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(Circulation. 1999;100:2491.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Abnormal Coronary Flow Velocity Reserve After Coronary Artery Stenting in Patients
Role of Relative Coronary Reserve to Assess Potential Mechanisms
From the Department of Internal Medicine, Division of Cardiology, Saint Louis University Health Sciences Center, Mo, and Service D’Explorations Fonctionnelles (P.D., E.A., J.-L.D.-R.), Unite D’Hemodynamique et de Cardiologie Interventionnelle, Henri Mondor University Hospital, University of Paris XII, Creteil, France.
Correspondence to Morton J. Kern, MD, Director, J.G. Mudd Cardiac Catheterization Laboratory, Saint Louis University Health Sciences Center, 3635 Vista Avenue at Grand Blvd, St. Louis, MO 63110. E-mail kernm{at}slu.edu
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Abstract |
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Background—Absolute coronary flow velocity reserve (CVR) after stenting may remain abnormal as a result of several different mechanisms. Relative CVR (rCVR=CVRtarget/CVRreference) theoretically normalizes for global microcirculatory disturbances and facilitates interpretation of abnormal CVR.
Methods and Results—To characterize potential mechanisms of
poststent physiology, CVR was measured using a Doppler-tipped
angioplasty guidewire in 55 patients before and after angioplasty,
after stenting, and in an angiographically normal reference vessel. For
the group, the percent diameter stenosis decreased from
75±13% to 40±18% after angioplasty and to 10±9% (all
P<0.05) after stent placement. After angioplasty, CVR
increased from 1.63±0.71 to 1.89±0.55 (P<0.05) and
after stent placement, to 2.48±0.75 (P<0.05 versus
pre- and postangioplasty). After angioplasty, rCVR increased from
0.64±0.26 to 0.75±0.23 and after stent placement to 1.00±0.34. In 17
patients with CVRstent 
2.0, increased basal
coronary flow, rather than attenuated hyperemia, was
responsible in large part for the lower CVRstent compared
with patients having CVRstent >2.0. In 8 patients with
CVRstent <2.0, a normal rCVR supported global
microvascular disease. The subgroup of 9 patients with
CVRstent <2.0 and abnormal rCVR (16% of the studied
patients) may require a pressure-derived fractional flow reserve to
differentiate persistent obstruction from diffuse atherosclerotic
disease or microvascular stunning.
Conclusions—Although a majority of patients after stenting normalize CVR for the individual circulation (ie, normal CVR or normal rCVR), in those with impaired CVRstent, the analysis of coronary flow dynamics suggests several different physiological mechanisms. Additional assessment may be required to fully characterize the physiological result for such patients to exclude remediable luminal abnormalities.
Key Words: coronary disease • blood flow • stents • stenosis
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Coronary balloon angioplasty and stent implantation enlarge luminal cross-sectional area and improve blood flow.1 2 3 4 Compared with balloon angioplasty, coronary stenting produces larger luminal areas and minimal residual stenoses.3 4 Due largely to symmetrical conduit morphological results, the scaffolding of the arterial segments after stenting provides better local flow conditions, a factor which is in large part responsible for the normalization of coronary vasodilatory reserve (CVR) in most patients after stenting.3 However, even after substantial conduit area enlargement with stenting, postprocedural CVR remains abnormal in some patients. Several potential mechanisms of the flow impairment have been suggested. These mechanisms include persistently elevated basal flow after transient ischemia, microvascular stunning due to particulate embolization, acute or chronic impairment of the microvascular circulatory response, an inadequate lumen at or adjacent to stent sites not recognized by conventional angiography due to residual stenosis or unappreciated thrombus, or diffuse epicardial atherosclerosis.
