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(Circulation. 1998;98:2695-2701.)
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports |
Effect of Glycoprotein IIb/IIIa Receptor Blockade on Recovery of Coronary Flow and Left Ventricular Function After the Placement of Coronary-Artery Stents in Acute Myocardial Infarction
From the Deutsches Herzzentrum and 1. Medizinische Klinik der Technischen Universität München, Munich, Germany.
Correspondence to Franz-Josef Neumann, MD, Deutsches Herzzentrum und 1. Medizinische Klinik der Technischen Universität, Lazarettstraße 36, 81636 München, Germany. E-mail neumann{at}dhm.mhn.de
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Abstract |
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Background—Apart from its established effects on vessel patency after percutaneous coronary revascularization, glycoprotein IIb/IIIa receptor blockade by abciximab may improve myocardial perfusion by inhibition of the interaction of platelets and platelet aggregates with the microvasculature. We investigated the effect of abciximab with stent placement in acute myocardial infarction.
Methods and Results—In a prospective randomized trial, patients undergoing stenting in acute myocardial infarction within 48 hours after onset of symptoms were randomly assigned to receive either standard-dose heparin or abciximab plus low-dose heparin. Immediately after the procedure and at 14-day angiographic follow-up, we assessed flow velocity in the recanalized vessel with the Doppler wire and regional wall motion by the centerline method. End points were changes in papaverine-induced peak flow velocities and in wall motion indices. We assigned 98 patients to standard heparin and 102 to abciximab. We obtained 152 paired flow measurements and 151 paired left ventricular function studies. Residual stenoses of the treated lesions did not differ between the 2 groups. Improvement of peak flow velocity (mean [95% CI]: 18.1 cm/s [13.6 to 22.6 cm/s], n=80, versus 10.4 cm/s [5.4 to 15.4 cm/s], n=72, P=0.024) and wall motion index (0.44 SD/chord [0.29 to 0.59 SD/chord], n=79 versus 0.15 SD/chord [0.00 to 0.30 SD/chord], n=72, P=0.007) was significantly greater in patients assigned to abciximab than in those on heparin alone. At follow-up, the abciximab group had a higher global left ventricular ejection fraction than the heparin group (62% [59% to 65%] versus 56% [53% to 59%], P=0.003).
Conclusions—Abciximab had important effects beyond the maintenance of large-vessel patency. It improved the recovery of microvascular perfusion and concomitantly enhanced the recovery of contractile function in the area at risk.
Key Words: myocardial infarction • stents • glycoproteins • blood flow • ventricles
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Introduction |
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In acute myocardial infarction (AMI), myocardial salvage after timely recanalization of the infarct-related artery is critically dependent on coronary blood flow to the area at risk.1 With regard to patency of the infarct-related artery, randomized trials have shown that direct PTCA is superior to established protocols of thrombolysis,2 3 and additional benefit may be derived from stent placement.4
The adequacy of reperfusion in AMI, however, depends not only on persistent patency of the infarct-related artery but also on the integrity of the distal circulation. At the microcirculatory level, distal embolization of platelet aggregates formed at the treated plaque,5 release of vasoconstrictive platelet mediators,6 and/or vascular reperfusion injury due to cardiac inflammatory responses may compromise the recovery of perfusion.7 To this end, it has been shown that the pattern of reperfusion after recanalization of the infarct-related artery with stent placement varies considerably between patients.8 In most patients, coronary flow reserve improves within the next 2 weeks, whereas in others, maximal coronary flow falls below the level achieved initially.8 Perfusion patterns are closely linked to the recovery of contraction in the infarct region and may thus be a target for pharmacological modification.8 9
Glycoprotein IIb/IIIa receptor blockade may not only maintain patency of the recanalized vessel but also prevent embolization of platelet aggregates into the distal circulation.10 11 In this prospective randomized trial on patients with AMI, we investigated microvascular and contractile recovery of the infarct region after revascularization with stent placement and compared the effect of peri-interventional glycoprotein IIb/IIIa blockade by abciximab with that of standard heparin therapy. Specifically, we tested the hypothesis that compared with conventional treatment, abciximab improves the recovery of papaverine-induced coronary peak flow velocity and of wall motion in the infarct area within 14 days after successful stent placement in the infarct-related artery.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Study Cohort and Procedural Outcome
The study included patients with AMI undergoing revascularization by stent placement within 48 hours after onset of pain. Inclusion criteria were (1) typical anginal pain lasting >30 minutes, (2) a coronary artery lesion that was deemed suitable for stent placement, (3) ST-segment elevation of
1 mm in 2 contiguous leads, (4) elevation in creatine
kinase to 3 times the upper limit of normal with a concomitant rise
in MB isoenzyme, and (5) coronary artery occlusion with
angiographic appearance of fresh thrombus. We recruited patients who
met criteria 1 and 2 plus at least 1 of criteria 3 through 5. Exclusion
criteria were inability to give informed consent, history of vasculitis
or chronic steroid treatment, and contraindications to 1 of the study
drugs. All eligible patients who gave written informed consent were
randomized by means of sealed envelopes. Patients, but not physicians,
were blinded to the assignment of treatment. The study was carried out
according to the Declaration of Helsinki and was approved by our
institutional ethics committee.
