Routine Thrombectomy in Percutaneous Coronary Intervention for Acute ST-Segment–Elevation Myocardial Infarction
A Randomized, Controlled Trial
Background— Distal embolization during primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction may result in reduced myocardial perfusion, infarct extension, and impaired prognosis.
Methods and Results— In a prospective randomized trial, we studied the effect of routine thrombectomy in 215 patients with ST-segment–elevation myocardial infarction lasting <12 hours undergoing primary PCI. Patients were randomized to thrombectomy pretreatment or standard PCI. The primary end point was myocardial salvage measured by sestamibi SPECT, calculated as the difference between area at risk and final infarct size determined after 30 days (percent). Secondary end points included final infarct size, ST-segment resolution, and troponin T release. Baseline variables, including ST-segment elevation and area at risk, were similar. Salvage was not statistically different in the thrombectomy and control groups (median, 13% [interquartile range, 9% to 21%] and 18% [interquartile range, 7% to 25%]; P=0.12), but 24 patients in the thrombectomy group and 12 patients in the control group did not have an early SPECT scan, mainly because of poor general or cardiac condition (P=0.04). In the thrombectomy group, final infarct size was increased (median, 15%; [interquartile range, 4% to 25%] versus 8% [interquartile range, 2% to 18%]; P=0.004).
Conclusions— Thrombectomy performed as routine therapy in primary PCI for ST-elevation myocardial infarction does not increase myocardial salvage. The study suggests a possible deleterious effect of thrombectomy, resulting in an increased final infarct size, and does not support the use of thrombectomy in unselected primary PCI patients.
Received October 15, 2005; revision received May 1, 2006; accepted May 4, 2006.
Despite restoration of epicardial blood flow with primary percutaneous coronary intervention (PCI), a significant proportion of patients with acute ST-segment–elevation myocardial infarction (STEMI) have impaired microvasculature and myocardial tissue perfusion, contributing to increased infarct size and reduced survival.1–5 The mechanisms responsible for impaired tissue perfusion may be numerous, and microvascular plugging caused by embolization of thrombotic or atheromatous debris occurring either spontaneously or after PCI may be a major factor.6,7 Different thrombectomy and distal protection devices have been developed that are both feasible and safe.8–10 However, the usefulness of thrombectomy as an adjunct therapy during primary PCI needs to be proved in randomized trials. Therefore, we conducted a prospective randomized trial to evaluate the effect of routine thrombectomy pretreatment with the Rescue catheter as an adjunct to primary PCI with stenting in STEMI.
Clinical Perspective p 47
The study was a prospective randomized trial in patients with STEMI. Inclusion criteria included symptoms lasting >30 minutes but <12 hours and cumulative ST-segment elevation of ≥2 mV in ≥2 contiguous leads. Exclusion criteria were left bundle-branch block, acute myocardial infarction within the previous 30 days, fibrinolytic treatment, previous coronary bypass surgery, left main stem stenosis, need for mechanical ventilation, and severe heart failure treated with intra-aortic balloon pump. The study was approved by the local ethics committee and was carried out in accordance with the Helsinki II declaration. All eligible patients provided written informed consent.
A coronary angiogram was performed to evaluate appropriateness for randomization. Patients were eligible if PCI was indicated and the treating physician found the infarct-related artery suitable for thrombectomy. Randomization was performed by a telephone line–accessible computer based on block randomization using varying block sizes (6/4/2) stratified by sex and diabetes. The system complies with international criteria for proper concealment of randomization.11
Before intervention, patients were pretreated with aspirin 300 mg orally or intravenously, clopidogrel 300 mg orally, and unfractionated heparin 10 000 IE intravenously. During the intervention, all patients were treated with abciximab.
