(Circulation. 1998;98:1172-1177.)
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports |
Plasma Lipoprotein(a) Is Not a Predictor for Restenosis After Elective High-Pressure Coronary Stenting
Flavio Ribichini, MD;
Giuseppe Steffenino, MD;
Antonio Dellavalle, MD;
Antonello Vado, MD;
Valeria Ferrero, MD;
Terenzio Camilla, BS;
Silvia Giubergia, BS;
; Eugenio Uslenghi, MD
From the Cardiac Catheterization Unit (F.R., G.S., A.D.), Division of
Cardiology (A.V., V.F., E.U.), and Laboratory for Clinical Biochemistry (T.C.,
S.G.), Ospedale Santa Croce, Cuneo, Italy.
Correspondence to Giuseppe Steffenino, MD, Laboratorio di Emodinamica, Ospedale Santa Croce, Via Michele Coppino 26, 12100 Cuneo, Italia. E-mail emodinam{at}www.lrcser.it
 |
Abstract
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Background—Lipoprotein(a) is a risk
factor for coronary artery disease. Although it has been
implicated in restenosis after balloon angioplasty, its role in
restenosis within coronary stents is unknown. The aim
of the study was to assess the role of plasma lipoprotein(a) as a
predictor for restenosis after elective coronary
stenting.
Methods and Results—Elective, high-pressure stenting of de novo
lesions in native coronary arteries with Palmaz-Schatz stents
was performed in 325 consecutive patients. Clinical, angiographic, and
biochemical data were analyzed prospectively. Angiographic
follow-up was performed at 6 months. Lipoprotein(a) levels were
compared in patients with and without restenosis. Angiographic
follow-up was obtained in 312 patients (96%); recurrence was
observed in 67 patients (21.5%). No clinical or biochemical
variable was associated with restenosis. Lipoprotein(a)
level was 37.81±49.01 mg/dL (median, 22 mg/dL; range, 3 to 262 mg/dL)
in restenotic patients and 36.95±40.65 mg/dL (median, 22
mg/dL; range, 0 to 244 mg/dL) in nonrestenotic patients
(P=NS). The correlations between percent diameter
stenosis, minimum luminal diameter, and late loss at follow-up
angiography and basal lipoprotein(a) plasma level after logarithmic
transformation were 0.006, 0.002, and 0.0017, respectively. Multiple
stents were associated with a higher incidence of restenosis
(P=0.006), but biochemical data in these patients were
similar to those treated with single stents.
Conclusions—The basal plasma level of lipoprotein(a) measured
before the procedure is not a predictor for restenosis after
elective high-pressure coronary stenting.
Key Words: stents • restenosis • lipoprotein(a)
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Introduction
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Although the plasma
level of lipoprotein (Lp) (a) has been proposed to be a major
independent risk factor for atherosclerosis and
progression of coronary artery
disease,1 2 3 the pathogenetic role of Lp(a)
remains unclear.4 5 Numerous case-control studies
that have compared Lp(a) levels in patients with known coronary
artery disease and in control subjects have demonstrated higher Lp(a)
concentrations in the former. In prospective studies, however, results
are uncertain, probably because of the potential importance of Lp(a)
heterogeneity in this
process.6
Lp(a) is involved in lipid metabolism, the coagulation and
fibrinolytic systems, and the stimulation of smooth muscle cell
proliferation.7 8 9 Plasma concentration of Lp(a)
in humans ranges from <1 mg/dL to >100 mg/dL, with risk for
cardiovascular disease associated with levels >25 to
30 mg/dL.10 11 According to epidemiological
studies, this threshold corresponds to the 75th12
or 90th13 percentile.
Most initial studies designed to assess the correlation between the
serum level of Lp(a) and restenosis after
percutaneous transluminal coronary angioplasty
(PTCA) have been limited to small groups of patients and have
considered restenosis as a simple binary phenomenon, with
incomplete angiographic follow-up; results of these studies are
inconsistent.14 15 16 17 18 19 20 21 A larger, more recent
study confirmed the association between recurrence after PTCA
and Lp(a), suggesting that its action may be crucial in the
arterial healing process after balloon
injury.21
Restenosis occurs less frequently after coronary
stenting than after balloon PTCA, with in-stent tissue proliferation
playing a key role in the former and negative remodeling in the
latter.22 23 The function of Lp(a) in
recurrence after balloon PTCA is open to new interpretations on
the basis of this understanding,22 and its role
after coronary stenting has not been studied previously. This
prospective study investigates the association between Lp(a) and
angiographic restenosis after elective, high-pressure stent
implantation in patients with de novo lesions of the native
coronary circulation.
