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(Circulation. 1999;100:1623-1629.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Preserved Endothelium-Dependent Vasodilation in Coronary Segments Previously Treated With Balloon Angioplasty and Intracoronary Irradiation
From the Thoraxcenter, Heartcenter, Rotterdam, Dijkzigt Academisch Ziekenhuis Rotterdam, The Netherlands (M.S., I.P.K., W.J.v.d.G., J.M.R.L., S.G.C., A.J.W., P.W.S.); Daniel den Hoed Cancer Center, Rotterdam, The Netherlands (V.L.M.A.C., J.P.A.M., P.C.L.); and Hospital de Bellvitge, Universitat de Barcelona, Barcelona, Spain (A.C., J.A.G.-H.).
Correspondence to P.W. Serruys, MD, PhD, Professor of Interventional Cardiology, Head of Department of Interventional Cardiology, Bd 412, Heartcenter, Academisch Ziekenhuis Rotterdam, Erasmus University, PO Box 1738, Dr Molewaterplein 40, 3000 DR Rotterdam, Netherlands. E-mail serruys{at}card.azr.nl
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionReferences |
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Background—Abnormal endothelium-dependent coronary vasomotion has been reported after balloon angioplasty (BA), as well as after intracoronary radiation. However, the long-term effect on coronary vasomotion is not known. The aim of this study was to evaluate the long-term vasomotion of coronary segments treated with BA and brachytherapy.
Methods and Results—Patients with single de novo lesions treated either with BA followed by intracoronary ß-irradiation (according to the Beta Energy Restenosis Trial-1.5) or with BA alone were eligible. Of these groups, those patients in stable condition who returned for 6-month angiographic follow-up formed the study population (n=19, irradiated group and n=11, control group). Endothelium-dependent coronary vasomotion was assessed by selective infusion of serial doses of acetylcholine (ACh) proximally to the treated area. Mean luminal diameter was calculated by quantitative coronary angiography both in the treated area and in distal segments. Endothelial dysfunction was defined as a vasoconstriction after the maximal dose of ACh (10-6 mol/L). Seventeen irradiated segments (89.5%) demonstrated normal endothelial function. In contrast, 10 distal nonirradiated segments (53%) and 5 control segments (45%) demonstrated endothelium-dependent vasoconstriction (-19±17% and -9.0±5%, respectively). Mean percentage of change in mean luminal diameter after ACh was significantly higher in irradiated segments (P=0.01).
Conclusions—Endothelium-dependent vasomotion of coronary segments treated with BA followed by ß-radiation is restored in the majority of stable patients at 6-month follow-up. This functional response appeared to be better than those documented both in the distal segments and in segments treated with BA alone.
Key Words: balloon • angioplasty • radioisotopes • endothelium • acetylcholine
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Abnormal endothelium-dependent coronary vasomotion has been reported both immediately after and up to 6 months after coronary balloon angioplasty (BA).1 2 3 4 The preservation of endothelial function is of the utmost importance to maintain the delicate balance between inhibition and promotion of vascular growth, vasoconstriction, and vasodilation, as well as antithrombotic and hemostatic mechanisms.5 Intracoronary radiation appears to be a promising new technique to prevent restenosis after BA.6 7 8 Experimental studies have demonstrated an impairment of endothelial function in the short term after high-dose intracoronary
-irradiation, which was
restored at follow-up.9 However, the effect of
brachytherapy after balloon-induced injury on vasomotor function in
patients remains unknown. The aim of the present study was to
assess the long-term effect of intracoronary radiation therapy
after successful BA on coronary vasomotion. |
Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patient Selection