Study Protocol
Before catheterization, all patients received
heparin 5000 U and aspirin 500 mg IV. Once the decision was made for
stent placement, patients were randomized to 1 of 2 treatment regimens.
Patients assigned to treatment with glycoprotein IIb/IIIa
receptor blockade received a bolus of abciximab 0.25 mg/kg body wt,
followed by continuous infusion of 10 µg/min for 12 hours, plus an
additional dose of heparin 25 000 U intra-arterially. In
patients assigned to usual care, we administered heparin 10 000 U
intra-arterially, followed by intravenous
heparin infusion 1000 U/h for the first 12 hours after sheath removal.
Immediately after reestablishing antegrade flow, we gave an
intracoronary bolus dose of 0.2 mg
nitroglycerin in both groups. Stent placement was
performed as described previously.12 We used 5
different types of slotted-tube stents, which were evenly distributed
between the study groups (Palmaz-Schatz, Multilink, Nir, Pura A, and
InflowDynamics). If, after stent placement, residual thrombus remained
and caused impairment of flow (TIMI grade 
2) or lumen narrowing of
>50%, operators were allowed to administer abciximab in the
usual-care group. In both groups, postinterventional antithrombotic
therapy consisted of ticlopidine 250 mg BID for 4 weeks and aspirin 100
mg BID throughout the study.
Immediately after completion of the intervention, coronary flow velocities in the stented segment were measured with the Doppler FloWire and analyzed by the FloMap system (Cardiometrics) as described previously.8 We positioned the tip of the Doppler wire at the proximal end of the stented segment to ensure a reproducible sampling site that is not subject to vasomotor changes. Doppler flow velocity spectra were analyzed on-line to determine time-averaged peak velocity. We determined basal and peak coronary flow velocities after intracoronary bolus doses of papaverine (10 mg for the right and 12 mg for the left coronary artery). Thereafter, we performed single-plane left ventriculography in the 30° right anterior oblique view. At 14±1 days after the initial intervention, coronary and left ventricular (LV) angiography and flow velocity measurements were repeated. When indicated, repeat PTCA was performed before the second flow velocity measurement.
Quantitative Angiography
We used nonionic contrast medium (ioversol) in all patients.
Images of coronary and LV angiograms (Hicor, Siemens) were
stored on compact disks and analyzed off-line (MEDIS Medical
Imaging Systems) by operators unaware of the study groups to which the
patients were assigned.8 12 Global LV ejection
fraction was determined by the area-length method. To quantify regional
LV wall motion, we used the centerline
method.8 13 Within the region of interest, the
mean wall motion of the abnormally contracting (-1 SD from
normal) contiguous chords was determined to yield the wall motion index
of that region.8 13 This result was expressed in
SD (from normal) per chord (SD/chord). In addition, we determined the
number of chords within the region of interest showing hypokinesis
(-1 SD).
Study End Points and Measures of Clinical Outcome
The differences in papaverine-induced coronary flow
velocity and in wall motion index between the initial study and 14-day
follow-up were primary end points. In addition, we analyzed
basal flow velocities, coronary flow reserve (ratio of peak
flow velocity and basal flow velocity), number of chords with
hypokinesis, and global LV ejection fraction. Secondary end point was
the clinical outcome during 30-day follow-up.
Statistical Analysis
All data were analyzed on an intention-to-treat basis.