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Methods
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From December 1993 to July 1997, 325 consecutive white patients
who had coronary artery disease treated with PTCA and elective
coronary stenting with Palmaz-Schatz stents and complete
assessment of factors associated with restenosis were enrolled
in this study. These patients are part of a larger prospective study of
biochemical and genetic risk factors for restenosis that is
ongoing in our institution. All patients fulfilled the following
criteria: patients of both sexes <80 years old with single-vessel or
multivessel disease of native coronary arteries, a new lesion
successfully treated with elective placement of 1 or 2 Palmaz-Schatz
stents, no contraindication to the administration of ticlopidine, and
agreement to undergo protocol follow-up coronary angiography at
6 months. Clinical and angiographic exclusion criteria were as follows:
coronary atherectomy followed by stenting, primary or rescue
PTCA, PTCA within 1 month of acute myocardial infarction, acute or
chronic inflammatory disease, renal insufficiency, liver dysfunction,
treatment with steroids, insulin-dependent diabetes, a severe comorbid
status, ostial lesions of the right coronary artery or the left
main stem, total coronary occlusions >2 weeks old, and lesions
>30 mm long. Thirteen patients included in the study were not
considered in the final analysis for the following reasons: 1
patient died, 2 developed subacute stent thrombosis (within 1 month
of the procedure), and 10 did not undergo follow-up angiography.
Angiographic follow-up at 6 months, or earlier when recurrence
of angina or ischemia was suspected, was thus available in 312
patients (96%).
Coronary intervention, angiographic assessment, and
quantitative coronary analysis were performed as
previously described.24 Immediate angiographic
success was considered to be the deployment of the stent(s) in the
target lesion, with a Thrombolysis in Myocardial Infarction
grade 3 coronary flow and a residual stenosis <20%.
Restenosis was defined as a percent diameter stenosis
50% at the site of the lesion treated with the stent(s) in at least
1 of 2 orthogonal incidences, 1 of these always including the "worst
view" of the segment being analyzed: only in-stent
restenosis was considered.
Analysis of Conventional Clinical and Laboratory Risk
Factors
Data for all patients were recorded as to age, sex, body
mass index, family history of coronary artery disease, current
smoking habits (>10 cigarettes/d), hypertension (diastolic
blood pressure >90 mm Hg or systolic blood pressure
>160 mm Hg), and non–insulin-dependent diabetes.
Biochemical Determination
Blood samples obtained in the morning before PTCA, after a
12-hour fast, were used to measure levels of plasma glucose, total
cholesterol, HDL cholesterol, and
triglycerides with enzymatic-colorimetric
methods. Apolipoprotein B was measured with a nephelometric method.
Lp(a) level was measured with a quantitative latex method for
nephelometric Lp(a) assay [N-latex Lp(a) and Behring Nephelometric
Analyzer, Behring Diagnostic Inc]. The N-latex
Lp(a) reagent consists of a rabbit polyclonal anti-human Lp(a)
antiserum as antibody for the nephelometric assay. The Lp(a) used in
the preparation of the antiserum is a mixture of Lp(a) isoforms; the
specificity of the antibody from Behring has been tested by
immunoelectrophoresis and Western blotting as reported
elsewhere.25 The method has intra-assay and
interassay coefficients of variation of 1.5% to 3.0% and 1.7% to
3.2%, respectively. The nephelometric method using a reagent
consisting of a polyclonal antibody is likely to recognize all of the
many genetic isoforms of Lp(a); the antibody is also specific, because
it does not precipitate plasminogen or any other
apolipoprotein as tested by
immunoelectrophoresis26 ; thus, this method should
be largely insensitive to variations related to the number of kringle 4
repeats. Its excellent precision and accuracy, the good correlation
with the electroimmunodiffusion method,26 27 and
the quick and easy use for the study of normal and pathological
concentrations are well suited for use in clinical and research
studies. All frozen assays were analyzed within 1 week to avoid
underestimation secondary to prolonged
freezing.21 28
Study Sample Size Calculation
The number of patients included in this analysis was
tailored to achieve a statistical significance as to the incidence of
restenosis in subjects with high (>30 mg/dL) or low Lp(a)
levels, with an expected frequency of restenosis of 30% in the
whole population and 49% in subjects with high Lp(a) levels, with
=0.5 and ß=0.20.