In patients with clinical conditions often associated with microvascular abnormalities (eg, diabetes mellitus, left ventricular hypertrophy, or myocardial ischemia/infarction), poststent CVR may be expected to be reduced even in the absence of any residual coronary artery stenoses.5 6 7 8 Assuming a relatively homogeneous distribution of global microcirculatory abnormalities,9 10 relative coronary flow velocity reserve ratio (rCVR), the ratio of CVR in the target vessel to CVR in an angiographically normal reference vessel, theoretically would normalize for the common microcirculatory abnormality and would be a more specific index of persistent conduit flow limitation.11 12 13
The purpose of this study was to examine absolute and relative CVR after balloon angioplasty and stenting to categorize the potential mechanisms of individual patient responses. We tested the hypothesis that rCVR would be normalized in most patients after stenting, but that patient subgroups with abnormal CVR and rCVR responses would identify several coexistent pathophysiologic alterations. An appreciation of different mechanisms would support the use of adjunctive techniques [eg, pressure-derived fractional flow reserve (FFR) and/or intravascular ultrasound] to establish the active process and direct further intervention, as indicated, in patients with impaired post-stent CVR.
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Methods |
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Study Patients
Fifty-five patients undergoing routine coronary angioplasty and elective stent placement were studied. Results in 19 of these patients were reported previously.3 Patients with recent (<4 weeks) myocardial infarction in the target or reference vessel territory or severe diffuse multivessel disease were excluded. Patients with clinical conditions of hypertension, diabetes mellitus, or myocardial infarction (remote in time from the study, >4 weeks) associated with impaired CVR were not excluded from the study. Oral and written consent was obtained from each patient before the study. The study protocol was approved by the Human Subjects Committee of the Institutional Review Board. No patient had a complication due to the study protocol. Anti-ischemic and antiplatelet medications were continued over the study period as clinically indicated.
Angioplasty and Stent Procedures
All patients received routine precatheterization
medications of diphenhydramine (25 mg orally) and diazepam (2 to 4 mg
intravenously) before the procedure. Vascular access was
obtained using the femoral approach with Seldinger technique. Heparin
(10 000 U intravenous bolus with 1 000 U/h
intravenous infusion) was administered before beginning
angioplasty. Angioplasty was performed in a routine manner using 6 or
8F guiding catheters and standard angioplasty balloon catheters. The
angioplasty guidewire was 0.014-inch Doppler-tipped guidewire
(FloWireTM, EndoSonics, Inc). All stents placed in this study were the
Johnson & Johnson Palmaz-Schatz sheathed stents varying in size from
3.0 to 4.0 mm.
Coronary Flow Velocity Technique
Coronary flow velocity was measured using the
Doppler-tipped guidewire 3 to 5 minutes after intracoronary
nitroglycerin (100 to 200 µg). The average peak
velocity (APV, cm/s) was obtained from the spectral velocity signals
averaged over 2 cardiac cycles. Coronary hyperemia was
induced with bolus administration of intracoronary
adenosine (8 to 12 µg for right coronary artery and
18 to 24 µg for the left coronary artery) as previously
reported.3 9 10 13 14 15 CVR was computed as the ratio of
hyperemic to basal average peak velocity. CVR measurements were
made in duplicate with previously reported variation of
15±9%.9 14 15 The CVR was measured in the reference
vessel (CVRreference), followed by the target
vessel at least 2 cm distal to the stenosis before angioplasty.
CVR was measured after angioplasty and again after stenting
(CVRstent). Data were obtained before and at
least 5 to 10 minutes after coronary angioplasty and stent
placement. rCVR was computed for each portion of the study as the ratio
of
CVRtarget/CVRreference3 11 12 13
and normal cut-off values (CVR >2.0, rCVR >0.8) were determined from
previous thresholds and receiver operating curves related to myocardial
perfusion imaging.16 17 18 An example of absolute and
relative coronary flow velocity data during stenting is shown
on Figure 1
.
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Quantitative Coronary Angiographic Technique
Quantitative coronary angiography (QCA) was performed
using the Phillips DCI-ACA or ADA imaging system. The percent diameter,
area stenosis, and minimal lumen diameter were computed in a
standard manner using the proximal normal reference vessel segments in
single plane, worst view angulation. The contrast-filled guiding
catheter was used as calibration for vessel dimension calculation. The
reproducibility of QCA from this laboratory has been previously
reported with inter- and intraobserver variability of 8% and 12%,
respectively.3 14 In patients with 3-vessel
coronary artery disease, a reference vessel was accepted as the
vessel with <40% narrowing by QCA.