Discrete variables, expressed as counts, were tested by Fisher's
exact test. Results of continuous variables, reported as mean±SD
or as mean (95% CI), were tested by the t test for paired
and unpaired samples, as appropriate. The effect of treatment and of
other covariables on changes in coronary flow velocity or
wall motion index was also assessed by stepwise multiple linear
regression analysis. We used the SPSS 7.5 software package for
all statistical analyses. A value of P<0.05 in the
2-tailed test was regarded as significant.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Study Cohort, Procedural Outcome, and Angiographic Follow-Up
The study enrolled 200 consecutive patients; 98 were assigned to usual care and 102 to abciximab treatment. Except for 2 patients with ST-segment elevation and early intervention, all developed significant creatine kinase elevation. The study groups were homogeneous with respect to baseline demographic, clinical, and angiographic characteristics (Table
1).
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In 4 patients, the intervention was unsuccessful for technical reasons. These were failure to recanalize the infarct-related occlusion and inability to cover a large residual dissection in 1 patient of each group. After stent placement in the usual-care group, large residual thrombi remained in 10 patients and were associated with TIMI grade 2 flow in 4 patients. In all patients with large residual thrombi, we administered abciximab secondarily, which dissolved the clots in 8 patients. Substantial residual thrombi or TIMI grade 2 flow was not encountered in any of the patients with successful stent placement assigned to abciximab. In the 4 patients with unsuccessful procedures and in 13 patients with hemodynamic instability, we did not perform flow velocity measurements and LV angiography.
Twelve patients with successful stent placement did not undergo repeat angiography at 14 days. This was because of death in 6 patients (see below), coronary artery bypass graft surgery for left main stenosis after successful recanalization of an occluded right coronary artery in 1 patient assigned to abciximab, severe peripheral vascular disease in 1 patient, and patient refusal after an uneventful clinical course in 4 patients.
We obtained paired coronary flow velocity measurements in
152 patients and paired LV angiographies in 151 patients. The causes
for missing studies are summarized in Table 2. Between the 2 groups, there were no
significant differences in the rate of paired flow velocity
measurements or LV angiograms (P>0.5), nor was the
distribution of causes for missing studies different between the 2
groups (P>0.6).
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Coronary Flow Velocities in the Infarct-Related
Artery
At the initial study, both treatment groups had similar
basal and peak flow velocities in the recanalized coronary
artery (Table 3). Within 14 days, peak
flow velocities increased significantly in both treatment groups and
basal flow velocity increased significantly in the abciximab group
(Figure 1). The increase in peak flow
velocity in patients assigned to abciximab was significantly larger
than that in patients assigned to usual care (Figure 1). Thus, at
follow-up, peak flow velocities in the abciximab group were
significantly higher than those in the usual-care group, and basal flow
velocities were higher by trend (Table 3). In both treatment groups, we
found significant increases in coronary flow reserve in the
infarct-related artery (Table 3). These were not affected by the
treatment regimen, however, and there were no significant differences
in coronary flow reserve between the abciximab group and the
usual-care group either at the initial study or at follow-up.
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With regard to potential determinants of coronary flow
velocity, the 2 treatment groups were homogeneous with
respect to vessel size, minimal luminal diameter, and residual
stenosis of the treated segment both in the initial study and
at follow-up (Table 3
). The same held true for arterial
blood pressure and pulse rate during the flow velocity measurements as
well as LV end-diastolic pressures (Table 3). Multiple
linear regression analysis revealed assignment to treatment
with abciximab as the single independent predictor (P=0.026)
for the increase in peak flow velocity. Apart from the assigned
treatment, the model included baseline demographic, clinical, and
angiographic characteristics (Table 1) as well as
hemodynamic and quantitative angiographic data (Table 3).
Regional and Global LV Function
Improvement of regional LV function within the first 2
weeks, assessed by wall motion index or number of chords with
hypokinesis, was significantly greater in patients assigned to
abciximab than in those assigned to usual care (Figure 2). By multiple linear regression
analysis with the same independent variables as in the
model for peak flow velocity (see above), the assigned treatment was a
significant (P=0.017) independent predictor for the increase
in wall motion index. The only other independent predictor was TIMI
flow grade before the intervention (P=0.007).