Statistical Analysis
Data are expressed as mean±SD or as median with ranges.
Student's t test was used to compare differences between
continuous variables. The 
2 statistic with
Yates's correction or Fisher's exact test when appropriate was used
to test associations of categorical data. Linear regression
analysis with logarithmic transformation was used to correlate
Lp(a) plasma level and angiographic parameters of
restenosis. For variables with nonnormal distribution, a
nonparametric test (Mann-Whitney U test)
was used. Recurrence rates were also calculated for each
quintile of Lp(a) concentration.
A value of P
0.05 was considered significant. SPSS
release 5.0.1 for Windows was used to perform all statistical
analysis.
This investigation was approved by the review committee of our
institution, and all patients gave informed consent for inclusion in
the study.
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Results
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Of 312 patients who had 6-month angiographic follow-up, 268 were
male and 44 female, and all were between 31 and 78 years old (60.3±9.5
years). Follow-up angiography was performed at 6.3±1.7 months after
coronary stenting for the whole cohort (range, 1.8 to 12
months). Angiographic restenosis was present in 67 patients
(21.5%) and absent in 245 patients at 5.4±1.4 and 6.5±1.6 months
after the procedure, respectively (P=0.0001). Lp(a)
concentrations and recurrence rates were not different in 45
patients (14.4%) receiving lipid-lowering therapy; none were using
drugs known to affect Lp(a) level.
No significant difference was present between patients with and
without restenosis as to demographic, clinical, and biochemical
variables or reference diameter before the procedure, after the
procedure, and at 6-month follow-up (Table 1
). Quantitative coronary
analysis data before angioplasty and after coronary
stenting were also similar in restenotic and
nonrestenotic patients except for the higher incidence of
restenosis among patients treated with multiple stents
(P=0.006). Multiple stents were used to treat patients with
more diffuse forms of coronary artery disease. However, levels
of Lp(a) in this subgroup were not significantly different between
patients with and without restenosis (37.8±33.06 mg/dL
[median, 23.0 mg/dL; range, 3.8 to 111.6 mg/dL] in 16 patients with
restenosis versus 36.93±28.03 mg/dL [median, 22.6 mg/dL;
range, 5.2 to 190 mg/dL] in 27 patients without restenosis,
P=NS).
A separate analysis of 6-month angiographic results was
performed considering subgroups of patients divided according to
conventional cutoff values of Lp(a) known to be associated with
ischemic events or coronary artery
disease10 11 12 13 (Table 2), but no difference was found in the
recurrence rate of patients with low or high plasma levels of
Lp(a). Analysis of the recurrence rates studied
according to Lp(a) concentration by quintile also demonstrated similar
restenosis rates in patients with the lowest and highest
concentrations (Figure).
View larger version (21K):
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Figure 1. Recurrence rate (%) for each quintile of patients
based on lipoprotein Lp(a) concentrations (mg/dL).
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Further analysis was performed considering restenosis
as a continuous variable; the correlation between plasma level of
Lp(a) and percent diameter stenosis, minimum luminal diameter,
and late loss at follow-up was not statistically significant
(r=0.006, r=0.002, and r=0.0017,
respectively).
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Discussion
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Our results show that the basal serum level of Lp(a) assessed by
nephelometry is not a predictor for angiographic restenosis
after elective, high-pressure coronary stenting using
Palmaz-Schatz stents in patients with de novo lesions of native
coronary arteries.
