Endovascular Thrombectomy for Acute Ischemic Stroke in Failed

Endovascular Thrombectomy for Acute Ischemic Stroke inFailed Intravenous Tissue Plasminogen Activator VersusNon–Intravenous Tissue Plasminogen Activator Patients

Revascularization and Outcomes Stratified by the Site ofArterial Occlusions

Zhong-Song Shi, MD; Yince Loh, MD; Gary Walker, PhD; Gary R. Duckwiler, MD;for the MERCI and Multi MERCI Investigators

Background and Purpose—Intracranial mechanical thrombectomy is a therapeutic option for acute ischemic strokepatients failing intravenous tissue plasminogen activator (IV tPA). We compared patients treated by mechanical embolusremoval in cerebral ischemia (MERCI) thrombectomy after failed IV tPA with those treated with thrombectomy alone.

Methods—We pooled MERCI and Multi MERCI study patients, grouped them either as failed IV tPA or non–IV tPA, andassessed revascularization rates, procedural complications, symptomatic hemorrhage rates, clinical outcomes, andmortality. We also evaluated outcomes stratified by the occlusion site and final revascularization.

Results—Among 305 patients, 48 failed, and 257 were ineligible for IV tPA. Nonresponders to IV tPA trended toward ahigher revascularization rate (73% versus 63%) and less mortality (27.7% versus 40.1%) and had similar rates ofsymptomatic hemorrhage and procedural complications. Favorable 90-day outcomes were similar in failed and non–IVtPA patients (38% versus 31%), with no difference according to occlusion site. Among patients failing IV tPA, goodoutcomes tended to occur more frequently in revascularized patients (47.1% versus 15.4%), although this relationshipwas attributable solely to middle cerebral artery and not internal carotid artery occlusions, with no difference inmortality. Among IV tPA–ineligible patients, revascularization correlated with good outcome (47.4% versus 4.4%) andless mortality (28.5% versus 59.6%).

Conclusions—The risks of hemorrhage and procedure-related complications after mechanical thrombectomy do not differwith respect to previous IV tPA administration. Thrombectomy after IV tPA achieves similar rates of good outcomes,a tendency toward lower mortality, and similar revascularization rates when stratified by clot location. Good outcomescorrelate with successful revascularization except with internal carotid artery occlusions in tPA-nonresponders. (Stroke.2010;41:1185-1192.)

Key Words: acute stroke � endovascular treatment � outcome � thrombectomy � thrombolysis

Revascularization rates in acute ischemic stroke patientswith intravenous tissue plasminogen activator (IV tPA)

treatment may be as low as 6% for internal carotid artery(ICA) terminus, 30% for middle cerebral artery (MCA) trunk,and 30% for basilar occlusions.1,2 Nonresponse to IV tPA isassociated with poor clinical outcomes.3 Although the initialIV tPA trials did not assess revascularization,4–6 failed IVtPA patients have emerged as a subgroup with persistentocclusions, confirmed by noninvasive or catheter angiogra-phy.7–10 The time window defining failed IV tPA has not beenestablished. Because revascularization after IV tPA is typi-

cally confirmed by transcranial Doppler ultrasonographywithin the first hour,11 this may be an appropriate windowwithin which to consider rescue reperfusion therapies for IVtPA nonresponders.

The Mechanical Embolus Removal in Cerebral Ischemia(MERCI) and Multi MERCI trials were prospective, multi-center, endovascular mechanical thrombectomy trials foracute ischemic stroke patients treated within 8 hours ofsymptom onset who were either ineligible for or failed IV tPAtherapy, introducing Merci Retriever thrombectomy as anoption for acute ischemic stroke patients.12–15 The Multi

Received November 18, 2009; final revision received December 16, 2009; accepted December 18, 2009.From the Division of Interventional Neuroradiology (G.R.D.), David Geffen School of Medicine at UCLA, Los Angeles, Calif; Concentric Medical,

Inc. (G.W.), Mountain View, Calif; the Department of Neurosurgery (Z.-.S.S.), The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, P.R.China; and the Neurovascular Service, Department of Medicine (Y.L.), Madigan Army Medical Center, Tacoma, Wash.

A list of the MERCI trial investigators appears in Appendix 1.A list of the Multi MERCI trial investigators appears in Appendix 2.Correspondence to Gary R. Duckwiler, MD, Division of Interventional Neuroradiology, David Geffen School of Medicine at UCLA, 757 Westwood

Plaza, Los Angeles, CA 90095-7437. E-mail [email protected]© 2010 American Heart Association, Inc.

Stroke is available at http://stroke.ahajournals.org DOI: 10.1161/STROKEAHA.109.568451

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MERCI trial also showed that significant hemorrhage fromthe combined use of IV tPA and thrombectomy (failed IVtPA group) was not significantly higher than with thrombec-tomy alone (non–IV tPA group).14,15 However, it is possiblethat the effect of nonresponse to IV tPA varies depending onocclusion location and final revascularization. We pooleddata from these 2 trials and analyzed outcomes and revascu-larization rates in patients with failed IV tPA versus non–IVtPA, stratified by vessel occlusion.

MethodsPooled data from the previously reported MERCI and Multi MERCItrials13,15 were analyzed retrospectively in this study. A family ofMerci Retrievers (Concentric Medical, Inc.) was used to extract clotfrom intracranial vessels. The MERCI trial only enrolled patientswho were ineligible for IV tPA. In Multi MERCI, patients receivingIV tPA (0.6 mg/kg or 0.9 mg/kg) within 3 hours of stroke onset wereincluded if persistent vessel occlusion was confirmed by angiogra-phy. Intra-arterial (IA) tPA was only allowed in cases of thrombec-tomy failure after 6 passes or to treat distal embolus after successfulproximal thrombectomy.

Patients were dichotomized into failed and non–IV tPA groups.Clinical variables, revascularization rates, symptomatic hemorrhagerates, clinical outcomes and mortality at 90 days, and clinicallysignificant procedural complications were compared. Clot locationswere confirmed by catheter angiography and were hierarchicallycategorized based on the most proximal occlusion location: ICA,MCA, or vertebro-basilar.

Successful revascularization was defined as achievingthrombolysis in myocardial infarction II or III flow in all treatablevessels (ICA, M1, M2, vertebral, and basilar) documented on finalpost-thrombectomy angiogram. CT or MRI brain imaging wasperformed at baseline, 24 hours, and at any time there was a declinein patient neurological status. Symptomatic intracranial hemorrhagewas defined as a point increase of �4 in the National Institutes ofHealth Stroke Scale (NIHSS) score within 24 hours with evidence ofany blood on 24-hour head CT/MRI scan or any intracranialhemorrhage in which no additional NIHSS scores were availablefollowed by patient death. Intracerebral hemorrhages were furthercategorized as hemorrhagic infarction type I and II, or parenchymalhematoma types I and II, as described previously.5 Procedure-relatedadverse events were adjudicated by an independent data safetymonitoring board and were defined as vascular perforation, intramu-ral arterial dissection, or embolization of a previously uninvolvedterritory, symptomatic hemorrhage, and access site complicationsrequiring surgery or transfusion. Clinically significant proceduralcomplications were defined as a procedure complication with declinein NIHSS score of �4 points or death, groin complication requiringsurgery, or blood transfusion.