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Immediately after recanalization of the
infarct-related artery, global and regional LV function of the infarct
zone were similar in both treatment groups (Table 4). At follow-up, the infarct-related
wall motion abnormalities were significantly less in the abciximab
group than in the usual-care group (Table 4). Concordant changes were
found in global LV ejection fraction (Table 4).
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We found a significant correlation between changes in peak flow velocity and changes in wall motion index (r=0.20, P=0.022). A similar trend was observed for the relation of changes in peak flow velocity to changes in LV ejection fraction (r=0.15, P=0.09).
Clinical Outcome
Although angiography at 14 days did not detect any
stent vessel occlusions, target lesion reintervention with
additional stent placement had to be performed in 4 patients of
the control group. During 30-day follow-up, 2 patients of the abciximab
group and 9 patients of the control group had adverse cardiac events
(OR [95% CI]: OR, 0.20 [0.04 to 0.94], P=0.031),
including death (2 versus 4; OR, 0.47 [0.08 to 2.93],
P=0.44), nonlethal reinfarction (0 versus 1; OR, 0 [0 to
18.3], P=0.49), and target lesion reintervention (0 versus
4; OR, 0 [0 to 1.05], P=0.056). Three patients assigned to
abciximab and 6 patients assigned to usual-care treatment needed blood
transfusions for bleeding at the access site (OR, 0.47 [0.11 to
1.91], P=0.32). Otherwise, there were no major bleeding
complications.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Various studies have shown that abciximab effectively prevents abrupt reocclusion after percutaneous coronary revascularization procedures, particularly when performed in high-risk settings such as AMI or unstable angina.10 Our present prospective randomized study presents evidence that in AMI, abciximab has important effects beyond the maintenance of large-vessel patency after stent placement. As our major finding, we showed that peri-interventional administration of abciximab improves the recovery of coronary vascular function and of regional wall motion compared with conventional heparin treatment.
Recovery of Coronary Flow to the Area at Risk
In patients assigned to abciximab, the increase in peak flow
velocity at the site of recanalization during the
first 2 weeks after the intervention was almost twice that in patients
assigned to usual care. This differential effect of the 2 treatment
regimens could not be attributed to differences in patency of the
infarct-related vessel. The 2 groups were homogeneous with
respect to vessel diameter and residual stenosis of the treated
lesion. Similarly, there were no inequalities in
hemodynamic conditions. These findings strongly suggest
a microvascular mechanism for the larger increase in peak flow velocity
after administration of abciximab compared with usual care. We did not
directly measure myocardial blood flow in the infarct region. However,
the stent ensured exact positioning and constant vessel diameters at
the sample volume of the Doppler wire in both flow velocity
studies. The changes in peak flow velocity thus may be taken as a
reliable indicator of changes in maximal myocardial blood flow in the
infarct region.
In the abciximab group, we also found a significant increase in basal flow velocity at the site of revascularization that was not observed in the usual-care group. Accordingly, coronary flow reserves at follow-up were not significantly different between the 2 treatment groups. Previous studies have shown that an increase in the number of functional vascular segments contributes substantially to the recovery of myocardial blood flow during reperfusion in AMI.8 14 The differential effect of our 2 treatment regimens may thus be explained by an increased number of functional vascular segments after abciximab treatment compared with usual care, rather than by an increase in flow reserve of the individual segments.
The beneficial effect of abciximab on recovery of vascular function in the infarct area can be explained by blockade of the glycoprotein IIb/IIIa receptor, which prevents embolization of platelet aggregates as well as platelet adhesion to the injured endothelium.11 15 In addition, blockade of the vitronectin receptor, another ß3-integrin, and of ß2-integrins, such as Mac-1 on leukocytes, may contribute by inhibition of the interaction of leukocytes with the reperfused microvasculature.16 Such interaction induces procoagulant and cytotoxic inflammatory responses.17 18
Recovery of Contraction in the Area at Risk
Previous clinical studies revealed a close relation between
recovery of perfusion and recovery of contraction in the infarct
region.8 9 14 Supporting a functional impact of
our findings on coronary flow velocity, we obtained a
significant correlation between the recovery of peak flow velocity and
the improvement of wall motion index. Most importantly, both the wall
motion index and the number of chords with hypokinesis indicated
improved recovery of LV function in the infarct area in patients
assigned to abciximab compared with usual care. Notably, these changes
translate into a higher global LV ejection fraction at follow-up in the
abciximab group. These findings underscore the important impact that
peri-interventional treatment with abciximab has on the recovery of
wall motion in the infarct region.