Statistical Analysis
All data were expressed as mean±SD. ANOVA was used to compare
baseline, postangioplasty and poststent hemodynamic
data, Doppler flow, and angiographic variables.
Scheffe’s test was used to compare mean values when significant
differences among the study periods were identified by ANOVA.
P<0.05 was considered statistically significant.
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Results |
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Patient Characteristics
The study included 55 patients (37 male, 18 female, mean age 58±12 years) with predominantly 1- or 2-vessel coronary disease (Table 1
). Hypertension was
present in 56% of patients, diabetes mellitus in 24%, and smoking
in 63%. A prior history of remote myocardial infarction was noted in
46% of the patients. The target vessel was the left anterior
descending artery in 21, circumflex in 10, and right coronary
artery in 24. Six patients had segmental left ventricular
hypokinesis in the distribution of the target stenosis (3
inferior-posterior, 2 anterior, 1 apical). The
angiographically normal reference vessels supplying regions of normal
left ventricular wall motion were the left anterior
descending in 24, circumflex in 26, obtuse marginal in 2, and diagonal
branch in 3 patients.
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Quantitative Coronary Angiographic and Hemodynamic
Data
Balloon angioplasty decreased the diameter stenosis from
75±13% (minimal luminal diameter 0.76±0.45 mm) to 40±18%
(minimal luminal diameter 1.77±0.61 mm, P<0.05).
Stent implantation further decreased the percent diameter
stenosis to 10±9% (minimal luminal diameter 2.91±0.52
mm, P<0.05 versus both before and after angioplasty). The
reference vessel segment mean diameter was similar, 2.94±0.52 mm
(Table 2). There was no
significant change in heart rate or mean arterial pressure
over the study period.
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Coronary Flow Velocity Data
For the entire group before angioplasty, basal
poststenotic APV increased from 14±6 to 23±12 cm/s at peak
hyperemia with a resulting CVR of 1.63±0.71. After
angioplasty, basal APV increased to 19±8 cm/s (P<0.05).
Hyperemic APV increased to 35±15 cm/s (P<0.05
versus preangioplasty) with CVR increasing to 1.89±0.55
(P=NS versus preangioplasty). After stent placement, resting
APV was unchanged (19±7 cm/s), hyperemic APV increased to
44±12 cm/s and CVR increased to 2.48±0.75 (P<0.05 versus
before and after angioplasty) (Table 3).
The reference vessel basal APV was 22±8 cm/s which increased to 51±15
cm/s with hyperemia yielding CVRreference
of 2.55±0.49, similar to the poststent result. Before angioplasty,
rCVR was 0.64±0.26. After angioplasty, rCVR increased to 0.75±0.23
(P<0.05) and after stent implantation to 1.00±0.34
(P<0.05 versus pre- and postangioplasty). When examined by
individual target vessel, CVR and rCVR were similar among the left
anterior descending, circumflex, and right coronary arteries.
Figure 2 shows CVR and rCVR and
corresponding percent diameter stenosis for the 3 study
periods.
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Stratification of CVR After Stenting
The results were also stratified by CVRstent
>2.0 or 2.0). There were 38 patients with
CVRstent >2.0. There were no significant
angiographic differences between the 2 groups.
In the CVRstent >2.0 group, the resting APV was
similar among pre- and postangioplasty, and poststent periods (15±5,
19±8, 17±6 cm/s, respectively, P=NS) (Figure 3). The CVR increased from 1.79±0.78 to
2.03±0.58 after angioplasty (P=NS) and to 2.82±0.61 after
stenting (P<0.05 versus pre- and postangioplasty). rCVR
increased from 0.69±0.28 before to 0.78±0.25 after angioplasty and to
1.11±0.35 after stenting (P<0.05 versus pre- and
postangioplasty).
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In the 17 patients with CVRstent 2.0 (8 left
anterior descending, 5 right coronary artery, and 4 circumflex
target vessels), resting APV was similar before (12±8 cm/s) and after
angioplasty (19±7 cm/s), but was higher after stenting (23±5 cm/s,
P<0.05 versus pre- and postangioplasty) and higher than
basal flow in CVRstent >2.0 patients
(P<0.05). Hyperemic APV increased from 17±14 to
31±13 cm/s after angioplasty, values lower than
CVRstent >2.0 patients (P<0.05).