Neurological status was quantified by the NIHSS and modifiedRankin Scale (mRS) at 90 days. Good outcome at 90 days wasdefined as mRS �2. Additional comparisons of revascularization,procedural complications, good outcomes, and mortality were strat-ified by the occlusion site, and outcomes were further stratified byfinal revascularization.

Categorical data were analyzed by the Fisher exact and �2 tests.Continuous data were assessed for normality by the Kolmogorov–Smirnov test; normally distributed continuous data were analyzed byStudent t test, and for unevenly distributed continuous data, theMann–Whitney U test was used. A P value �0.05 was consideredstatistically significant. No adjustment was made for multiplicity.Statistical analyses were performed using SAS software (version 8.2;SAS Institute Inc).

ResultsDemographicsA total of 305 patients were enrolled in the 2 trials: 141patients in MERCI and 164 patients in Multi MERCI.

Forty-eight (15.7%) failed IV tPA, and 257 (84.3%) were noteligible to receive IV tPA before mechanical thrombectomy.In the failed IV tPA group, the mean age was 67.8�12.7years, and 56.3% (27 of 48) were women. Mean baselineNIHSS score was 19.1�5.5. The mean IV tPA dose was57�16 mg. In the non–IV tPA group, the mean age was67.6�16.3 years, and 51.4% (132 of 257) were women. Meanbaseline NIHSS score was 19.8�6.7. Baseline characteristics(Table 1) for these 2 populations were similar with theexception of a higher distribution of comorbid dyslipidemiain those failing IV tPA (46.8% versus 31.6%; P�0.05).

Patients with failed IV tPA tended to have a shorter time tointervention and shorter procedure duration (4.0 versus 4.4hours). Table 1 shows the distribution of occlusion locations,categorized hierarchically by the most proximal occlusion.The distribution of occlusion location was not differentbetween groups, with the MCA being the most common, thenthe ICA, and then the vertebro-basilar system.

Revascularization RatesThe final revascularization rates were similar between groups(72.9% versus 63.0%), with comparable intergroup IA tPAuse. In tPA-nonresponders, revascularization was achieved in66.7% (12 of 18) of ICA, 74.1% (20 of 27) of MCA, and100% (3 of 3) of vertebro-basilar occlusions (Table 2). In thenon–IV tPA patients, revascularization was achieved in61.7% (50 of 81), 61.6% (93 of 151), and 76.0% (19 of 25),respectively (Table 3). There was no intergroup difference.

Symptomatic Hemorrhage and ComplicationsSymptomatic hemorrhage was similar between groups(10.4% versus 8.6%). The 2.1% rate of symptomatic paren-chymal hematoma II in patients with failed IV tPA wassimilar to the 1.9% rate in the non–IV tPA patients. Symp-tomatic hemorrhage rates by occlusion site were as followsfor the failed and non–IV tPA groups, respectively: ICA,11.1% for both; MCA, 11.1% versus 5.3%; and vertebro-basilar, 0% versus 20.0% (Tables 2 and 3). Symptomatichemorrhage in ICA occlusions was similar between groups.Although all parenchymal hematoma II hemorrhages oc-curred with MCA occlusions in the failed IV tPA group, therates of all symptomatic hemorrhages for both MCA andvertebro-basilar occlusions were similar to the non–IV tPAgroup.

Hemorrhage by Revascularization StatusIn tPA-nonresponders, symptomatic hemorrhage occurredequally by revascularization status (8.6% [3 of 35] versus15.4% [2 of 13]). In the non–IV tPA group, revascularizedpatients had less symptomatic hemorrhage (4.3% [7 of 162]versus 15.8% [15 of 95]; P�0.002).

Procedural Adverse EventsBoth groups had a similar rate of clinically significantprocedural complications (4.2% versus 6.6%). In the failedIV tPA group, procedural complications only occurred withMCA occlusions, at a rate of 7.4%. In the non–IV tPA group,clinically significant complication rates by occlusion sitewere: ICA, 8.6%; MCA, 4.6%; and vertebro-basilar, 12.0%.

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Clinical OutcomesThe rates of good clinical outcomes (mRS, 0 to 2) at 90 dayswere similar in the failed and non–IV tPA groups (38.3%versus 31.3%). Good outcomes by occlusion site in the failedand non–IV tPA groups were as follows, respectively (Tables2 and 3): ICA, 29.4% (5 of 17) versus 28.8% (23 of 80);MCA, 40.7% (11 of 27) versus 33.3% (46 of 138); andvertebro-basilar, 66.7% (2 of 3) versus 28.0% (7 of 25). Therate of good outcome at 90 days was similar between groupsfor each occlusion location.

Outcomes by Postprocedure Revascularization StatusIn both groups, good clinical outcomes at 90 days occurredmore frequently in subjects for whom revascularization wassuccessful (Figure 1). In the failed IV tPA group, 47.1% (16

of 34) of revascularized patients had a good neurologicaloutcome compared with 15.4% (2 of 13) of nonrevascularizedpatients (P�0.09), powered by MCA (55% versus 0%) butnot ICA occlusions (27% versus 33%). In the non–IV tPAgroup, 47.4% (72 of 152) of revascularized patients had agood neurological outcome compared with 4.4% (4 of 91) ofnonrevascularized patients (P�0.001). When stratified byocclusion site, a positive relationship existed between revas-cularization and good outcome, with the exception of ICAocclusions failing IV tPA.

Across cohorts, revascularized patients had a similar rate ofgood outcomes in both groups (47.1% versus 47.4%),whereas nonrevascularized patients in the failed IV tPAgroup trended toward better outcome than nonrevascularizedpatients in the non–IV tPA group (15.4% versus 4.4%;

Table 2. Revascularization Rates and Outcomes by Site of Vascular Occlusion in Failed IV tPA Patients

Overall (n�48) ICA (n�18) MCA (n�27) Posterior (n�3) P

Final revascularization, n (%) 35 (72.9%) 12 (66.7%) 20 (74.1%) 3 (100%) 0.32

Intracranial hemorrhage

Symptomatic, n (%) 5 (10.4%) 2 (11.1%) 3 (11.1%) 0 (0.0%) 0.71

Asymptomatic, n (%) 17 (35.4%) 6 (33.3%) 10 (37.0%) 1 (33.3%) 0.97

Good outcome at 90 days, n (%) 18 of 47 (38.3%) 5 of 17 (29.4%) 11 (40.7%) 2 (66.7%) 0.44

Mortality at 90 days, n (%) 13 of 47 (27.7%) 6 of 17 (35.3%) 6 (22.2%) 1 (33.3%) 0.63

Procedural complication, n (%) 2 (4.2%) 0 (0.0%) 2 (7.4%) 0 (0.0%) 0.31

P values are from the likelihood ratio chi-square test.