Clinical Relevance
We investigated the effect of abciximab in a cohort that
comprised the entire spectrum of patients with AMI referred to a
tertiary-care hospital within 48 hours after onset of pain. Thus, apart
from patients with Q-wave AMI within the first 12 hours, our study
included patients with non–Q-wave AMI, those with persistent angina
for >12 hours, and those with failed thrombolysis.
Multiple regression analysis demonstrated that the beneficial
effect of abciximab was independent of these clinical covariables.
Abciximab thus improved the recovery of coronary flow and
regional LV function in a very broad spectrum of patients with AMI.
Although our study was not sufficiently powered to address the differential effect of the treatment regimens on clinical outcome, adverse cardiac events were significantly fewer in the abciximab group than in the usual-care group. This beneficial effect of abciximab is consistent with the results of the recently published EPISTENT study.19 In addition, our studies of contractile function strongly support the administration of abciximab in patients undergoing stent placement in AMI.
Methodological Considerations and Limitations of the Study
In accordance with our preceding study on recovery of
coronary flow in AMI, we used papaverine to assess
coronary vasodilator capacity.8
Papaverine has been extensively validated in the analysis of
coronary flow dynamics.20 21
Adenosine exerts a comparable vasodilator
effect,22 but it is preferred by some
investigators because of a lower risk of torsade de pointes
tachycardia. Nevertheless, we did not experience any
adverse event due to side effects of papaverine.
The fact that physicians were not blinded to the assignment of treatment represents a limitation of our study. Consequently, bias on the part of the investigators cannot be fully excluded as a factor influencing clinical treatment. However, flow velocities were ascertained by automated computerized evaluation, and the angiographic evaluations were performed by blinded operators. Bias in the assessment of the primary end points can thus be excluded. In 10 patients of the usual-care group, operators administered abciximab to deter a detrimental outcome of the intervention. These crossovers do not confound the principal trial results, because the functional and clinical outcome of the usual-care group most probably would have been even less favorable without them. In some patients, we could not obtain paired LV angiograms or flow wire measurements. This problem was similar in previous studies and affected both study groups to the same extent.13 Moreover, the distribution of the causes for missing studies was similar in both groups. Therefore, we cannot assume a relevant distortion of the trial results by missing studies.
Implications
Our study shows that in patients undergoing coronary
stent placement in AMI, peri-interventional administration of abciximab
has important beneficial effects beyond the maintenance of
large-vessel patency. Abciximab improves the recovery of
coronary perfusion at the level of the distal vascular bed and
concomitantly enhances the restoration of LV function in the infarct
area. Our findings support the concept that not only large-vessel
patency but also improvement of microvascular perfusion is an
achievable and rewarding goal in the treatment of patients with AMI.
Glycoprotein IIb/IIIa receptor blockade offers a novel
strategy toward this goal.
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Acknowledgments |
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This study was supported in part by a grant from Lilly, Deutschland. The authors appreciate the invaluable assistance of Leila Fakhoury, Rainer Huppmann, Sergej Kammerzell, and Michael Schlief.
Received May 29, 1998; revision received August 28, 1998; accepted September 9, 1998.