These results cannot be compared with others aimed at studying the role
of Lp(a) in the recurrence of lesions after balloon PTCA,
mainly because of the different mechanism of restenosis after
coronary stenting. In fact, classic concepts of
restenosis after balloon dilatation consist of immediate
recoil, platelet deposition, and thrombus formation, followed by
smooth muscle cell proliferation and matrix
formation,23 a mechanism analogous to wound
healing after balloon injury,29 in which Lp(a)
may be involved. Following this line of evidence, Desmarais et
al21 found that the basal level of Lp(a) is a
strong predictor of restenosis, suggesting that the link
between the structural and physiological properties
of Lp(a) and the mechanisms controlling fibrinolysis,
coagulation, and cellular mitogenesis, which occur at sites of deep
arterial injury after balloon dilatation, may be
responsible for this effect. More recently, Horie et
al30 described a higher basal Lp(a) level and a
significant reduction after balloon PTCA in patients who developed
restenosis at 4 months, elaborating the hypothesis of a most
important inhibition of thrombolysis and promotion of
thrombus formation that may contribute to restenosis in these
patients.
Studies with intracoronary ultrasound have demonstrated that
recurrence after balloon PTCA is mainly due to a process of
negative arterial remodeling in response to balloon injury,
accounting for >70% of late lumen loss.22 On
the other hand, stents create a larger final lumen cross-sectional area
and practically abolish arterial remodeling because the
metallic scaffold does not recoil. Neointimal hyperplasia
is therefore the main factor responsible for in-stent
restenosis after coronary stenting, offering a pure
proliferative model for the study of
restenosis.31 A neointimal
proliferative effect has been attributed to Lp(a), and evidence of this
action has been obtained in vitro.9 32 Although
neointimal proliferation after coronary stenting
may be activated or stimulated by many biochemical mediators,
our results suggest that the basal level of Lp(a) does not play a
leading role in this setting.
Our study was designed to minimize interference by the variables
that might affect the incidence of restenosis after
coronary stenting or might influence basal levels of Lp(a). The
nephelometric assay used in this study is sensitive to all the isoforms
of Lp(a), which adds uniformity to the values found in our patients and
limits problems that arise from the spectrum of
isoforms.33
In agreement with other series of white subjects, Lp(a) concentrations
were not distributed normally in our population but rather were skewed
toward lower values.21 34 Bearing in mind that
pathological effects of Lp(a) occur in patients with high levels (>30
mg/dL), the relatively small number of patients "at risk" is
apparent when the usual distribution is respected; therefore, our study
was sized to detect a difference in the recurrence rate of 19%
among patients with low or high Lp(a) levels.
From univariate analysis, no relationship was
observed between clinical variables and restenosis after
coronary stenting. Unstable angina and diabetes are among the
strongest predictors of recurrence after balloon
PTCA35 36 ; however, the restenosis rate
in unstable patients treated with elective high-pressure implantation
of Palmaz-Schatz stents is uncertain. Diabetes seems to be related to
restenosis after coronary stenting as
well37 ; this was not observed in our population
or in a recently published series of diabetic
patients.38 The exclusion of insulin-dependent
diabetic patients and the strict metabolic control exerted
by drug or dietary treatment in our patients may have blunted the
effect of this variable.39
From the analysis of angiographic characteristics, a higher
restenosis rate was observed in patients treated with multiple
stenting. Multiple stents were used to treat patients with more diffuse
forms of coronary disease, and the degree of coronary
artery disease is known to be correlated with serum levels of
Lp(a).2 This was also apparent in our population,
although the difference did not reach statistic significance: Lp(a)
levels in patients with focal versus diffuse disease were 33.29±36.18
mg/dL (median, 22 mg/dL) versus 46.33±43.87 (median, 22 mg/dL),
respectively (P=0.22). Therefore, Lp(a) concentration was
not significantly different among patients with single or multiple
stents (37.12±43.16 mg/dL [median, 22 mg/dL] and 37.26±38.63 mg/dL
[median, 22 mg/dL], respectively), but because of the small number of
patients in the latter subgroup, a statistical error cannot be excluded
(Table 1
).
None of the biochemical variables tested were related to
restenosis (Table 1), and the analysis of a subgroup of
patients with elevated Lp(a) levels yielded negative results (Table 2).
Furthermore, no correlation was found between Lp(a) and
restenosis as a continuous variable analyzing the
recurrence rate for each quintile of Lp(a) concentration
(Figure 1) or using regression analysis after logarithmic
transformation.