Two groups of patients were compared: patients with single de novo lesions successfully treated with BA followed by intracoronary ß-irradiation (n=23) and patients with single de novo lesions successfully treated only with BA (n=16). Patients receiving radiation were included in the Beta Energy Restenosis Trial (BERT-1.5). Patients in the control group were individuals treated with BA alone and matched for age, sex, and vessel size. Those patients in stable condition who returned for 6-month angiographic follow-up formed the study population (n=19, irradiated group and n=11, control group). BERT-1.5 was a prospective multicenter feasibility study. The isotope selected was pure ß-emitting 90Sr/90Y, and patients were randomized to receive 12, 14, or 16 Gy at 2 mm from the source. The inclusion and exclusion criteria of this trial have been reported previously.10
Radiation Delivery System
The Beta-Cath System (Novoste Corp) was used to deliver
localized ß-radiation to a coronary artery at the site of
coronary intervention. The device consists of 3 components: (1)
the transfer device, which stores the radiation source train and allows
the positioning of these sources within the catheter; (2) the delivery
catheter, which is a 5F multilumen, over-the-wire, noncentered catheter
that uses saline solution to send and return the radiation source
train; and (3) the radiation source train, which consists of a series
of 12 independent 2.5-mm-long cylindrical seeds that contain the
radioisotope 90Sr/90Y
sources and is bordered by 2 gold radiopaque markers at the distal and
proximal parts of the 30-mm source train.11
Dose Calculation
The actual dose received by the luminal surface was
retrospectively calculated by means of dose-volume
histograms.12 This method is based on quantitative
intravascular ultrasound (IVUS) under the assumption that the radiation
source is positioned at the same place as the IVUS catheter. The method
of selection of the area of interest on IVUS has been reported
previously.13 The IVUS system used was a sheath-based IVUS
catheter (ClearView, CVIS, Boston Scientific Corporation) incorporating
a 30-MHz single-element transducer rotating at 1800 rpm (Ultracross,
CVIS). Image acquisition and digitization were performed by means of an
ECG-gated pullback at a step size of 0.2
mm/step.14 15 Volumetric analysis of the
irradiated area was performed by a semiautomatic contour detection
program developed at our institution.16 The feasibility
and intraobserver and interobserver variabilities of this system have
been reported previously.17 18 19 The distance between the
center of the catheter and both the lumen-intima and media-adventitia
interfaces was calculated in 24 pie slices (15° each) in all cross
sections corresponding to the irradiated area (30-mm length of the
train source). Considering the prescribed dose and the accurate
geometric data obtained from the IVUS, the cumulative curve of the
dose-volume histogram for a predefined volume (ie, intima or
adventitia) can be obtained (Figure 1
).
From this curve, for example, the minimal dose received by 90% of
either the intimal volume (Dv90 lumen) or the
adventitial volume (Dv90 Adv) was calculated.
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Endothelial Function Study
Long-acting vasoactive drugs were discontinued 
48 hours before
the study. A percutaneous femoral artery approach and
8F guiding catheter were used in all cases.
Endothelium-dependent and -independent coronary
vasomotion were studied as described previously in
detail20 : after the administration of 10 000 IU of
heparin, a 3F infusion catheter (Transit, Cordis) was advanced over a
guidewire and placed proximally to the irradiated segment. To avoid
wire-induced coronary spasm, the wire was removed. The
irradiated segment was identified on the basis of the anatomic
landmarks visible on the angiogram performed at the time of the
placement of the radiation source. To ensure that the segments were
fully bathed by the infusion of acetylcholine chloride (ACh), the tip
of the infusion catheter was placed 2 to 3 mm proximal to the
proximal border of the irradiated area. To determine the baseline
vasomotion, an initial infusion of saline solution for 1 minute through
the infusion catheter was performed and a baseline angiogram taken.