After stent implantation, hyperemic APV increased to 40±10
cm/s (P<0.05 versus pre- and postangioplasty). Figure 3
summarizes the changes in basal and hyperemic velocity
in the CVRstent subgroups.
After angioplasty in the group with CVRstent
<2.0, CVR increased from 1.27±0.31 to 1.57±0.28 (P<0.05)
and to 1.73±0.14 after stent implantation (P<0.05 versus
preangioplasty; P<0.05 versus
CVRstent >2.0). In this group,
CVRstent was less than
CVRreference (1.73±0.14 versus 2.38±0.39,
P<0.05). rCVR increased from 0.54±0.15 at baseline to
0.68±0.25 after angioplasty and further increased after stent
implantation to 0.75±0.13 (P<0.05 versus preangioplasty
and CVRstent >2.0). Figure 4 summarized the changes in CVR and rCVR
for the CVRstent subgroups.
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Microvascular Disease, Multivessel Coronary Artery Disease,
and CVR
Microvascular disease was based on
CVRreference <2.0 and was present in 9
patients (Table 4, Figure 5). Compared with patients with
CVRreference >2.0, patients with
CVRreference 2.0 had higher reference vessel
basal APV (31±7 versus 20±7 cm/s, P<0.05) and higher
postangioplasty basal APV (P<0.05). In addition, after
stenting, the hyperemic APV was lower than hyperemic
reference APV (40±12 versus 56±9 cm/s, P<0.05) compared
with patients without microvascular disease (44±12 versus 50±16 cm/s,
P=NS). However, these variations in flow velocity did not
result in the mean CVRstent being significantly
different than patients with CVRreference >2.0.
All patients with CVRreference <2.0, including 5
patients with CVRstent <2.0, had normalized rCVR
after stenting (Figure 6). There was no
significant difference between CVRstent and rCVR
for patients with single- and multivessel coronary artery
disease (Figure 6).
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Coronary Flow Velocity Responses After Stenting and
Potential Mechanisms
Using previously established thresholds of
CVRstent (>2.0) and rCVR (>0.8), 4 subgroups of
patients were identified that have potentially different mechanisms
accounting for the physiological end result (Figure 6). Four patients had normal CVRstent with
abnormal rCVR (group I: CVR 2.25±0.17, rCVR 0.72±0.03); 34 patients
had normal CVRstent with normal (or supranormal)
rCVR (group II: CVR 2.89±0.66, rCVR 1.16±0.34); 8 patients had
abnormal CVRstent with normal rCVR (group III:
CVR 1.76±0.15, rCVR 0.86±0.6); and 9 patients had abnormal
CVRstent and abnormal rCVR (group IV: CVR
1.70±0.14, rCVR 0.65±0.09). The mean values for
CVRstent and rCVR for each group are shown in
Figure 6 (right panel). The potential mechanisms by subgroup are
discussed below.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study demonstrates that although impaired CVR (<2.0) after stenting was observed in some patients (30%), rCVR could be normalized in most patients. In the examination of these results, CVRstent and the associated rCVR suggest several potential different mechanisms for the resultant physiology which include, individually or combined, 1) increased baseline flow after stenting, 2) residual conduit obstruction, 3) microvascular stunning or small vessel disease, or 4) diffuse epicardial atherosclerosis. Dissection of specific flow velocity parameters can aid in differentiating these mechanisms.