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M. Marzilli, G. Sambuceti, R. Testa, and S. Fedele Platelet glycoprotein IIb/IIIa receptor blockade and coronary resistance in unstable angina J. Am. Coll. Cardiol., December 18, 2002; 40(12): 2102 - 2109. [Abstract] [Full Text] [PDF]
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M Dalby and G Montalescot Transfer for primary angioplasty: who and how? Heart, December 1, 2002; 88(6): 570 - 572. [Abstract] [Full Text] [PDF]
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F.-J. Neumann and N. Jander How to best counteract the enemies? By ensuring adequate oxygen delivery Eur. Heart J. Suppl., November 1, 2002; 4(suppl_G): G35 - G42. [Abstract] [PDF]
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M. J. Kern Patterns of Left Ventricular Dilatation With an Opened Artery After Acute Myocardial Infarction: Missing Links to Long-Term Prognosis Circulation, October 29, 2002; 106(18): 2294 - 2295. [Full Text] [PDF]
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H. C. Herrmann, G. W. Stone, C. L. Grines, and J. E. Tcheng Comparison of Angioplasty with Stenting in Acute Myocardial Infarction N. Engl. J. Med., August 1, 2002; 347(5): 367 - 368. [Full Text] [PDF]
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T. Palmerini, M. A. Nedelman, L. E. Scudder, M. T. Nakada, R. E. Jordan, S. Smyth, R. E. Gordon, J. T. Fallon, and B. S. Coller Effects of abciximab on the acute pathology of blood vessels after arterial stenting in nonhuman primates J. Am. Coll. Cardiol., July 17, 2002; 40(2): 360 - 366. [Abstract] [Full Text] [PDF]
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J.P.S. Henriques, F. Zijlstra, J.P. Ottervanger, M.-J. de Boer, A.W.J. van 't Hof, J.C.A. Hoorntje, and H. Suryapranata Incidence and clinical significance of distal embolization during primary angioplasty for acute myocardial infarction Eur. Heart J., July 2, 2002; 23(14): 1112 - 1117. [Abstract] [Full Text] [PDF]
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E. D. Aymong, M. J. Curtis, M. Youssef, M. M. Graham, L. Shewchuk, W. Leschuk, and T. J. Anderson Abciximab Attenuates Coronary Microvascular Endothelial Dysfunction After Coronary Stenting Circulation, June 25, 2002; 105(25): 2981 - 2985. [Abstract] [Full Text] [PDF]
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S Constantinides, T S N Lo, M Been, and M F Shiu Early experience with a helical coronary thrombectomy device in patients with acute coronary thrombosis. Heart, May 1, 2002; 87(5): 455 - 460. [Abstract] [Full Text] [PDF]
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J. A. Ambrose and E. E. Martinez A New Paradigm for Plaque Stabilization Circulation, April 23, 2002; 105(16): 2000 - 2004. [Abstract] [Full Text] [PDF]
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P Andrassy, M Zielinska, R Busch, A Schomig, and C Firschke Myocardial blood volume and the amount of viable myocardium early after mechanical reperfusion of acute myocardial infarction: prospective study using venous contrast echocardiography Heart, April 1, 2002; 87(4): 350 - 355. [Abstract] [Full Text] [PDF]
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G. W. Stone, C. L. Grines, D. A. Cox, E. Garcia, J. E. Tcheng, J. J. Griffin, G. Guagliumi, T. Stuckey, M. Turco, J. D. Carroll, et al. Comparison of Angioplasty with Stenting, with or without Abciximab, in Acute Myocardial Infarction N. Engl. J. Med., March 28, 2002; 346(13): 957 - 966. [Abstract] [Full Text] [PDF]
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B R Brodie and T D Stuckey Mechanical reperfusion therapy for acute myocardial infarction: Stent PAMI, ADMIRAL, CADILLAC and beyond Heart, March 1, 2002; 87(3): 191 - 192. [Full Text] [PDF]
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G. W. Stone, M. A. Peterson, A. J. Lansky, G. Dangas, R. Mehran, and M. B. Leon Impact of normalized myocardial perfusion after successful angioplasty in acute myocardial infarction J. Am. Coll. Cardiol., February 20, 2002; 39(4): 591 - 597. [Abstract] [Full Text] [PDF]
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S. H. Rezkalla and R. A. Kloner No-Reflow Phenomenon Circulation, February 5, 2002; 105(5): 656 - 662. [Full Text] [PDF]
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J. Mehilli, A. Kastrati, J. Dirschinger, J. Pache, M. Seyfarth, R. Blasini, D. Hall, F.-J. Neumann, and A. Schomig Sex-Based Analysis of Outcome in Patients With Acute Myocardial Infarction Treated Predominantly With Percutaneous Coronary Intervention JAMA, January 9, 2002; 287(2): 210 - 215. [Abstract] [Full Text] [PDF]
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C. Loubeyre, M.-C. Morice, T. Lefevre, J.-F. Piechaud, Y. Louvard, and P. Dumas A randomized comparison of direct stenting with conventional stent implantation in selected patients with acute myocardial infarction J. Am. Coll. Cardiol., January 2, 2002; 39(1): 15 - 21. [Abstract] [Full Text] [PDF]
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