Table 1. Characteristics of Patients With Failed IV tPA Vs Non–IV tPA

Failed IV t-PA (n�48) No IV t-PA (n�257) P Value

Mean age, years�SD 67.8�12.7 67.6�16.3 0.93*

Female, % 27 (56.3%) 132 (51.4%) 0.64†

Hypertension 38 of 48 (79.2%) 181 of 256 (70.7%) 0.29†

Diabetes mellitus 9 of 47 (19.1%) 52 of 255 (20.4%) 0.85‡

Dyslipidemia 22 of 47 (46.8%) 73 of 231 (31.6%) �0.05‡

Coronary artery disease 20 of 46 (43.5%) 102 of 250 (40.8%) 0.75†

Congestive heart failure 7 of 45 (15.6%) 49 of 254 (19.3%) 0.55‡

Smoking 11 of 47 (23.4%) 54 of 237 (22.8%) 0.93‡

Atrial fibrillation 22 of 48 (45.8%) 106 of 254 (41.7%) 0.64†

Baseline NIHSS score 19.1�5.5 19.8�6.7 (256) 0.51*

Symptom onset to IA access (hours) 3.95�1.16 4.43�1.84 (255) 0.08*

Site of vascular occlusion, % 0.06‡

ICA 1 (2.1%) 27 (10.5%)

ICA-T 17 (35.4%) 54 (21.0%)

MCA M1 21 (43.8%) 129 (50.2%)

MCA M2 6 (12.5%) 22 (8.6%)

Vertebro-basilar 3 (6.3%) 25 (9.7%)

Time to treatment (hours) 3.95�1.16 4.43�1.84 0.08*

Mean procedure duration (hours) 1.68�0.78 1.93�0.91 (250) 0.08*

Attempts to remove clot, mean�SD 2.79�1.71 2.94�1.55 0.57*

IA lytic use, % 17 (35.4%) 80 (31.1%) 0.56‡

Final TIMI II/III flow 35 (72.9%) 162 (63.0%) 0.25†

*P value is from the 2-sample t test; †P value is from the Fisher exact test; ‡P value is from the likelihood ratiochi-square t test.

TIMI indicates thrombolysis in myocardial infarction.

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P�0.16). Figure 2 shows 90-day good outcomes stratified byrevascularization status, IV tPA status, and occlusionlocation.

MortalityThere was a trend toward less mortality at 90 days in thefailed IV tPA group (27.7% [13 of 47] versus 40.1% [101 of252]; P�0.08). Mortality rates in patients failing and notreceiving IV tPA, by occlusion site, were as follows, respec-tively (Tables 2 and 3): ICA, 35.3% (6 of 17) versus 50.6%(41 of 81); MCA, 22.2% (6 of 27) versus 33.6% (49 of 146);and vertebro-basilar, 33.3% (1 of 3) versus 44.0% (11 of 25).The rate of 90-day mortality was the same between groups foreach occlusion location.

Mortality by PostprocedureRevascularization StatusNonrevascularized patients had higher rates of mortality inboth the failed IV tPA and non–IV tPA groups (Figure 1).Revascularized and nonrevascularized patients in the failedIV tPA groups had similar mortality at 90 days (23.5% versus38.5%). In contrast, the mortality in the revascularizednon–IV tPA group (28.5%) was lower than those not revas-cularized (59.6%; P�0.001).

Across cohorts, revascularized patients had a similar rate ofmortality in both groups (23.5% versus 28.5%), althoughamong nonrevascularized patients, there was trend toward

decreased mortality in the failed IV tPA cohort (38.5% versus59.6%; P�0.23). Mortality results, stratified by revascular-ization status and site of vascular occlusion, are shown inFigure 3.

DiscussionThe combination of IV tPA followed by mechanical throm-bectomy achieves similar rates of good outcomes comparedwith thrombectomy alone. Previous IV tPA use does notincrease symptomatic hemorrhage risk or procedure-relatedcomplications after thrombectomy. Revascularization ratesare similar between the failed and non–IV tPA groups whenstratified by occlusion location. Revascularized patients havebetter outcomes regardless of occlusion site.

Results from 2 different IV thrombolysis studies showedthat the ICA, MCA, and basilar artery occlusions responddifferently to thrombolytics, and revascularization was morefrequent in distal occlusions.1,2 Revascularization and goodoutcomes may be improved by a combined multimodalapproach.7–10,16–21 In a series of 69 patients (50 MCA, 18ICA, and 1 basilar occlusion) treated by IA thrombolysis afternonresponse to IV tPA,9 the revascularization rate was72.5%, similar to the 75% rate in another series of 16 patientswith MCA and ICA occlusions.8

Two studies also demonstrated improved revascularizationwith mechanical clot disruption after failed IV tPA. In 32patients with persistent MCA or ICA occlusion after IA or IV

Figure 1. Ninety-day (90d) mRS by revasculariza-tion status in the cohort of failed IV tPA subjects(A; n�47) and the cohort that did not receive IVtPA (B; n�243). Brackets indicate the percentageof subjects achieving a good mRS score of 0 to 2.mRS scores of 3, 4 to 5, and 6 represent interme-diate, poor neurological outcome, and death,respectively.

Table 3. Revascularization Rates and Outcomes by Site of Vascular Occlusion in Non–IV tPA Patients

Overall (n�257) ICA (n�81) MCA (n�151) Posterior (n�25) P

Final revascularization, n (%) 162 (63.0%) 50 (61.7%) 93 (61.6%) 19 (76.0%) 0.35

Intracranial hemorrhage

Symptomatic, n (%) 22 (8.6%) 9 (11.1%) 8 (5.3%) 5 (20.0%) �0.05

Asymptomatic, n (%) 72 (28.0%) 21 (25.9%) 46 (30.5%) 5 (20.0%) 0.48

Good outcome at 90 days, n (%) 76 of 243 (31.3%) 23 of 80 (28.8%) 46 of 138 (33.3%) 7 (28.0%) 0.73

Mortality at 90 days, n (%) 101 of 252 (40.1%) 41 (50.6%) 49 of 146 (33.6%) 11 (44.0%) 0.04

Procedural complication, n (%) 17 (6.6%) 7 (8.6%) 7 (4.6%) 3 (12.0%) 0.28

P values are from the likelihood ratio chi-square test.