Abnormal CVR After Stenting
An augmentation of basal flow velocity, more than a significant
attenuation of maximal hyperemic flow velocity appears to
account for the failure to achieve an CVRstent
>2.0 in most patients. The current data reproduces the findings of van
Liebergen et al,4 wherein patients with impaired CVR after
stenting had a mean baseline APV that was nearly double the APV after
balloon angioplasty and after stenting in patients with
CVRstent >2.5. As in the current study, the
hyperemic APVstent was similar for both
groups immediately after the procedure. The exact mechanism of an
increased basal APVstent in these patients is
unclear but may be due to atherosclerotic plaque compression during
stent implantation and release of factors and/or particulates that
produce a sustained hyperemic stimulus or transiently alter
coronary autoregulation or vasomotion.19 20 21
Abnormal rCVR After Stenting
In the 2 groups with normal CVRstent (I,
II), the abnormal rCVR in group I suggests that although the CVR
exceeds 2.0, this value doe not achieve 80% of the reference flow
potential resulting from either continued unappreciated epicardial
stenosis or regional microvascular abnormalities. Conversely,
in group II the reference vessel flow in some patients (eg, those with
rCVR >1.2) fails to equal or exceed poststent flow. This response
suggests potential regional reference vessel microvascular disease,
diffuse atherosclerosis of the reference vessel, or
unappreciated reference vessel obstruction. Our laboratory has recently
demonstrated significant spatial heterogeneity of the
coronary circulation in some cardiac transplant
recipients,10 a factor which confounds the usefulness of
rCVR in some circumstances. Transcoronary guidewire
pressure-derived FFR would discriminate between impaired flow due to
diffuse disease in the reference vessel
(FFRnormal) or occult reference or target vessel
obstruction (FFRabnormal).22 23
In the 2 groups with abnormal CVRstent (III, IV), rCVR suggests other mechanisms. In group III, the normal rCVR suggests that impaired CVRstent is sufficient for globally reduced microcirculatory function. CVR may be reduced by comorbid conditions such as diabetes mellitus, hypertension, or hypercholesterolemia, conditions associated with abnormal microcirculatory responses.5 6 7 8 It is interesting to note that the 9 patients with CVRreference <2.0 had normal rCVR poststenting, with 5 having an abnormal CVRstent. The 4 patients with normal CVRstent had supranormal rCVR (>1.4), suggesting that an alternative mechanism may also be present. Although van Liebergen et al4 had no patients immediately after angioplasty or stenting with a CVRreference <2.0, a supranormal rCVR was also demonstrated, occurring exclusively in stent patients at the 6-month follow-up evaluation. Although the reference vessel appeared angiographically normal, diffuse atherosclerosis, unappreciated by angiography, may have again reduced CVRreference (akin to group II) in the absence of focal epicardial narrowing.24 Mintz et al25 indicated that intravascular ultrasound imaging commonly identifies diffuse atherosclerosis in angiographically normal vessels, a factor confounding any evaluation when angiography represents the imaging modality used.24
In group IV, the abnormal rCVR suggests 2 mechanisms: either residual conduit obstruction (eg, occult stenosis or thrombus) or regional microvascular stunning. Impaired CVRstent may be due to an acute attenuation of the microcirculatory vasomotor responses by distal embolization and microvascular stunning following balloon angioplasty or stent deployment. In this case, both CVRstent and rCVR would initially be abnormal and normalize at follow-up. Persistent microvascular vasoconstriction may also be a contributing factor, one that should be minimized by postprocedure nitrates. An alternative mechanism is unappreciated luminal obstruction. Although stent implantation nearly always leads to a significant increase in cross-sectional area with generally concentric and cylindrical conduits, inapparent stent edge dissections, and new accumulation of focally extruded plaque into the nonstented vessel segments may occur.26 In this circumstance, both CVRtarget and rCVR would also be abnormal. In this subgroup, FFR would be particularly useful to differentiate conduit obstruction (FFRabnormal) from microvascular stunning (FFRnormal).
Durability of Improved Physiology After Angioplasty and
Stenting
Haude et al,2 using densitometric angiographic
methods, as well as van Liebergen et al,4 demonstrated
that improved myocardial perfusion reserve and CVR immediately after
stenting is associated with normalized maximal blood flow ratios, an
effect that was generally sustained for 6 months. A durable normalized
anatomy coupled with physiology for both balloon angioplasty,
and most recently stenting, has also translated to enhanced clinical
outcomes.27 28 A prospective multicenter trial reported
that an optimized coronary lumen area produced by conventional
balloon angioplasty, sufficient to increase
CVRPTCA >2.5, produced stent-like outcomes with
6-month target lesion revascularization and
angiographic restenosis rates of 16%.28
Limitations
The technical limitations of Doppler CVR have been described
in detail elsewhere.29 It is recognized that the current
study population is small, a factor limiting the strength of
conclusions regarding mechanisms of impaired poststent CVR. However,
the role of rCVR, especially in patients with microvascular disease,
appears promising to identify potential mechanisms and, when coupled
with FFR, can fully define the proposed mechanisms of impaired flow and
direct further intervention.