The Rescue catheter (Boston Scientific/Scimed, Inc, Maple Grove, Minn) is a thrombectomy system made up of a 4.5F polyethylene catheter to be advanced over a guidewire through a 7F guiding catheter. The proximal end of the catheter has an extension tube connected to a vacuum pump (0.8 bar) with a collection bottle. While the catheter is slowly advanced and pulled back through the thrombus, continuous suction is applied. Several runs can be performed, and in case of distal embolization, the catheter can be advanced distally over the guidewire to remove the embolized material. The Rescue catheter has previously been proved safe and effective in removing thrombus material.10
In the present study, thrombectomy was performed stepwise: (1) The catheter was advanced to the culprit lesion, and suction was performed proximal and distal to the lesion until no thrombus was visible; (2) in patients with resistance against advancement of the catheter distal to the lesion, predilatation with a 2.0- to 2.5-mm balloon was performed, followed by thrombectomy as described above; and (3) if the lesion could not be reached even after balloon predilatation, the technical end point of “device success” was negative.
Postintervention medications consisted of infusion of abciximab for 12 hours and aspirin 75 mg/d and clopidogrel 75 mg/d for 12 months. Troponin T (TnT) levels were measured immediately after PCI and at 12, 24, and 96 hours after symptom onset. Clinical follow-up was performed at 30 days.
Study End Points
The primary end point was myocardial salvage estimated by 99mTc-sestamibi SPECT. Secondary end points were final infarct size (FIS) and markers of effective reperfusion: TIMI flow, corrected TIMI frame count (CTFC), ST-segment resolution (STR) measured immediately and 90 minutes and 6 hours after PCI, and the release of TnT. Distal embolization visible at the end of the procedure, total procedure time, major adverse clinical events at 30 days (death, reinfarction, and disabling stroke), left ventricular ejection fraction after 30 days, and technical success of the thrombectomy (device success), as described above, also were secondary end points.
Before initiation of the assigned invasive therapy, patients received an intravenous injection of 700±10% MBq 99mTc-sestamibi to assess the area at risk (AAR). Gated SPECT was performed within 8 hours after injection of the radionuclide and performed using a dual-headed rotating gamma camera (ADAC) with a high-resolution, parallel-hole collimator. To ensure equal count statistics, the acquisition time varied between 25 and 60 seconds per projection, depending on the time elapsed since injection of the tracer. Images were gated at 8 frames per cardiac cycle. No scatter or attenuation correction was used. A follow-up myocardial scintigraphy was scheduled 30 days after PCI to assess the FIS using the same protocol as in the initial study. Two experienced readers of nuclear cardiology studies who were blinded to the assigned treatment analyzed data independently. Images were analyzed with the commercially available automatic quantitative programs QPS and QGS, (Cedars-Sinai Medical Center),12 which has been extensively described and validated.13–16 In each study, we calculated the initial perfusion defect (AAR) and the FIS. The difference between these 2 measurements provided the degree of myocardial salvage. AAR, FIS, and myocardial salvage were expressed as a percentage of the left ventricular volume. Salvage index was calculated as the ratio between myocardial salvage and the AAR. In the final infarct scan, we also determined the left ventricular ejection fraction.
Four experienced observers who were blinded to randomization performed all measurements. Angiographic TIMI flow grade was visually estimated, and the CTFC was measured as previously described.17,18 In case of a totally occluded vessel, CTFC was set to 100.19
ECG recordings were analyzed at the DANAMI 2 Electrocardiographic Core Laboratory (Rigshospitalet, Copenhagen, Denmark).20 A snapshot 12-lead ECG was recorded immediately before PCI, immediately after PCI, and at 90 minutes and 6 hours after PCI. ST-segment elevation was calculated 20 ms after the J point. The sum of ST-segment elevation (ΣST) was calculated in leads I, aVL, and V1 through V6 for anterior and leads II, III, aVF, V5, and V6 for nonanterior myocardial infarctions.2 With the ECG recorded before PCI as baseline, STR was calculated immediately and 90 minutes and 6 hours after PCI, given as the magnitude of the resolution (percent),5 and categorized using the Schroeder classification as complete (70% to 100%), partial (30% to 70%), or absent (<30%).21,22
Power Calculation and Statistical Analysis
Previous studies of primary PCI with stenting have demonstrated an AAR within the magnitude of 30% of the left ventricle and a salvage index of 0.50.23,24 We chose a target FIS of ≤12% because an infarct size of this magnitude is associated with very low mortality.25,26 A 20% reduction in FIS from 15% to 12% corresponds to an increase in salvage index from 0.5 [(30−15)/30] to 0.6 [(30−12)/30]. Assuming an SD of the salvage index of 0.2323,24 and that data conformed with a parametric distribution, we calculated that demonstration of a reduction in salvage index of 0.1 would require a sample size of 85 patients in each group with a power of 80% and a 2-sided α value of 0.05. From this, we aimed to include 200 patients in the study. The analysis was done according to the intention-to-treat principle. Because data were skewed and did not conform to a normal distribution, they are presented as median counts (interquartile range [IQR]) or proportions (percentages). Continuous data were compared by use of the Mann-Whitney U test. Categorical data were compared with χ2 test or Fisher exact test when expected cell values were <5. The release of TnT was compared by use of 1-way ANOVA. All comparisons are 2 sided, and all statistical analyses were performed with SPSS 13.0.