This was followed by infusion of serial doses of intracoronary
ACh, with final estimated intracoronary concentrations of
10-8 to 10-6 mol/L, to
assess endothelium-dependent coronary
vasomotion. The duration of each infusion was 2.5 minutes, followed
immediately by angiography. All angiograms were taken with identical
views and radiographic characteristics. All infusions were
delivered at a rate of 2 mL/min by use of a precision pump injector
(Mark V, Medrad, Europe BV). The final blood concentrations of ACh were
estimated with the assumption that blood flow in the coronary
artery was 80 mL/min.21 Finally, to evaluate
endothelium-independent vasomotion, a
nitroglycerin (NTG) bolus (2 mg) was administered
through the guiding catheter, after which an angiogram identical to
those performed previously was done.20 Throughout each
infusion, the heart rate, systemic arterial pressure, and
ECG were monitored continuously. Because ACh causes
endothelium-dependent vessel relaxation in experimental
models and in humans,22 23 a paradoxical vasoconstriction
after the infusion of this substance is an indicator of
endothelial dysfunction.20
The study was approved by the Medical Ethics Committee of our institution, and written informed consent was obtained from all patients in accordance with the guidelines established by the Committee for the Protection of Human Subjects.
Quantitative Coronary Angiography
Quantitative coronary angiography was performed after
the infusion of saline solution, at the end of each ACh infusion, and
after NTG bolus. Angiograms were performed in the 2 orthogonal
projections that best showed the artery of interest, without
overlapping of side branches and with less foreshortening. Offline
analysis was performed by means of the CAAS II system (Pie
Medical BV). Calibration of the system was based on dimensions of the
catheters not filled with contrast medium. The intraobserver and
interobserver variabilities of this method of analysis have
been reported previously.24 25 26 Mean luminal diameter was
determined after the infusion of each substance in the irradiated area,
in a 15- to 20-mm-long segment distal to the irradiated area and in a
contralateral nontreated artery that served as a control. Mean luminal
diameter was averaged for the 2 projections, and the percentage of
change relative to baseline was noted. All quantitative measurements
were performed by the same investigator (M.S.). Intraobserver
variability was assessed by reanalysis of the quantitative
coronary angiography of a series of 15 studies (150 repeated
measures in total) 3 months apart. Intraobserver differences (mean±2
SD) in mean luminal diameter were as follows: 0.7±2.7% for baseline
values, 0.8±2.9% after maximal dose of ACh, and 0.7±2.6% after NTG.
The intraclass correlation coefficient
(R2) for repeated measures was 0.97
for baseline values, 0.96 for maximal-dose ACh values, and 0.98 for NTG
values. We considered endothelial dysfunction a
vasoconstriction of the segment studied after the maximal dose of ACh
beyond the variability of the method of analysis (>3%).
Statistical Analysis
Data are presented as mean±SD or proportions. To
compare continuous variables, 2-tailed Student's t
test, ANOVA for repeated measurements, and linear regression
analysis were performed when appropriate. A value of
P<0.05 was considered statistically significant.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Baseline Characteristics
Baseline characteristics of both irradiated and control patients are presented in Table 1
.
Angiographic restenosis (diameter stenosis >50%) was
observed within the irradiated area in 3 patients (16%). Fourteen
patients (74%) remained asymptomatic, whereas 5 (26%)
presented with angina pectoris Canadian
Cardiovascular Society (CCS) class 1 (n=1), 2 (n=1), or
3 (n=3). None of the patients in the control group showed angiographic
restenosis, and only 2 presented with angina pectoris
CCS class 1. No differences were observed between groups regarding age,
sex, coronary risk factors, or minimal luminal diameter and
diameter stenosis in the diagnostic angiogram
performed at the time of the functional study. The left anterior
descending coronary artery was assessed more often in the
control group.
|
Coronary Vasomotion Study
No significant changes in mean aortic pressure and heart rate were
observed during the ACh infusion in either group. Mean luminal
diameters after infusion of each substance in irradiated and distal
nonirradiated segments and in the control group are presented
in Table 2. Seventeen irradiated segments
(89.5%) demonstrated normal endothelium-dependent
coronary vasomotion (16 segments with a vasodilatory response
[5.0±3% of change in mean luminal diameter after Ach] and 1 with no
change in mean luminal diameter [–0.1% of change after Ach
infusion]). On the other hand, endothelial dysfunction
was demonstrated in 2 irradiated segments (10.5%): 1 with angiographic
restenosis and angina pectoris CCS class 3 and the other with
angina pectoris CCS class 1 without restenosis (–5.2% and
–7.8% of vasoconstriction after maximal dose of ACh, respectively).