The link between Lp(a) and coronary artery disease as an
independent risk factor is still not straightforward. Most of the
discrepancies observed in prospective studies may be in part secondary
to a large number of confounding variables that are still unknown
about the "mysteries of Lp(a)."40
Furthermore, no studies have been performed to evaluate the impact of
method inaccuracy on the interpretation of clinical data, and this may
explain why results are not consistent.41
Although the present study does not address the potential role of
different isoforms of Lp(a) in restenosis after stent
implantation, our negative data strongly suggest that the basal serum
level of Lp(a) screened with a simple, reliable, and quick
nephelometric method is not a valuable predictor of 6-month outcome
after coronary stenting. Additional studies could be useful to
validate this observation.
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Acknowledgments
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Dr Ribichini was supported by a research fellowship from the
European Society of Cardiology at the OLV
Cardiovascular Center, Aalst, Belgium. We are indebted
to Marilena Tomatis, RN, and Maria Stefanina Dutto, RN, for their help
in data collection.
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Footnotes
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Reprint requests to Flavio Ribichini, MD, Laboratorio di Emodinamica, Ospedale Santa Croce, Via Michele Coppino 26, 12100 Cuneo, Italia.
Presented in part at the 69th Scientific Sessions of the American Heart Association, New Orleans, La, November 11–14, 1996.
Received February 19, 1998;
revision received May 13, 1998;
accepted May 16, 1998.
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References
|
|---|
1.
Genest J Jr, McNamara JR, Ordovas JM, Jenner JL,
Silberman SR, Anderson KM, Wilson PW, Salem DN, Schaefer EJ.
Lipoprotein cholesterol, apolipoprotein A1 and B and
lipoprotein (a) abnormalities in men with premature coronary
artery disease. J Am Coll Cardiol. 1992;19:792–802.[Abstract]
2.
Dahlen GH, Guyton JR, Attar M, Farmer JA, Kautz JA,
Gotto AM. Association of levels of lipoprotein Lp(a), plasma lipids,
and other lipoproteins with coronary artery disease documented
with angiography. Circulation. 1986;4:758–765.
3.
Orth-Gomér K, Mittleman MA, Schenck-Gustafsson
K, Wamala SP, Eriksson M, Belik K, Kirkeeide R, Svane B, Rydén L.
Lipoprotein (a) as a determinant of coronary heart disease in
young women. Circulation. 1997;95:329–334.[Abstract/Free Full Text]
4.
Simons L, Friedlander Y, Simons J, McCallum J.
Lipoprotein (a) is not associated with coronary heart disease
in the elderly: cross-sectional data from the Dubbo Study.
Atherosclerosis. 1993;99:87–95.[Medline]
[Order article via Infotrieve]
5.
Kinlay S, Dobson AJ, Heller RF, McElduff P, Alexander
H, Dickenson J. Risk of primary and recurrent acute myocardial
infarction from lipoprotein (a) in men and women. J Am Coll
Cardiol. 1996;28:870–875.[Abstract]
6.
Koschinsky ML, Marcovina SM. Lipoprotein (a):
structural implications for pathophysiology. Int J Clin Lab
Res. 1997;27:14–23.[Medline]
[Order article via Infotrieve]
7.
Hajjar KA, Gavish D, Breslow JL, Nachman RL.
Lipoprotein (a) modulation of endothelial cell surface
fibrinolysis and its potential role in
atherosclerosis. Nature. 1989;339:303–305.[Medline]
[Order article via Infotrieve]
8.
Miles LA, Fless GM, Levin EG, Scanu AM, Plow EF. A
potential basis for the thrombotic risk associated with lipoprotein
(a). Nature. 1989;339:301–303.[Medline]
[Order article via Infotrieve]
9.
Grainger DJ, Kirschenlohr HL, Metcalfe JC, Weissberg
PL, Wade DP, Lawn RM. Proliferation of human smooth muscle cells
promoted by lipoprotein (a). Science. 1993;260:1655–1658.[Abstract/Free Full Text]
10.
Bruckert E, Truffert J, Degennes JL, Lagarde JP,
Bernard C, Federspiel MC, Giral P, Dairou F. Does electrophoresis
reliably screen for high serum lipoprotein Lp(a)? Clin Chim
Acta. 1990;188:71–78.[Medline]
[Order article via Infotrieve]
11.
Hoefler G, Harnoncourt F, Paschke E, Mirtl W, Pfeiffer
KH, Kostner GM. Lipoprotein Lp(a): a risk factor for myocardial
infarction. Arteriosclerosis. 1988;8:398–401.[Abstract/Free Full Text]
12.