FFR was not routinely used in the current study due to the limited availability of pressure sensor wires during the study period. FFR is theoretically more specific for conduit obstruction than CVR in that the effect of the microcirculation is nullified in the derived calculations. Baumgart et al13 demonstrated that rCVR, but not CVRtarget, had a significant correlation to FFR (r=0.95, P<0.001; CVRtarget versus FFR, r=0.45, P=0.09), an expected result considering the confounding influence of the microcirculation on CVR. The mechanisms postulated in group IV patients with abnormal CVR and rCVR can be further defined using FFR.
The selection of normal CVR and rCVR values has been derived from studies of angioplasty outcomes and myocardial perfusion imaging.4 13 16 17 18 30 The validity of the rCVR concept assumes that there is a uniform microcirculation across the target and reference vessel regions. Previous studies9 10 support a relatively uniform CVR distribution in patients without coronary artery disease, but this finding may not apply in patients with active ischemia or moderate multivessel coronary artery disease.31 32
Intravascular ultrasound was also not routinely used in this study but would have confirmed both diffuse atherosclerotic disease or focal obstructions. Ziada et al26 demonstrated persistent haziness in 15% of patients after high-pressure coronary stent implantation, which was associated with angiographically occult but intravascular ultrasound-identified coronary dissections.
Clinical Implications
In most patients, stent implantation significantly augments
coronary blood flow with improvement in both absolute CVR and
normalization of rCVR. Failure to normalize CVR after stenting,
observed in a minority of patients, may be due to multiple mechanisms
which may be investigated using coronary flow velocity. The
rCVR can assist in identifying a need for further examination by
pressure-derived FFR, additional angiographic views, or possibly
intravascular ultrasound imaging to exclude remediable luminal
abnormalities. Identifying the mechanism of persistently abnormal
coronary blood flow after stenting will assist in decisions for
additional interventions with the potential to reduce stent
restenosis or limit adverse clinical outcomes.
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Acknowledgments |
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The authors wish to thank the J.G. Mudd Cardiac Catheterization Laboratory team for technical support and Donna Sander for manuscript preparation.
Received April 27, 1999; revision received July 21, 1999; accepted August 4, 1999.
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References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Haude M, Erbel R, Issa H, Meyer J. Quantitative analysis of elastic recoil after balloon angioplasty and after intracoronary implantation of balloon-expandable Palmaz-Schatz stents. J Am Coll Cardiol. 1993;21:26–34.[Abstract]
2.
Haude M, Caspari G, Baumgart D, Brennecke R, Meyer J,
Erbel R. Comparison of myocardial perfusion reserve before and after
coronary balloon predilatation and after stent implantation in
patients with postangioplasty restenosis.
Circulation. 1996;94:286–297.
3. Kern MJ, Dupouy P, Drury JH, Aguirre FV, Aptecar E, Bach RG, Caracciolo EA, Donohue TJ, Dubois Rande J, Geschwind HJ, Mechem CJ, Kane G, Teiger E, Wolford TL. Role of coronary artery lumen enlargement in improving coronary blood flow after balloon angioplasty and stenting: a combined intravascular ultrasound Doppler flow and imaging study. J Am Coll Cardiol. 1997;29:1520–1527.[Abstract]
4.
van Leibergen RAM, Piek JJ, Koch KT, de Winter RJ, Lie
KI. Immediate and long-term effect of balloon angioplasty or stent
implantation on the absolute and relative coronary blood flow
velocity reserve. Circulation. 1998;98:2133–2140.
5. Strauer B. The significance of coronary reserve in clinical heart disease. J Am Coll Cardiol. 1990;15:775–783.[Abstract]
6. Rossen JD, Winniford MD. Effect of increases in heart rate and arterial pressure on coronary vasodilatory reserve in humans. J Am Coll Cardiol. 1993;21:343–348.[Abstract]
7.