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thrombolysis, aggressive mechanical clot disruption (angio-plasty or stenting, catheter or wire clot maceration, and snaredevice) achieved successful revascularization (thrombolysisin myocardial infarction II/III) in 87.5% of MCA occlusionsand 62.5% of ICA occlusions.16 In 7 patients with basilarocclusions treated by combined IV tPA and mechanicalthrombectomy (snares and suction devices) or IA tPA, 87.5%of patients were revascularized.10

In our analysis, successful revascularization of ICA, MCA,and basilar artery occlusions was achieved with the Mercidevice in IV tPA nonresponders, with no difference incomplications. Revascularization rates in our cohort of66.7%, 74.1%, and 100% of ICA, MCA, and basilar occlu-sions, respectively, were comparable to those of previouscombined approach cohorts.

We demonstrate no difference in the rates of symptomatichemorrhage between patients either failing or ineligible forIV tPA who are subsequently treated with mechanical throm-

bectomy. The overall 10.4% rate of symptomatic hemorrhagein the combined IV tPA and thrombectomy group is compa-rable to the 8.2% rate from the pooled data of IV tPA trials.22

Our observed rate is also lower than the 12.2% rate observedin IA thrombolysis and 20% rate in IA plus IV thrombolysisfrom one multicenter study23 but slightly higher than the 6.2%and 5.8% rates from 2 other series of combined IA and IVthrombolysis.8,9

In our study, an 11.1% rate of symptomatic hemorrhage wasfound in patients with either ICA or MCA occlusions treatedwith a combined approach, whereas rates of symptomatichemorrhage after thrombectomy alone were 11.1% in ICA, 5.3%in MCA, and 20% in basilar artery occlusions. Our rates ofsymptomatic hemorrhage in ICA occlusions in both groups werelower than the 18.8% rate seen in 16 patients treated withmechanical clot disruption after failed IV tPA.16

Patients in our study also experienced parenchymal hema-toma II hemorrhage less frequently than described in Inter-

Figure 2. Ninety-day good outcomes (mRS �2) by revascularization and IV tPA status overall and by occlusion site. BA indicates basi-lar artery. The number above each bar indicates the number of patients in the cohort.

Figure 3. Ninety-day mortality by revascularization and IV tPA status overall and by occlusion site. BA indicates basilar artery. Thenumber above each bar indicates the number of patients in the cohort.



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ventional Management of Stroke studies I and II, whichoccurred in 7.5% and 8.8% of patients, respectively.24,25 Thedecreased incidence of parenchymal hematoma II hemor-rhages with the Merci device may be associated with thedecreased use of thrombolytic drugs. Despite the theoreticallyincreased risk of symptomatic hemorrhage with mechanicalthrombectomy after failed IV tPA, there were numericallyfewer procedure-related complications and mortality in thefailed IV tPA group than the non–IV tPA group.

We found no difference in good outcomes and mortalitybetween patients undergoing mechanical thrombectomy afterfailing or being ineligible for IV tPA. Similar rates of goodoutcomes have been reported in previous combined approachstudies.7–10,16–21,25 In one study, 33 patients treated endovas-cularly (IA thrombolysis, Merci device, snare, or angioplasty)after IV tPA demonstrated lower mortality than 30 patientstreated with IV tPA alone.19 In our study, good outcomes andmortality rates were similar in patients with MCA, ICA, andbasilar artery occlusions treated with the combined approach.In patients undergoing thrombectomy alone, the rates of goodclinical outcomes were similar among the different sites ofocclusion, but there was a trend toward lower mortality inpatients with MCA occlusions than basilar or ICA occlusions.The only group in this entire cohort with no notable relation-ship between good outcome and revascularization was intPA-nonresponders with ICA occlusions. The implications ofthis finding are unclear at this time, although they may be aresult of an uneven distribution of pre-MERCI disability orhigher hemorrhage transformation rates after revasculariza-tion in this subgroup.

Previous endovascular studies have shown a strong asso-ciation between successful revascularization and favorableclinical outcomes,13,15,26–28 and our analysis supports thisassertion. In the non–IV tPA group, revascularized patientshad a higher proportion of good outcomes and a lower rate ofmortality. In addition, patients with revascularized MCA orbasilar occlusions had better outcomes and less mortality thanthe nonrevascularized patients in both treatment groups. WithICA occlusions, good outcome was more frequent in revas-cularized patients in the non–IV tPA group but not in thefailed IV tPA group.

This study has several limitations. Although the MERCItrial did not include failed IV tPA patients (by trial design),they contributed a greater number of non–IV tPA subjects forthis analysis, facilitating a more meaningful comparison.Since the MERCI study, there has been progress in the Mercidevice, operator experience, and case selection, which mayfavor the failed IV tPA group (all from Multi MERCI). Inaddition, the failed IV tPA group presented earlier than thenon IV tPA group, and since time from symptom onset to tPAbolus has also been shown to affect outcomes in the IV tPAtrials, this may have contributed to detected differences.

In conclusion, the risk of symptomatic hemorrhage andprocedural complication using the Merci Retriever afterfailed IV tPA is the same as using thrombectomy alone.Thrombectomy after IV tPA achieves similar rates of goodoutcomes, a tendency toward lower mortality, and similarrevascularization rates when stratified by clot location. Good

outcomes correlate with successful revascularization exceptwith ICA occlusions in tPA-nonresponders.

Appendix 1MERCI Trial InvestigatorsWade S. Smith, MD, PhD, University of California, San Franciscowas the national principal investigator.

The data safety monitoring board included: chair, Gene Sung,MD, University of Southern California; biostatistician, Phil Hormel,MS; members, Tim W. Malisch, MD, University of Illinois atChicago, Steven L. Giannotta, MD, University of Southern Califor-nia, Steven Rudolph, MD, Lenox Hill Hospital, and Fady T. Charbel,MD, University of Illinois at Chicago.

The imaging core laboratory consisted of Paul Kim, MD, Univer-sity of Southern California.

The writing committee included: Ronald Budzik, MD; Y. PierreGobin, MD; Thomas Grobelny, MD; Randall T. Higashida, MD;Chelsea Kidwell, MD; Helmi L. Lutsep, MD; Michael Marks, MD;Gary Nesbit, MD; Marilyn M. Rymer, MD; Jeffrey Saver, MD; IsaacE. Silverman, MD; Wade S. Smith, MD, PhD; Sidney Starkman,MD; and Gene Sung, MD.