Sandholzer C, Saha N, Kark JD, Rees A, Jaross W,
Dieplinger H, Hoppichler F, Boerwinkle E, Utermann G. Apo(a) isoforms
predict risk for coronary heart disease: a study of six
populations. Arterioscler Thromb. 1992;12:1214–1226.[Abstract]
13.
Kostner GM, Avogaro P, Cazzolato G, Marth E, Bittolobon
G, Quinci GB. Lipoprotein Lp(a), and the risk for myocardial
infarction. Arteriosclerosis. 1981;38:51–61.
14.
Reis GJ, Kuntz RE, Silverman DI, Pasternak RC. Effects
of serum lipid levels on restenosis after coronary
angioplasty. Am J Cardiol. 1991;68:1431–1435.[Medline]
[Order article via Infotrieve]
15.
Shah PK, Amin J. Low high density lipoprotein level is
associated with increased restenosis rate after
coronary angioplasty. Circulation. 1992;85:1279–1285.[Abstract/Free Full Text]
16.
Hearn JA, Donohue BC, Ba'albaki H, Douglas JS, King SB
III, Lembo NJ, Roubin GS, Sgoutas DS. Usefulness of serum lipoprotein
(a) as a predictor of restenosis after
percutaneous transluminal coronary angioplasty.
Am J Cardiol. 1992;69:736–739.[Medline]
[Order article via Infotrieve]
17.
Benchimol D, Bonnet J, Benchimol H, Drouillet F, Duplaa
C, Couffinhal T, Desgranges C, Bricaud H. Biological risk factors for
restenosis after percutaneous transluminal
coronary angioplasty. Int J Cardiol. 1993;38:7–18.[Medline]
[Order article via Infotrieve]
18.
Daida H, Lee YJ, Yokoi H, Kanoh T, Ishiwata S, Kato K,
Nishikawa H, Takatsu F, Kato H, Kutsumi Y, Yamada N, Noma A, Yamaguchi
H, and the Low-Density Lipoprotein Apheresis Angioplasty
Restenosis Trial (L-ART) Group. Prevention of
restenosis after percutaneous transluminal
coronary angioplasty by reducing lipoprotein (a) levels with
low-density lipoprotein apheresis. Am J Cardiol. 1994;73:1037–1040.[Medline]
[Order article via Infotrieve]
19.
Cooke T, Sheahan R, Foley D, Reilly M, D'Arcy G, Jauch
W, Gibney M, Gearty G, Crean P, Walsh M. Lipoprotein (a) in
restenosis after percutaneous transluminal
coronary angioplasty and coronary artery disease.
Circulation. 1994;89:1593–1598.[Abstract/Free Full Text]
20.
Yamamoto H, Imazu M, Yamabe T, Ueda H, Hattori Y,
Yamakido M. Risk factors for restenosis after
percutaneous transluminal coronary angioplasty:
role of lipoprotein (a). Am Heart J. 1995;130:1168–1173.[Medline]
[Order article via Infotrieve]
21.
Desmarais RL, Sarembock IJ, Ayers CR, Vernon SM, Powers
ER, Gimple LW. Elevated serum lipoprotein (a) is a risk factor for
clinical recurrence after coronary balloon angioplasty.
Circulation. 1995;91:1403–1409.[Abstract/Free Full Text]
22.
Mintz GS, Popma JJ, Hong MK, Pichard AD, Kent KM,
Satler LF, Leon MB. Intravascular ultrasound to discern device-specific
effects and mechanism of restenosis. Am J
Cardiol. 1996;78(suppl A):18–22.
23.
Currier JW, Faxon DP. Restenosis after
percutaneous transluminal coronary angioplasty:
have we been aiming at the wrong target?. J Am Coll
Cardiol. 1995;25:516–520.[Abstract]
24.
Ribichini F, Steffenino G, Dellavalle A, Matullo G,
Colajanni E, Camilla T, Vado A, Benetton G, Uslenghi E, Piazza A.
Plasma activity and insertion/deletion polymorphism of
angiotensin I–converting enzyme: a major risk factor and a
marker of risk for coronary stent restenosis.
Circulation. 1998;97:147–154.[Abstract/Free Full Text]
25.