The authors had full access to the data and take full responsibility for their integrity. All authors have read and agree to the manuscript as written.
Between January 15, 2004, and February 24, 2005, we randomized 215 patients presenting to the Department of Cardiology at Aarhus University Hospital (Skejby, Denmark) with STEMI to either PCI with thrombectomy pretreatment (n=108) or PCI alone (n=107). Patient flow is shown in the Figure.
Baseline clinical and angiographic characteristics were well matched between groups (Table 1).
Procedural Results and Angiographic Outcome
Thrombectomy resulted in an additional median 10-minute increase in total procedure time (P<0.0001) and was successfully performed in 89% (96 of 108) (Table 2). Procedural failure occurred in 12 patients (11%) and was due to inability to reach the lesion with the Rescue catheter despite predilatation. There was no difference in final TIMI flow or CTFC between groups, and angiographically documented distal embolization after the procedure also was similar in the 2 groups.
Primary End Point: Scintigraphic Evaluation
All patients had tracer injected before PCI. Paired initial and follow-up SPECT examinations could be obtained in 79 patients (73%) assigned to thrombectomy and in 89 patients (83%) in the control group (P=0.08). Incomplete scintigraphic studies were due to lack of either the early or the late scan. As shown in Table 3, more patients in the thrombectomy group were not able to be transported to acute SPECT scan (24 [22%] versus 12 [11%]; P=0.04), primarily because of cardiac or clinical instability. FIS was available in 96 (89%) and 93 (87%) patients (P=0.67). The primary end point, salvage, was not significantly different between groups regardless of the presence of visible thrombus and infarct localization (Tables 4 and 5⇓). There was a trend toward less salvage in the thrombectomy group (13% [IQR, 9% to 21%] versus 18% [IQR, 7% to 25%]; P=0.12). FIS was significantly larger in the thrombectomy group (15% [IQR, 4% to 25%] versus 7.5% [IQR, 2% to 18%]; P=0.004; Table 3), which was explained mainly by a difference in FIS in anterior infarcts (Table 5). Among the 12 patients with device failure, scintigraphic data were available in 7 and FIS in 10 patients. Scintigraphic data of these patients were as follows: AAR, 30%; FIS, 12.5%; salvage, 19%; and salvage index, 69. Lack of the initial scan was due to intra-aortic balloon pump, cardiac instability, and withdrawal of consent. Lack of the final scan was due to withdrawal of consent. Predilatation before thrombectomy was performed in 21 of 108 patients (19%). These patients did not differ from the remaining patients with respect to FIS (12% versus 15%; P=0.77) and salvage (14% versus 13%; P=0.22).
There was no significant difference between groups in STR at any of the postprocedural time points (Table 6).
The release of TnT was significantly higher in the thrombectomy group (P<0.01) (Table 7).
There was no difference in the occurrence of major adverse clinical events between groups. Left ventricular ejection fraction at 30 days was similar (Table 7).
In the present study, STEMI patients were randomized to thrombectomy pretreatment regardless of visible thrombus. There was no crossover between treatment groups, and thrombectomy was successfully performed in 89% of patients randomized to this treatment. Thrombectomy was not associated with better outcome evaluated by myocardial salvage and indirect measures of reperfusion. On the contrary, we found a significantly increased FIS in the thrombectomy group.