Opherk D, Mall G, Zebe H, Schwarz F, Weihe E, Manthey
J, Kubler W. Reduction of coronary reserve: a mechanism for
angina pectoris in patients with arterial hypertension and
normal coronary arteries. Circulation. 1984;69:1–7.
8. Nitenberg A, Foult JM, Blancet F, Zouioueche S. Multifactorial determinants of reduced coronary flow reserve after dipyridamole in dilated cardiomyopathy. Am J Cardiol. 1985;55:748–754.[Medline] [Order article via Infotrieve]
9. Kern MJ, Bach RG, Mechem CJ, Caracciolo EA, Aguirre FV, Miller LW, Donohue TJ. Variations in normal coronary vasodilatory reserve stratified by artery, gender, heart transplantation and coronary artery disease. J Am Coll Cardiol. 1996;28:1154–1160.[Abstract]
10.
Wolford TL, Donohue TJ, Bach RG, Drury JH, Caracciolo
EA, Kern MJ, Miller LW. Heterogeneity of
coronary flow reserve in the examination of multiple individual
allograft coronary arteries. Circulation. 1999;99:626–632.
11. Gould KL, Kirkeeide RL, Buchi M. Coronary flow reserve as a physiologic measure of stenosis severity. J Am Coll Cardiol. 1990;15:459–474.[Abstract]
12. Gould KL. Noninvasive assessment of coronary stenosis by myocardial perfusion imaging during pharmacologic coronary vasodilation. Am J Cardiol. 1978;41:267–278.[Medline] [Order article via Infotrieve]
13.
Baumgart D, Haude M, Goerge G, Ge J, Vetter S, Dagres
N, Heusch G, Erbel R. Improved assessment of coronary
stenosis severity using the relative flow velocity reserve.
Circulation. 1998;98:40–46.
14. Donohue TJ, Kern MJ, Aguirre FV, Bach RG, Wolford T, Bell CA, Segal J. Assessing the hemodynamic significance of coronary artery stenoses: analysis of translesional pressure-flow velocity relations in patients. J Am Coll Cardiol. 1993;22:449–458.[Abstract]
15. Ofili EO, Kern MJ, Labovitz AJ, St. Vrain JA, Segal J, Aguirre FV, Castello R. Analysis of coronary blood flow velocity dynamics in angiographically normal and stenosed arteries before and after endolumen enlargement by angioplasty. J Am Coll Cardiol. 1993;21:308–316.[Abstract]
16.
Miller DD, Donohue TJ, Younis LT, Bach RG, Aguirre FV,
Wittry MD, Goodgold HM, Chaitman BR, Kern MJ. Correlation of
pharmacologic 99 mTc-sestamibi myocardial perfusion imaging with
poststenotic coronary flow reserve in patients with
angiographically intermediate coronary artery stenoses.
Circulation. 1994;89:2150–2160.
17. Joye JD, Schulman DS, Lasorda E, Farah T, Donohue BC, Reichek N. Intracoronary Doppler guide wire versus stress single-photon emission computed tomographic thallium-201 imaging in assessment of intermediate coronary stenoses. J Am Coll Cardiol. 1994;24:940–947.[Abstract]
18.
Heller LI, Cates C, Popma J, Deckelbaum LI, Joye JD,
Dahlberg ST, Villegas BJ, Arnold A, Kipperman R, Grinstead WC, Balcom
S, Ma Y, Cleman M, Steingart RM, Leppo JA, for the FACTS study group.
Intracoronary Doppler assessment of moderate
coronary artery disease: comparison with 201Tl imaging and
coronary angiography. Circulation. 1997;96:484–490.
19. Nato S, Kodama K, Hori M, Mishima M, Hirayama A, Inoie M, Kamada T. Temporal increase in resting coronary blood flow causes an impairment of coronary flow reserve after coronary angioplasty. Am Heart J. 1992;124:28–36.
20.
Bates ER, McGillem MJ, Beals TJ, DeBoe SF, Mikelson JK,
Mancini GBJ, Vogel RA. Effect of angioplasty-induced
endothelial denudation compared with medial injury on
regional coronary blood flow. Circulation. 1987;76:710–716.