The site principal investigators, coinvestigators, and study coor-dinators in order of enrollment are as follows. University ofCalifornia at Los Angeles Medical Center (22): Sidney Starkman,MD; Gary Duckwiler, MD; Megan Leary, MD; Chelsea Kidwell,MD; Jeffrey Saver, MD; Fernando Vinuela, MD; Reza Jahan, MD;Y. Pierre Gobin, MD; and Judy Guzy, RN. Oregon Health ScienceUniversity (22): Helmi Lutsep, MD; Stanley Barnwell, MD; WayneClark, MD; Ted Lowenkopf, MD; Elizabeth North, MD; JosephQuinn, MD; Robert Egan, MD; Todd Kuether, MD; John Roll, MD;George Luh, MD; Gary Nesbit, MD; and Barbara Dugan, RN. SaintLuke’s Hospital (21): Thomas Grobelny, MD; Naveed Akhtar, MD;Steven Arkin, MD; Irene Bettinger, MD; Marilyn Rymer, MD;Charles Weinstein, MD; Michael Schwartzman, MD; ChristineBoutwell, MD; and Barbara Gruenenfelder, RN. MassachusettsGeneral Hospital (11): Walter Koroshetz, MD; Johnny Pryor, MD;Neeraj Badjatia, MD; Ferdinando Buonarmo, MD; Lawrence Con-rad, MD; David Greer, MD; Raul Nogueira, MD; James Rabinov,MD; Guy Rordorf, MD; Jonathan Rosand, MD; Lee Schwamm, MD;John Sims, MD; Eric Smith, MD; Brian Hoh, MD; Joshua Hirsch,MD; Cenk Ayata, MD; Leigh Hochberg, MD; and Joanie Cacciola,RN. NY Presbyterian Hospital–Columbia (11): John Pile-Spellman,MD; Sean Lavine, MD; Sundeep Mangla, MD; Philip Meyers, MD;and Leslie Schmidt, NP. The Stroke Center at Hartford Hospital (11):Isaac Silverman, MD; Stephen Ohki, MD; Gary Speigel, MD;Martha Ahlquist, LPN, CCRP; and Dawn Beland, MSN. NYPresbyterian Hospital–Cornell (6): Alan Segal, MD; Ai-His Liu,MD; Igor Ougrets, MD; Howard Riina, MD; Y. Pierre Gobin, MD;and Kimberly Salvaggio, NP. University of California at SanFrancisco Medical Center (6): Randall Higashida, MD; ChristopherDowd, MD; Van Halbach, MD; Vineeta Singh, MD; Nerissa Ko,MD; Jacob Elkins, MD; S. Claiborne Johnston, MD, PhD; J. ClaudeHemphill, MD, MSc; David C. Bonovich, MD; Sharon Filler, RN;and Melissa Meighan, RN. Florida Hospital Neuroscience Institute(5): Frank Huang-Hellinger, MD; and Susan Mitchell, RN. RiversideMethodist Hospital (5): Ronald Budzik, MD; Geoffrey Eubank, MD;Erik Arce, MD; Jim Fulop, MD; John Lippert, MD; Tom Davis, MD;J. Kevin McGraw, MD; Peter Pema, MD; and Paula Meyers, RN.Stanford University Medical Center (5): Michael Marks, MD; HuyDo, MD; Gregory Albers, MD; Amie Hsia, MD; David Tong, MD;Christine Wijamn, MD; and Mary Marcellus, RN. Carolina Neuro-surgery and Spine (4): Joseph Bernard, MD; Gary DeFilipp, MD;Richard Bellon, MD; Barry McGinnis, MD; Andrea Dietrich, MD;Steve Putnam, MD; and Peggy Boltes, RN. Georgetown University(2): Vance Watson, MD; John DeSimone, MD; Manual Yepes, MD;and Theresa Kowal, RN. University of Maryland (2): JoanneStallmeyer, MD; Abraham Obuchowski, MD; Greg Zoarski, MD;Marian LaMonte, MD; Marcella Wozniack, MD; and DeborahSchofield, RN. University of Pennsylvania (2): David Liebeskind,MD; Scott Kasner, MD; Brett Cucchiara, MD; Steven Messe, MD;



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Robert Taylor, MD; Michael McGarvey, MD; Robert Hurst, MD;Linda Bagley, MD; John Weigele, MD; Jessica Clarke, RN, BSN.Brigham and Women’s Hospital (1): Walter Koroshetz, MD; KaiFrerichs, MD; Steven Feske, MD; Alexander Norbash, MD; GalenHendersen, MD; Farzanah Sorond, MD; John Baker, MD; PengChen, MD; and Joanne O’Hara, RN. Latter-Day Saints Hospital (1):John Jacobs, MD; Lisa Yananse, MD; Duane Blatter, MD; AlbertLee Bahr, MD; Collen Harker MD; David Pisani, MD; and KathyWalker, RN. Louisiana State University at Shreveport (1): ClaudioSchonoholz, MD; Horacio D’Agostino, MD; Anil Nanda, MD;Roger Kelley, MD; and Donna Singleton, RN. State University ofNew York at Buffalo (1): L. Nelson Hopkins, MD; Lee Guterman,MD; Elad Levy, MD; Jay Howington, MD; Mark Harrigan, MD;Ricardo Hanel, MD; and Annemarie Crumlish. University of NorthCarolina–Chapel Hill (1): Sten Solander, MD; Ana Felix, MD;Souvik Sen, MD; David Huang, MD; Nydia Melendez, MD; andSusan Wilson, MSN, FNP. Washoe Medical Center (1): Paul Katz,MD; Bradley Glenn, MD; Timothy Koci, MD; Anthony Bruno, MD;Mark Algood, MD; and Marta Heffner, RN. Baptist MemorialClinical Research Center: John Barr, MD; Paul Broadbent, MD;Soren A. Singer, MD; Stephen D. Morris, MD; Sanat Dixit, MD; andGrace Miller. Barrow Neurological Institute: James Frey, MD;Cameron McDougall, MD; Felipe Albuquerque, MD; Mark Hekler,MD; David Fiorella, MD; Seth Larson, MD; Shafeeq Ladha, MD;Darin Okuda, MD; and Mary Harrigan, RN, MN. Baton RougeGeneral Hospital: Albert Alexander, MD; Joseph Acosta, MD; JonOlson, MD; Kevin Callerame, MD; Rodney Hillis, MD; and Kim-berly Hendricks, RN, MN. Emory University: Frank Tong, MD;Jacques Dion, MD; Michael Frankel, MD; Barney Stern, MD; OwenSamuels, MD; and Marc Chimowitz, MD. University of Texas,Houston: Morgan Campbell, MD; John Choi, MD; Frank Yatsu,MD; Marc Malkoff, MD; James Grotta, MD; Edwin Cacayorin, MD;Christina Hall, MD; Lise Labiche, MD; Elizabeth Noser, MD; JoonSong, MD; Ken Uchino, MD; and Doralene Smith.

Appendix 2Multi MERCI Trial InvestigatorsWade S. Smith, MD, PhD, University of California, San Francisco,was the international principal investigator.

The data safety monitoring board included: chair, Gene Sung,MD, MPH, University of Southern California; biostatistician, PhilHormel, MS; and members, Tim W. Malisch, MD, Alexian BrothersMedical Center; Steven Rudolph, MD, Maimonides Medical Center;and Arun Amar, MD, Stanford University.

The imaging core laboratory consisted of Paul Kim, MD, Univer-sity of Southern California. The biostatistician was Phil Hormel, MS.

