [Medline] [Order article via Infotrieve]
3. Sherman CT, Litvack F, Grundfest W, Lee M, Hickey A, Chaux A, Kass R, Blanche C, Matloff J, Morgenstern L, Ganz W, Swan HJC, Forrester J. Coronary angioscopy in patients with unstable angina pectoris. N Engl J Med. 1986;315:913-919. [Abstract]
4. Mizuno K, Satomura K, Miyamoto A, Arakawa K, Shibuya T, Arai T, Kurita A, Nakamura H, Ambrose JA. Angioscopic evaluation of coronary artery thrombi in acute coronary syndromes. N Engl J Med. 1992;326:287-291. [Abstract]
5. Uchida Y, Hasegawa K, Kawamura K, Shibuya I. Angioscopic observation of the coronary luminal changes induced by percutaneous transluminal coronary angioplasty. Am Heart J. 1989;117:769-776. [Medline] [Order article via Infotrieve]
6. Siegel RJ, Chae J-S, Forrester JS, Ruiz CE. Angiography, angioscopy, and ultrasound imaging before and after percutaneous balloon angioplasty. Am Heart J. 1990;120:1086-1090. [Medline] [Order article via Infotrieve]
7. Ramee SR, White CJ, Collins TJ, Mesa JE, Murgo JP. Percutaneous angioscopy during coronary angioplasty using a steerable microangioscope. J Am Coll Cardiol. 1991;17:100-105. [Abstract]
8. Itoh A, Miyazaki S, Nonogi H, Ozono K, Daikoku S, Saito K, Goto Y, Haze K. Angioscopic and intravascular ultrasound imagings before and after percutaneous holmium-YAG laser coronary angioplasty. Am Heart J. 1993;125:556-558. [Medline] [Order article via Infotrieve]
9. Inoue K, Kuwaki K, Ochiai H, Ueda K, Takano E, Minato H. Percutaneous transluminal coronary angioscopy as a guiding therapy for intracoronary thrombolysis and angioplasty. In: Vogel JHK, King SB III, eds. Interventional Cardiology: Future Directions. St Louis, Mo: CV Mosby Co; 1989:1-27.
10. Mandelkorn JB, Wolf NM, Singh S, Shechter JA, Kersh RI, Rodgers DM, Workman MB, Bentivoglio LG, Laporte SM, Meister SG. Intracoronary thrombus in nontransmural infarction and in unstable angina pectoris. Am J Cardiol. 1983;52:1-6. [Medline] [Order article via Infotrieve]
11.
Dorros G, Cowly MJ, Simpson J, Bentivoglio LG, Block PC,
Bourassa M, Ketre K, Gosselin AJ, Gruntzig AR, Kelsey SF, Kent KM, Mock
MB, Mullin SM, Myler RK, Passamani ER, Stertzer SH, Williams DO.
Percutaneous transluminal coronary angioplasty: report of complications
from the National Heart, Lung, and Blood Institute PTCA registry.
Circulation. 1983;67:723-730.
12. Serruys PW, Reiber JHC, Wijns W, van den Brand M, Kooijman CJ, ten Katen HJ, Hugenholtz PG. Assessment of percutaneous transluminal coronary angioplasty by quantitative coronary angiography: diameter versus densitometric area measurements. Am J Cardiol. 1984;54:482-488. [Medline] [Order article via Infotrieve]
13. Mizuno K, Arai T, Satomura K, Shibuya K, Arakawa K, Okamoto Y, Miyamoto A, Kurita A, Kikuchi M, Nakamura H, Utsumi A, Takeuchi K. New percutaneous transluminal coronary angioscope. J Am Coll Cardiol. 1989;13:363-368. [Abstract]
14.
Franzen D, Hopp HW, Korsten J, Hilger HH. A prospective study
on percutaneous coronary angioscopy with different guiding techniques
in patients with coronary heart disease. Eur Heart J. 1992;13:655-660.
15.
Nissen SE, Gurley JC, Grines CL, Booth DC, McClure R, Berk M,
Fischer C, DeMaria AN. Intravascular ultrasound assessment of lumen
size and wall morphology in normal subjects and patients with coronary
artery disease. Circulation. 1991;84:1087-1099.