In the largest study published so far, the Enhanced Myocardial Efficacy and Recovery by Aspiration of Liberated Debris (EMERALD) trial,27 501 patients were randomized to PCI with or without distal protection with the Guard Wire system (Medtronic). The coprimary end points were infarct size measured by SPECT and complete ST resolution, and no differences in either primary or secondary end points were detected. On the contrary, in high-risk subgroups, defined as patients presenting with totally occluded vessels or large thrombus burden, infarct size was increased in the distal protection group. The Angiojet Rheolytic Thrombectomy in Patients Undergoing Primary Angioplasty for Acute Myocardial Infarction (AIMI) trial has not been published, but similar results with larger infarcts in the thrombectomy group have been reported.28 Recently, the results of the Protection Devices in PCI Treatment of Myocardial Infarction for Salvage of Endangered Myocardium (PROMISE) study testing the Filter Wire-EX (Boston Scientific) in a randomized study of 200 patients revealed no benefit of distal protection when evaluated by coronary flow velocity and infarct size estimated by MRI.29 The Randomized Evaluation of the Effect of Mechanical Reduction of Distal Embolization by Thrombus-Aspiration in Primary and Rescue Angioplasty (REMEDIA) trial30 and other studies using indirect measures of reperfusion such as TIMI flow, CTFC, blush, and STR31–33 indicate that reperfusion is improved after thrombectomy or distal protection, but whether these results transform into smaller infarcts or better outcome has not been reported.
In contrast to the indirect measures of reperfusion (TIMI flow, CTFC, blush, and STR), myocardial perfusion estimated by sestamibi SPECT is an objective, quantitative measure of perfusion and a well-validated measure of infarct size.34 Even with this sensitive marker, we were unable to demonstrate a beneficial effect of routine thrombectomy in primary PCI.
Our primary end point was prespecified as myocardial salvage, and the study was powered to test the hypothesis that thrombectomy yields a 20% increase in salvage. This hypothesis cannot be confirmed by our data. On the contrary, there is a tendency toward lower salvage in the thrombectomy group. Paired scintigraphic data were not obtained in 22% of the patients, primarily because of no early scan. This scarcity affects the power of the salvage analysis, but we consider our results valid because primary and secondary end points are consistent. FIS was significantly higher in the thrombectomy group, suggesting that the reported value for salvage in this group may be an overestimation as a result of a statistical imbalance in the number of patients who underwent acute scintigraphic scanning in the study groups. We also believe that the difference between clinical event rates in the study groups may support our conclusion because the lack of an early scan was due to clinical events and was more frequent in the thrombectomy than in the control group. Importantly, all patients were scheduled for transport to the nuclear facilities within 8 hours from tracer injection, and the decision not to perform the initial scan was made by the cardiac care unit attending physician, who was unaware of the treatment modality.
Clinical instability was not a predefined end point and encompassed a variety of conditions such as episodes of ventricular tachycardia, prolonged hypotension, prolonged chest pain, and severe general discomfort. The finding that more patients in the thrombectomy group were clinically unstable was unexpected. Baseline ST-segment elevation, distribution of the infarct related vessel, and baseline TIMI flow were similar before intervention. Consequently, we would not expect that differences in the preintervention status could explain the difference. We observed a 10-minute increase in procedural time in the thrombectomy group, thus resulting in a nonsignificant increase in symptom duration. However, with a median reperfusion time of 4 hours, we would not expect this to influence clinical outcome.35,36 The reason why more patients in the thrombectomy group were unstable in the first hours after the PCI procedure remains unclear, but the possibility that factors related to the thrombectomy procedure itself may be harmful has to be considered.
We observed a substantial difference in the FIS (7.5% versus 15%; P=0.004), which may have prognostic implications.25,26 It is noteworthy that none of the surrogate end points such as STR or CTFC showed any difference despite the difference in FIS, suggesting that these commonly used end points may be insensitive for detecting a difference. Our sample size does not allow extensive subgroup analysis, but when we look at the subgroup of anterior infarcts, we find the difference between treatment groups even more pronounced, with infarct sizes in the thrombectomy group >20% of the left ventricle.