The writing committee included: Ronald Budzik, MD; GaryDuckwiler, MD; Donald Frei, MD; Y. Pierre Gobin, MD; ThomasGrobelny, MD; Randall T. Higashida; Frank Hellinger, MD; DanHuddle, MD, MD; Chelsea Kidwell, MD; Walter Koroshetz, MD;David S. Liebeskind, MD; Helmi L. Lutsep, MD; Michael Marks,MD; Gary Nesbit, MD; Marilyn M. Rymer, MD; Jeffrey Saver, MD;Isaac E. Silverman, MD; Wade S. Smith, MD, PhD; SidneyStarkman, MD; and Gene Sung, MD, MPH.

The site principal investigators, coinvestigators, and study coor-dinators in order of number of patients treated are as follows. StLuke’s Hospital (50): Naveed Akhtar, MD, Thomas Grobelny, MD;Annette Allen, RN; Steven Arkin, MD; Irene Bettinger, MD;Christine Boutwell, MD; Charlene Grau, RN; Barbara Gruenen-felder, RN; Marilyn Rymer, MD; Michael Schwartzman, MD; andCharles Weinstein, MD. Riverside Methodist Hospital (32): RonaldBudzik, MD; Erik Arce, MD; Albert Berarducci, MD; Tom Davis,MD; Mark Dean, MD; Eric Dolen; Geoffrey Eubank, MD; JimFulop, MD; Xiamei Gao-Hickman, MD; John Lippert, MD; WilliamMayr, MD; J. Kevin McGraw, MD; Paula Meyers, RN; Peter Pema,MD; and Robert Wyatt, MD. Oregon Stroke Center (21): HelmiLutsep, MD; Stanley Barnwell, MD; Wayne Clark, MD; BarbaraDugan, RN; Robert Egan, MD; Todd Kuether, MD; Ted Lowenkopf,MD; Gary Nesbit, MD; Elizabeth North, MD; Bryan Peterson, MD;John Roll, MD; and Lisa Yanase, MD. The Stroke Center at Hartford

Hospital (14): Isaac Silverman, MD; Martha Ahlquist, LPN, CCRP;Dawn Beland, MSN; Joao Gomes, MD; Stephen Ohki, MD; andGary Speigel, MD. University of California at Los Angeles MedicalCenter (12): Sidney Starkman, MD; Latisha Ali; Brian Buck, MD;Dennis Chute, MD; Gary Duckwiler, MD; Judy Guzy, RN; RezaJahan, MD; Doojin Kim, MD; David S. Liebeskind, MD; VictorMarder, MD; Bruce Ovbiagele, MD; Venkatakrishna Rajajee, MD;Lucas Restrepo, MD; Nerses Sanossian, MD; Jeffrey Saver, MD;Scott Selco, MD; Samir Shah, MD; Maria Shukman, RN; SatoshiTateshima, MD; Amytis Towfighi, MD; Paul Vespa, MD; J. PabloVillablanca, MD; Harry Vinters, MD; and Fernando Vinuela, MD.Swedish (Denver) Medical Center (9): Don Frei, MD; Dan Huddle,MD; Richard Bellon, MD; Christopher Finale, MD; Carol Green-wald, MD; and Don Smith, MD. Florida Hospital NeuroscienceInstitute (8): Frank Hellinger, MD; Laura Billanovic, RN; and SusanMitchell, RN. NY Presbyterian Hospital–Cornell (4): Alan Segal,MD; Y. Pierre Gobin, MD; Jeffrey Katz, MD; Igor Ougrets, MD;Howard Riina, MD; and Kimberly Salvaggio, NP. University ofCalgary, Foothills Hospital: (4) PI: Michael Hill, MD; Philip Barker,MD; Andrew Demchuk, MD; Imanuel Dzialowski; Karyn Fischer,RN, MD; William Hu; Mark Hudon, MD; Will Morrish, MD; SureshSubramanian, MD; Tim Watson, MD; and John Wong, MD. NYPresbyterian Hospital–Columbia (3): John Pile-Spellman, MD; SeanLavine, MD; Philip Meyers, MD; and Leslie Schmidt, NP.Georgetown University (3): Vance Watson, MD; John DeSimone,MD; Timea Hodics, MD; Theresa Kowal, RN; Farid Parham, MD;Susan Sutten, MPH; and Manual Yepes, MD. Stanford UniversityMedical Center (2): Michael Marks, MD; Gregory Albers, MD;James Castle, MD; Huy Do, MD; Mahesh Jayerman, MD; MartenLansberg, MD; Mary Marcellus, RN; Chitra Venkatsubmaran, MD;and Christine Wijman, MD. University of Alberta, Edmonton (2):Ashfaq Shuaib, MD; Robert Ashforth, MD; Derek Emery, MD;Faraz Al-Hussain, MD; Muhammad Hussain, MD; Thomas Jeer-akathil, MD; Kurshid Khan, MD; Mikael Murtaoghu, MD; NazirRizvi, MD; Maher Saqqur, MD; James Scozzafava, MD; BrendaScwindt, RN; Muzaffar Siddiqui, MD; and Khalida Tariq, MD.Baptist Memorial Clinical Research Center: John Barr, MD; PaulBroadbent, MD; Sanat Dixit, MD; Grace Miller; and Stephen D.Morris, MD. University of Pittsburgh Medical Center: Tudor Jovin,MD; Max Hammer, MD; Michael Horowitz, MD; Vivek Reddy,MD; Tibetha Santucci, RN; Ken Uchino, MD; Nirav Vora, MD; andLawrence Wechsler, MD.

AcknowledgmentsWe thank Phil Hormel, MS, biostatistician, for his programming andassistance of the analysis.

DisclosuresGary R. Duckwiler is a scientific advisor and stockholder in ConcentricMedical, Inc. Gary Walker is an employee of Concentric Medical, Inc.

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11. Ribo M, Alvarez-Sabín J, Montaner J, Romero F, Delgado P, Rubiera M,Delgado-Mederos R, Molina CA. Temporal profile of recanalization afterintravenous tissue plasminogen activator: selecting patients for rescuereperfusion techniques. Stroke. 2006;37:1000–1004.

12. Gobin YP, Starkman S, Duckwiler GR, Grobelny T, Kidwell CS, JahanR, Pile-Spellman J, Segal A, Vinuela F, Saver JL. MERCI 1: a phase 1study of Mechanical Embolus Removal in Cerebral Ischemia. Stroke.2004;35:2848–2854.

13. Smith WS, Sung G, Starkman S, Saver JL, Kidwell CS, Gobin YP, LutsepHL, Nesbit GM, Grobelny T, Rymer MM, Silverman IE, Higashida RT,Budzik RF, Marks MP. Safety and efficacy of mechanical embolectomyin acute ischemic stroke: results of the MERCI trial. Stroke. 2005;36:1432–1438.

14. Smith WS. Safety of mechanical thrombectomy and intravenous tissueplasminogen activator in acute ischemic stroke. Results of the MultiMechanical Embolus Removal in Cerebral Ischemia (MERCI) trial, partI. AJNR Am J Neuroradiol. 2006;27:1177–1182.