21. Fischell TA, Bausback KN, McDonald TV. Evidence for altered epicardial coronary artery autoregulation as a cause of distal coronary vasoconstriction after successful percutaneous transluminal coronary angioplasty. J Clin Invest. 1990;86:575–584.
22.
Pijls NJJ, van Son AM, Kirkeeide RL, de Bruyne B, Gould
KL. Experimental basis of determining maximum coronary,
myocardial, and collateral blood flow by pressure measurements for
assessing functional stenosis severity before and after
percutaneous transluminal coronary angioplasty.
Circulation. 1993;87:1354–1367.
23.
Pijls NH, de Bruyne B, Peels K, Van Der Voort PH,
Bonnier HJ, Bartunek J, Koolen JJ, Koolen JJ. Measurement of fractional
flow reserve to assess the functional severity of
coronary-artery stenosis. N Engl J
Med. 1996;334:1703–1708.
24. Marcus ML, Harrison DG, White CW, McPerson DD, Wilson RF, Kerber RE. Assessing the physiologic significance of coronary obstructions in patients: importance of diffuse undetected atherosclerosis. Prog Cardiovasc Dis. 1988;31:39–56.[Medline] [Order article via Infotrieve]
25. Mintz GS, Painter JA, Pichard AD, Kent KM, Statler LF, Popma JJ, Chuang YC, Bucher TA, Sokolowicz LE, Leon MB. Atherosclerosis in angiographically "normal" coronary artery reference segments: an intravascular ultrasound study with clinical correlations. J Am Coll Cardiol. 1995;25:1479–1485.[Abstract]
26. Ziada KM, Tuzcu M, De Franco AC, Kim MH, Raymond RE, Franco I, Whitlow PL, Ellis SG, Nissen SE. Intravascular ultrasound assessment of the prevalence and causes of angiographic "haziness" following high-pressure coronary stenting. Am J Cardiol. 1997;80:116–121.[Medline] [Order article via Infotrieve]
27.
Serruys PW, de Jaegere P, Kiemeneij F, Macaya C,
Rutsch W, Heyndrickx G, Emanuelsson H, Marco J, Legrand V, Materne P. A
comparison of balloon-expandable-stent implantation with balloon
angioplasty in patients with coronary artery disease.
N Engl J Med. 1994;331:489–495.
28.
Serruys PW, Di Mario C, Piek J, Schroeder E, Vrintz C,
Probst P, de Bruyne B, Hanet C, Fleck E, Haude M, Verna E, Voudris V,
Geschwind H, Emanuelsson H, Muhlberger V, Danzi G, Peels HO, Ford AJ
Jr, Boersma E, for the DEBATE study group. Prognostic value of
intracoronary flow velocity and diameter stenosis in
assessing the short- and long-term outcomes of coronary balloon
angioplasty: the DEBATE study (Doppler Endpoints Balloon
Angioplasty Trial Europe). Circulation. 1997;96:3369–3377.
29. Kern MJ. Intracoronary Doppler flow. In: Geschwind HJ, Kern MJ, eds. Guidebook to Endovascular Coronary Diagnostic Techniques. Armonk, NY: Futura Publishing; 1997:335–442.
30. Donohue TJ, Miller DD, Bach RG, Tron C, Wolford T, Caracciolo EA, Aguirre FV, Younis LT, Chaitman BR, Kern MJ. Correlation of poststenotic hyperemic coronary flow velocity and pressure with abnormal stress myocardial perfusion imaging in coronary artery disease. Am J Cardiol. 1996;77:948–954.[Medline] [Order article via Infotrieve]
31. Sestier FJ, Mildenberger RR, Klassen GA. Role of augmentation in spatial and temporal perfusion heterogeneity of canine myocardium. Am J Physiol. 1978;235:H64–H71.
32.
Austin RE Jr, Aldea GS, Coggins DL, Flynn AE, Hoffman
JIE. Profound spatial heterogeneity of coronary
reserve: discordance between patterns of resting and maximal myocardial
blood flow. Circ Res. 1990;67:319–331.
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