16. Gussenhoven EJ, Essed CE, Lancee CT, Mastik F, Frietman P, Van Egmond FC, Reiber J, Bosch H, Van Urk H, Roelant J, Bom N. Arterial wall characteristics determined by intravascular ultrasound imaging: an in vitro study. J Am Coll Cardiol. 1989;14:947-952. [Abstract]
17. Nishimura RA, Edwards WD, Warnes CA, Reeder GS, Holmes DR, Jr, Tajik AJ, Yock PG. Intravascular ultrasound imaging: in vitro validation and pathologic correlation. J Am Coll Cardiol. 1990;16:145-154. [Abstract]
18.
Leimgruber PP, Roubin GS, Hollman J, Cotsonis GA, Meier B,
Douglas JS, King SB III, Gruentzig AR. Restenosis after successful
coronary angioplasty in patients with single-vessel disease.
Circulation. 1986;73:710-717.
19.
Leisch F, Schutzenberger W, Herbinger W. Influence of a
variant angina on the results of percutaneous transluminal coronary
angioplasty. Br Heart J. 1986;56:341-345.
20. Holmes DR Jr, Vlietstra RE, Smith HC, Vetrovec GW, Kent KM, Cowley MJ, Faxon DP, Gruentzig AR, Kelsey SF, Detre KM, Van Raden MJ, Mock MB. Restenosis after percutaneous transluminal coronary angioplasty (PTCA): a report from the PTCA registry of the National Heart, Lung, and Blood Institute. Am J Cardiol. 1984;53:77C-81C. [Medline] [Order article via Infotrieve]
21. Myler RK, Topol EJ, Shaw RE, Stertzer SH, Clark DA, Fishman J, Murphy MC. Multivessel coronary angioplasty: classification, results, and patterns of restenosis in 494 consecutive patients. Cathet Cardiovasc Diagn. 1987;13:1-15. [Medline] [Order article via Infotrieve]
22. Vandormael MG, Deligonul U, Kern MJ, Happer M, Presant S, Gibson P, Galan K, Chaitman BR. Multilesion coronary angioplasty: clinical and angiographic follow-up. J Am Coll Cardiol. 1987;10:246-252. [Abstract]
23.
Serruys PW, Umans V, Heyndrickx GR, van den Brand M, de Feyter
PJ, Wijns W, Jaski B, Hugenholtz PG. Elective PTCA of totally occluded
coronary arteries not associated with acute myocardial infarction:
short-term and long-term results. Eur Heart J. 1985;6:2-12.
24. Urban P, Meier B, de Bruyne B, Steffenino G, Rutishauser W. Coronary wedge pressure: a predictor of restenosis after coronary balloon angioplasty. J Am Coll Cardiol. 1987;10:504-509.[Abstract]
25. Guiteras Val P, Bourassa MG, David PR, Bonan R, Crepeau J, Dyrda I, Lesperance J. Restenosis after successful percutaneous transluminal coronary angioplasty: the Montreal Heart Institute experience. Am J Cardiol. 1987;60:50B-55B. [Medline] [Order article via Infotrieve]
26. Mata LA, Bosch X, David PR, Rapold HJ, Corcos T, Bourassa MG. Clinical and angiographic assessment 6 months after double vessel percutaneous coronary angioplasty. J Am Coll Cardiol. 1985;6:1239-1244. [Abstract]
27. Schwartz RS, Huber KC, Murphy JG, Edwards WD, Camrud AR, Vlietstra RE, Holmes DR. Restenosis and the proportional neointimal response to coronary artery injury: results in a porcine model. J Am Coll Cardiol. 1992;19:267-274. [Abstract]
28. Urry DW. On the molecular basis for vascular calcification. Perspect Biol Med. 1974;18:68-84. [Medline] [Order article via Infotrieve]
29. Farb AF, Virmani R, Atkinson JB, Kolodgie FD. Plaque morphology and pathologic changes in arteries from patients dying after coronary balloon angioplasty. J Am Coll Cardiol. 1990;16:1421-1429. [Abstract]
30. De Morais CF, Lopes EA, Checchi H, Arie S, Pileggi F. Percutaneous transluminal coronary angioplasty: histopathological study of nine necropsy cases. Virchows Arch A Pathol Anat Histopathol. 1986;410:195-202. [Medline] [Order article via Infotrieve]
31.
Fitzgerald PJ, Ports TA, Yock PG. Contribution of localized
calcium deposits to dissection after angioplasty: an observational
study using intravascular ultrasound. Circulation. 1992;86:64-70.
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