15. Smith WS, Sung G, Saver J, Budzik R, Duckwiler G, Liebeskind DS,Lutsep HL, Rymer MM, Higashida RT, Starkman S, Gobin YP, Frei D,Grobelny T, Hellinger F, Huddle D, Kidwell C, Koroshetz W, Marks M,Nesbit G, Silverman IE. Mechanical thrombectomy for acute ischemicstroke: final results of the multi MERCI trial. Stroke. 2008;39:1205–1212.

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17. Zaidat OO, Suarez JI, Santillan C, Sunshine JL, Tarr RW, Paras VH,Selman WR, Landis DM. Response to intra-arterial and combined intra-venous and intra-arterial thrombolytic therapy in patients with distalinternal carotid artery occlusion. Stroke. 2002;33:1821–1826.

18. Suarez JI, Zaidat OO, Sunshine JL, Tarr R, Selman WR, Landis DM.Endovascular administration after intravenous infusion of thrombolyticagents for the treatment of patients with acute ischemic strokes.Neurosurgery. 2002;50:251–259.

19. Burns TC, Rodriguez GJ, Patel S, Hussein HM, Georgiadis AL, Laksh-minarayan K, Qureshi AI. Endovascular interventions following intrave-nous thrombolysis may improve survival and recovery in patients withacute ischemic stroke: a case-control study. AJNR Am J Neuroradiol.2008;29:1918–1924.

20. Qureshi AI, Siddiqui AM, Suri MF, Kim SH, Ali Z, Yahia AM, LopesDK, Boulos AS, Ringer AJ, Saad M, Guterman LR, Hopkins LN.Aggressive mechanical clot disruption and low-dose intra-arterial third-generation thrombolytic agent for ischemic stroke: a prospective study.Neurosurgery. 2002;51:1319–1327.

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23. Singer OC, Berkefeld J, Lorenz MW, Fiehler J, Albers GW, LansbergMG, Kastrup A, Rovira A, Liebeskind DS, Gass A, Rosso C, Derex L,Kim JS, Neumann-Haefelin T. MR Stroke Study Group Investigators.Risk of symptomatic intracerebral hemorrhage in patients treated withintra-arterial thrombolysis. Cerebrovasc Dis. 2009;27:368–374.

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25. IMS II. Trial Investigators. The Interventional Management of Stroke(IMS) II Study. Stroke. 2007;38:2127–2135.

26. Tomsick T, Broderick J, Carrozella J, Khatri P, Hill M, Palesch Y,Khoury J. Revascularization results in the Interventional Management ofStroke II trial. AJNR Am J Neuroradiol. 2008;29:582–587.

27. Furlan A, Higashida R, Wechsler L, Gent M, Rowley H, Kase C, PessinM, Ahuja A, Callahan F, Clark WM, Silver F, Rivera F. Intra-arterialpro-urokinase for acute ischemic stroke. The PROACT II study: a ran-domized controlled trial. Prolyse in Acute Cerebral Thromboembolism.J Am Med Assoc. 1999;282:2003–2011.

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for the MERCI and Multi MERCI InvestigatorsZhong-Song Shi, Yince Loh, Gary Walker and Gary R. Duckwiler

Revascularization and Outcomes Stratified by the Site of Arterial OcclusionsIntravenous Tissue Plasminogen Activator Patients:−Plasminogen Activator Versus Non

Endovascular Thrombectomy for Acute Ischemic Stroke in Failed Intravenous Tissue

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 2010 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Stroke doi: 10.1161/STROKEAHA.109.568451

2010;41:1185-1192; originally published online April 29, 2010;Stroke.

http://stroke.ahajournals.org/content/41/6/1185World Wide Web at:

The online version of this article, along with updated information and services, is located on the

/content/43/10/e111.full.pdfAn erratum has been published regarding this article. Please see the attached page for:

http://stroke.ahajournals.org/content/suppl/2016/03/31/STROKEAHA.109.568451.DC1Data Supplement (unedited) at:

http://stroke.ahajournals.org//subscriptions/

is online at: Stroke Information about subscribing to Subscriptions:

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document. Permissions and Rights Question and Answer process is available in the

Request Permissions in the middle column of the Web page under Services. Further information about thisOnce the online version of the published article for which permission is being requested is located, click

can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office.Strokein Requests for permissions to reproduce figures, tables, or portions of articles originally publishedPermissions:


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Correction

The article, “Endovascular Thrombectomy for Acute Ischemic Stroke in Failed Intravenous TissuePlasminogen Activator Versus Non–Intravenous Tissue Plasminogen Activator Patients: Revas-cularization and Outcomes Stratified by the Site of Arterial Occlusions” by Shi et al (Stroke.2010;41:1185–1192) included an error in Appendix 2. Dr Fawaz Al-hussain’s name and affiliationwere incorrect. The correct information appears below as well as in the current online version.

The investigator’s name should appear as Fawaz Al-hussain, MD, King Saud University.

(Stroke. 2012;43:e111.)© 2012 American Heart Association, Inc.

Stroke is available at http://stroke.ahajournals.org DOI: 10.1161/STR.0b013e318273db6f

e111

22

Stroke May 2010

Original Contributions

大脑中动脉主干闭塞与第二段闭塞机械取栓术的临床结局：脑缺血机械取栓 (MERCI) 和多中心 MERCI 试验的汇总分析

Clinical Outcomes in Middle Cerebral Artery Trunk Occlusions Versus Secondary Division Occlusions After Mechanical Thrombectomy:

Pooled Analysis of the Mechanical Embolus Removal in Cerebral Ischemia (MERCI) and Multi MERCI Trials

Zhong-Song Shi, MD; Yince Loh, MD; Gary Walker, PhD; Gary R. Duckwiler, MD; for the MERCI and Multi-MERCI Investigators

背景和目的：血管内血管再通术对急性缺血性卒中患者有益，但其益处是否在大脑中动脉(MCA)第二段(M2)闭塞与MCA主干(M1)闭塞存在差异尚不清楚。本文对由血管造影术确定的MCA M1闭塞患者与单独M2闭塞患

者，用Merci Retriever装置进行机械取栓后的血管再通状态和临床结局进行了比较。

方法：回顾性分析了脑缺血机械取栓(MERCI)和多中心MERCI试验中MCA卒中患者的汇总数据。患者分成两

组：MCA M1闭塞和单独M2闭塞，评价了两组的基线特征、血管再通率、出血率、并发症、结局和死亡率。

结果：MERCI和多中心MERCI试验中的178例MCA闭塞患者，84.3%为M1闭塞，15.7%为单独M2闭塞。单独

M2闭塞患者与M1闭塞患者相比有更高的血管再通率，更少的平均机械疏通次数，且具有更短平均操作时间

的趋势。尽管在所有患者中，M2的结局从数字上看是优于M1，但M2与M1组之间在症状性出血、有临床意义

的操作不良反应、90天良好结局或90天的死亡率等方面无统计学差异。在多因素分析中，最终的血管再通是

90天良好结局最强的预测因素。

结论：MCA M1闭塞和单独M2闭塞的患者在接受机械取栓后可以达到相对高的血管再通率和良好的临床结

局。而事实上，与M1闭塞的患者相比，单独M2闭塞患者具有更高的血管再通率，需要更少的机械疏通次数

且没有增加并发症。

关键词：急性脑卒中血管内治疗大脑中动脉结局取栓术

(Stroke.2010;41;953-960. 林森译曾进胜校)

From the Division of Interventional Neuroradiology (Z.S.S., Y.L., G.R.D.), David Geffen School of Medicine at UCLA, Los Angeles, Calif; and Concentric Medical, Inc (G.W.), Mountain View, Calif.