In contrast, 10 (53%) of the distal nonirradiated segments
demonstrated endothelial dysfunction (–19.5±17% of
vasoconstriction after maximal dose of ACh). No significant de novo
stenosis was observed at distal segments. No significant
correlation was demonstrated between the degree of stenosis at
follow-up and the vasomotor response. Five patients in the control
group (45%) showed endothelial dysfunction in the
treated area (–9.0±5% of vasoconstriction at ACh
10-6 mol/L). Mean percentages of change in mean
luminal diameter after infusion of the different substances between the
irradiated and control patients and between irradiated and distal
nonirradiated segments are presented in Figures 2 and 3.
Mean percentage change in diameter after ACh was 3.8±7.1% in the
irradiated segments compared with -3.2±7% and -6.6±10% in the
control group and in the distal nonirradiated segments, respectively
(P=0.01). No significant differences in percentage of change
in mean luminal diameter either in irradiated or in distal segments
were observed between the 3 coronary vessels after either ACh
or NTG. Examples of coronary segments with vasodilation of the
irradiated area and vasoconstriction of the distal nonirradiated
segment after ACh infusion are depicted in Figures 4 and 5.
All of the segments experienced vasodilation after NTG, which is
indicative of normal smooth muscle vasomotion (Figures 2 and 3).
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Radiation Dose Calculation
Mean prescribed radiation dose was 14±1.9 Gy at 2 mm to the
source. However, when dose-volume histograms were applied, the
calculated minimal dose received by 90% of the luminal surface was
8.2±3.8 Gy, whereas DV90 Adv was 5.2±1.9 Gy.
Only 6 patients (31.5%) received on average >10 Gy at luminal
surface, and only 2 patients (10.5%) received on average >8 Gy at the
adventitial layer. No significant correlation was found between
endothelium-dependent coronary vasomotion and
the calculated Dv90 lumen (r=-0.03;
P=NS). Similarly, no significant correlation was observed
between the coronary vasomotor response to NTG and
Dv90 Adv (r=0.03;
P=NS).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study demonstrates for the first time that the endothelium-dependent vasomotor function of coronary segments treated with BA followed by ß-radiation is restored in the majority of stable patients at 6-month follow-up. This functional response observed in irradiated segments appeared to be better than that documented both in distal nonirradiated segments and in segments treated only with BA.
An impairment of endothelial function has been reported at up to 3 to 6 months after BA.4 It has been demonstrated that soon after balloon-induced injury, there is a release of von Willebrand factor27 and endothelin28 as markers of endothelial injury. Experimental studies have demonstrated that the endothelium regenerates at follow-up. However, the endothelium appeared to still be dysfunctional,29 30 which may cause the release of endothelium-dependent contracting factors and the alteration of endothelial muscarinic receptors.31 32 33
Endothelial dysfunction in distal nontreated segments is a common finding in atherosclerotic coronary arteries after percutaneous interventions.3 An alteration of autoregulation due to chronic hypoperfusion may be implicated in the distal abnormal responsiveness to ACh.2 Furthermore, the presence of coronary risk factors may have a deleterious effect on distal coronary vasomotion.34 35
In contrast, most of the irradiated segments exhibited normal
endothelium-dependent vasomotion, and all of them
presented a normal response to NTG. Wiedermann et
al9 demonstrated restoration of
endothelial function after high-dose (20 Gy)
-radiation in a non–balloon-injured animal model. However, a
diffuse fibrosis of the smooth muscle layer, probably responsible for
the loss of response to NTG, was detected on
histological analysis.9 Our
findings confirmed these experimental observations in terms of
endothelium-dependent coronary vasomotion. The
lack of paradoxical vasoconstriction may be explained by an alteration
of the muscular media, which may demonstrate an impairment in response
to endothelium-dependent vasoregulatory signals.