Karadi I, Kostner GM, Gries A, Nimpf J, Romies L, Malle
E. Lipoprotein (a), and plasminogen are immunochemically
related. Biochim Biophys Acta. 1988;960:91–97.[Medline]
[Order article via Infotrieve]
26.
Tiran A, Tiran B, Hojas S, Kostner GM, Wilders-Trushnig
MM. Immunoquantification of lipoprotein (a): comparison of nephelometry
with electroimmunodiffusion. J Clin Lab Anal. 1993;7:256–262.[Medline]
[Order article via Infotrieve]
27.
Labeur C, Sheperd J, Rosseneu M. Immunological assays
of apolipoproteins in plasma: methods and instrumentation. Clin
Chem. 1990;36:591–597.[Abstract/Free Full Text]
28.
Robert B, Grandhomme M, Mainard F, Madec Y. Effect of
storage of sera and lipoprotein (a) phenotypes on detection of
lipoprotein (a) by a new agarose gel. Clin Chim Acta. 1994;225:195–201.[Medline]
[Order article via Infotrieve]
29.
Forrester JS, Fishbein M, Helfant R, Fagin J. A
paradigm for restenosis based on cell biology: clues for the
development of new preventive therapies. J Am Coll
Cardiol. 1991;17:758–769.[Abstract]
30.
Horie H, Takahashi M, Izumi M, Takaoka A, Fujita T,
Sakamoto T, Kito O, Okamura H, Kinoshita M. Association of an acute
reduction in lipoprotein (a) with coronary artery
restenosis after percutaneous transluminal
coronary angioplasty. Circulation. 1997;96:166–173.
31.
Hoffmann R, Mintz GS, Dussaillant GR, Popma JJ, Pichard
AD, Satler LF, Kent KM, Griffin J, Leon MB. Patterns and mechanism of
in-stent restenosis: a serial intravascular ultrasound study.
Circulation. 1996;94:1247–1254.[Abstract/Free Full Text]
32.
Loscalzo J. The relation between
atherosclerosis and thrombosis. Circulation.
1992;86(suppl III):III-95-III-99.
33.
Albers JJ, Marcovina SM, Lodge MS. The unique
lipoprotein (a): properties and immunochemical measurement. Clin
Chem. 1990;36:2019–2026.[Abstract/Free Full Text]
34.
Jenner JL, Ordovas JM, Lamon-Fava S, Schaefer MM,
Wilson PW, Castelli WP, Schaefer EJ. Effects of age, sex, and
menopausal status on plasma lipoprotein (a) levels: the Framingham
Offspring Study. Circulation. 1993;87:1135–1141.[Abstract/Free Full Text]
35.
Weintraub WS, Kosinski AS, Brown CL, King SB. Can
restenosis after coronary angioplasty be predicted from
clinical variables? J Am Coll Cardiol. 1993;21:6–14.[Abstract]
36.
Rensing BJ, Hermans RM, Tijssen JG, Rutch W,
Danchin N, Heyndrickx GR, Mast EG, Wijns W, Serruys PW.
Luminal narrowing after percutaneous transluminal
coronary angioplasty. Circulation. 1993;88:975–985.[Abstract/Free Full Text]
37.
Carrozza JP, Kuntz RE, Fishman RF, Baim DS.
Restenosis after arterial injury caused by
coronary stenting in patients with diabetes mellitus. Ann
Intern Med. 1993;118:344–349.[Abstract/Free Full Text]
38.
Van Belle E, Bauters C, Hubert E, Bodart JC, Abomaali
K, Meurice T, McFadden EP, Lablanche JM, Bertrand ME.
Restenosis rates in diabetic patients: a comparison of
coronary stenting and balloon angioplasty in native
coronary vessels. Circulation. 1997;96:1454–1460.[Abstract/Free Full Text]
39.
Aronson D, Bloomgarden Z, Rayfield EJ. Potential
mechanisms promoting restenosis in diabetic patients.
J Am Coll Cardiol. 1996;27:528–535.[Abstract]
40.
Uterman G. The mysteries of lipoprotein (a).
Science. 1989;246:904–910.[Abstract/Free Full Text]
41.
Fortmann SP, Marcovina SM. Lipoprotein (a), a
clinically elusive lipoprotein particle. Circulation. 1997;95:295–296.[Free Full Text]
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Abstract
Introduction