Our results suggest that routine thrombectomy, as performed in this study, may have a deleterious rather than a beneficial effect. Although thrombectomy was intuitively expected to be beneficial, the EMERALD trial found similar evidence of an opposite effect with higher infarct sizes in several high-risk groups.27 Obvious explanations for these results are lacking, but a possible harmful effect of the devices on the infarct-related arteries is a possibility. There might be a risk that the devices cause physical damage to the vessel endothelium, thereby creating areas that, if not covered by a stent, potentially can promote further creation of new thrombi and distal embolization. The increase in FIS in anterior but not in nonanterior infarct-related vessels after thrombus aspiration may indicate that more extensive vascular damage may affect the smaller left anterior descending artery more than the right coronary artery after additional instrumentation of the vessel with the thrombectomy catheter. In addition, introduction of the devices and/or predilatation might, at least in some patients, shift embolic material into side branches or distally into the main artery.
The 30-day mortality in our study population is lower than usually observed in randomized trials in STEMI. The Killip class characterization indicates that our patients have a favorable risk profile, although the exclusion criteria were conservative. The outcome might reflect the fact that informed consent from the patient was required before randomization, which excluded seriously ill patients. We cannot exclude another outcome in more severe disease states. As discussed earlier, we did not obtain paired scintigraphic data in 22% of the patients. The reduced power of the salvage analysis is a limitation of the study.
We used thrombectomy in all patients presenting with STEMI regardless of visible thrombus. Filtering of the aspirates was done at the discretion of the operator. Ample amounts were infrequent, and the aspirate did not undergo a systematic analysis. If there is a potential harmful effect of the thrombectomy device, it should probably be restricted to those who potentially can benefit from the treatment, ie, patients with visible thrombus. However, analysis of this subgroup did not reveal a beneficial effect of thrombectomy. Because the study was underpowered for subgroup analyses, we cannot exclude the possibility that thrombectomy might be beneficial in a selected subset of patients.
Conclusions and Clinical Implications
Our study demonstrates that thrombectomy performed with the Rescue catheter as routine adjunct therapy in primary PCI for STEMI does not increase myocardial salvage. The study suggests a deleterious effect of thrombectomy, resulting in increased FIS, and does not support the use of thrombectomy as routine adjunct therapy in unselected patients.
We thank Karrina Clausen, RN, for excellent work in all phases of the study and the entire staffs of the catheterization laboratory, coronary care unit, and Department of Nuclear Medicine for enthusiasm during the study.
Source of Funding
Boston Scientific, Denmark, funded part of the study by supplying an unrestricted grant to the Department of Cardiology B, Aarhus University Hospital, Skejby, Section of PCI Research. None of the authors received individual funding from Boston Scientific. The sponsor did not interfere with design, conduction of the trial, analyses of the results, or drafting of the manuscript.
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When treating ST-segment myocardial infarction with primary percutaneous coronary intervention (PCI), it has been increasingly evident that distal embolization of either thrombus or atherosclerotic debris may result in reduced myocardial perfusion, infarct extension, and impaired prognosis. Several technical devices to protect the microvasculature have been developed: devices to remove thrombus by aspiration or thrombectomy before balloon dilatation and devices to protect the distal vessel by placing a filter to catch liberated debris or thrombus material. These devices, including the Rescue thrombectomy catheter, have proved feasible and safe; therefore, we wanted to evaluate whether routine thrombectomy as an adjunct therapy to primary PCI reduced perfusion impairment and infarct size. We conducted a prospective randomized trial of 215 patients and evaluated routine thrombectomy pretreatment with respect to the degree of myocardial salvage compared with the estimated area at risk and to the final infarct size. Myocardial perfusion imaging, sestamibi SPECT, was used to assess perfusion defects, and both area at risk (the amount of myocardium without perfusion before PCI) and final infarct size after 30 days were estimated. The study demonstrated that thrombectomy performed with the Rescue catheter as routine adjunct therapy in primary PCI for STEMI did not increase myocardial salvage. However, final infarct size was significantly larger in the thrombectomy group. The results suggest a deleterious effect of thrombectomy, resulting in increased final infarct size, and does not support the use of thrombectomy as routine adjunct therapy in unselected patients.