However, vasodilation rather than lack of constriction was the
vasomotor response demonstrated in all but 1 of the irradiated segments
with normal endothelial function. The vasomotor
response to NTG remained unaltered and comparable between groups, which
suggests an absence of radiation-induced impairment of the medial
layer. In an experimental model, endothelial cells as
well as vascular smooth muscle cells were inhibited in a dose-dependent
manner. However, at a moderate range of ß-particle delivery (0.4 to 6
Gy), but not at a high dose (10 Gy), endothelial cells
appeared to be more radioresistant than vascular smooth muscle
cells.36 The relatively low dose of radiation received by
the treated segments may account for this normal functional behavior.
In fact, none of the patients actually received on average >10 Gy at
the level of the adventitia, as assessed by dose-volume histograms.
On the other hand, an experimental model of porcine coronary arteries subjected to balloon overstretch injury and either placebo or radiation with 18 Gy37 demonstrated that expression of enzyme-inducible nitric oxide synthase (iNOS), responsible for NO production, was enhanced, whereas expression of the cytokine transforming growth factor-ß1 (TGF-ß1) was suppressed in the irradiated group. iNOS is potentially responsible for inhibition of neointimal hyperplasia and stimulation of reendothelialization, whereas TGF-ß1 would enhance intimal hyperplasia and fibrosis by negatively modulating the expression of iNOS.37 Moreover, it has been demonstrated in experimental models that radiation causes dose- and time-dependent impairment of endothelium-dependent relaxation38 and that low-dose radiation would induce an anti-inflammatory reaction through specific dose-dependent modulation of the NO pathway.39 It remains to be seen whether this chain reaction after radiation would result in a late reduction in the restenosis rate. However, restoration of endothelial function may play an important role in this regard.
Study Limitations
Because the use of ACh in unstable patients is not exempt of
risk of coronary occlusion, only stable patients were
evaluated.
This study assessed patients receiving ß-radiation by means of a noncentering device. The actual dose received by the treated segment was rather low; thus, the effect of a higher dose or of different devices that allow a more homogeneous dose distribution remains to be evaluated.
We assessed the vasomotion of the 3 coronary arteries in the irradiated group, which have a potentially different degree of vasoreactivity to ACh. However, the 3 arteries demonstrated comparable vasomotor responses to ACh and NTG both at the irradiated and the distal segments, which overcomes this potential limitation.
We assumed that coronary vasomotion immediately after treatment is markedly impaired, as demonstrated in experimental models and in humans.1 2 3 4 9 Taking into account the risk of coronary occlusion in such situation, it was considered unethical to determine endothelium-dependent vasomotion immediately after the coronary intervention. Thus, the degree of recovery of coronary vasomotion could not be evaluated.
We also assumed that the IVUS and delivery catheters were lying in the
same position in the treated coronary segment. The size of the
IVUS catheter is smaller (2.9F, 
1 mm) than the brachytherapy
device (5F), which is thus to some extent more centered in the lumen.
Although the catheters should be on the shortest 3D path in the lumen,
coronary arteries have a complex curved geometry in space and
can be partially deformed by the catheters. Thus, catheters with
different rigidity may occupy different positions. The development of
new systems that incorporate the IVUS imaging element on the delivery
catheter might resolve this drawback.
During irradiation, the position of the delivery catheter inside the lumen is not fixed and may vary during the cardiac cycle because of ventricular contractions, which may lead to some degree of inhomogeneity not assumed by data derived from the static end-diastolic IVUS images.
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Acknowledgments |
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Dr Sabaté is the recipient of the 1997 BEAI200043 grant from the Generalitat de Catalunya for research in endothelial function after brachytherapy. Dr Kay is supported by The National Heart Foundation of New Zealand. The authors are indebted to the personnel of the catheterization laboratory for their help during the study protocol. The Wenckebach prize was awarded to P.W. Serruys by the Dutch Heart Foundation for brachytherapy research in the catheterization laboratory.
Received April 13, 1999; revision received June 21, 1999; accepted June 28, 1999.
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