Current affiliation for Z.S.S.: Department of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, P.R.China.Current affiliation for Y.L.: Neurovascular Service, Department of Medicine, Madigan Army Medical Center, Tacoma, Wash.Correspondence to Gary R. Duckwiler, MD, Division of Interventional Neuroradiology, David Geffen School of Medicine at UCLA, 757 Westwood Plaza, Los Angeles, CA

90095-7437. E-mail [email protected]© 2010 American Heart Association, Inc.

颅内大动脉闭塞引起的急性缺血性卒中患者对

溶栓治疗的反应不尽相同，可能取决于动脉闭塞的

位置不同。在美国神经疾病与卒中研究所、欧洲急

性卒中协作研究 (ECASS) 以及阿替普酶静脉注射

(IV) 非介入治疗急性缺血性卒中的临床试验中，使

用组织型纤溶酶原激活剂 (tPA) 静脉溶栓，由于缺乏

对血栓的准确定位，动脉闭塞类型既不影响血管再

通状态也不影响临床结局 [1–4]。大脑中动脉 (MCA)供血区的卒中在缺血性卒中的所占比例最大。然而， IV 和动脉内 (IA) 溶栓治疗则很少报道血管再通状态

和临床结局在MCA主干 (M1)闭塞和单独第二段 (M2)闭塞中的差别 [1–8]。最近应用经颅多普勒超声和 / 或CT 血管成像的研究发现在 IV tPA 治疗后，MCA M2

闭塞的血管再通状态优于 MCA M1 闭塞 [9,10]。具有

良好临床结局的 MCA M2 闭塞患者约两倍于 MCA M1 闭塞患者 [9]。

急性脑血栓栓塞溶栓试验Ⅱ (PROACT II) 研究

纳入的 MCA M1 闭塞患者占患者总数的 61.7%，其

余大多是单独 MCA M2 闭塞；然而，根据 M1 与

M2 闭塞分层比较临床结局的研究罕有报告 [5]。最近

的尿激酶 IA 溶栓治疗的研究显示 MCA M1 闭塞的

血管再通状态要优于单独 M2 闭塞，但却没有描述

不同闭塞部位与临床结局的关系 [11,12]。

对于起病 8 小时内 IV tPA 治疗不适用或失败的

急性缺血性卒中患者，应用 Merci 器械进行机械取

栓是一种很有前景的替代疗法 [13-17]。脑缺血机械取

23

Shi et al Outcomes in MCA Occlusions With the Merci Retriever

栓 (MERCI) 和多中心 MERCI 第一部分试验的汇总

分析已经证明，颈内动脉闭塞的患者可以达到相对

较高的血管再通率 [17]。然而，它并没有评估 MCA M2 闭塞与 MCA M1 闭塞的机械性血管再通的结

局差异。本研究的目的是评价经过血管造影确定的

MCA M1 闭塞与单独 M2 闭塞的急性缺血性卒中患

者使用 Merci Retriever 装置进行机械取栓术是否会

影响其血管再通状态。同时本研究也旨在通过血管

再通状态比较不同组 (M1 vs. M2) 中所有 MCA 闭塞

患者使用机械取栓术的安全性和有效性。

方法MERCI 与多中心 MERCI 试验的汇总数据对确

定的急性 MCA 卒中进行了回顾分析。汇总数据包

括总共 305 例缺血性卒中患者，其中 141 例来自于

MERCI 试验，164 例来自于多中心 MERCI 试验。

这两个试验的详细计划书在之前的研究中已经作了

描述 [13-17]。简单来说，纳入试验的患者不是不适合

进行 IV tPA 治疗，就是经过导管法血管造影确认接

受 IV tPA 治疗后闭塞的血管未再通。试验使用一类

X 系列和 L5 Merci Retriever 装置 (Concentric Medi-cal, Inc, Mountain View, Calif) 从管腔取出血栓试图

来使闭塞的颅内血管再通。第一代装置 (X4、X5 和

X6 Retriever) 在两个试验中都有应用，而第二代装

置 (L5 Retriever 装置 ) 只用在多中心 MERCI 试验中。

IA tPA 被允许在治疗中装置 6 次疏通依然失败或成

功施行近端血栓去除术后，溶解装置无法靠近的远

端血栓时应用。两个研究方案中，任何部位的闭塞

都不允许使用血管成形术或支架。

本研究纳入经数字减影血管造影确定的单独

MCA M1 和 / 或 M2 闭塞的患者。分析中排除了那

些 ICA/MCA 串联闭塞或 ICA-T 闭塞的患者。患者

分为 MCA M1 闭塞组和单独 MCA M2 闭塞组。成功

的血管再通定义为经数字减影血管造影所确认的所

有应治疗的血管经治疗后达到心肌梗塞溶栓 (TIMI)血流分级的 II 级或 III 级。CT 或 MRI 扫描在基线、

24 小时以及患者神经状态下降的任何时间进行。根

据 ECASS 试验的分类，大脑内出血分为出血性梗

死 I 和 II 型或脑实质血肿 I 和 II 型。症状性出血是

指 24 小时内 NIHSS 分数增加≧ 4 分，且 24 小时

内头部 CT/MRI 扫描发现有出血的证据，或在除和

之外无更多合适的 NIHSS 分数比基线线时没变化，

但患者死亡有的任何颅内出血。操作相关的不良事

件由独立的数据安全与监督委员会裁定，且被定义

为血管穿孔、动脉壁内夹层、或之前未受累区域栓

塞、症状性出血，以及需要外科手术或输血处理的

操作区并发症。临床上操作相关的严重并发症是指

NIHSS 降低≧ 4 分的操作并发症或死亡、需要外科

手术或输血处理的腹股沟区并发症。

神经状态由 NIHSS 和 30 及 90 天的改良 Rankin评分 (mRS) 来评定。各闭塞组患者的评估内容包括血

管再通率、出血转化率、临床上严重的操作相关并发

症、90 天临床结局及死亡率。90 天良好的结局被定义

为 mRS ≤ 2。由于单独 M2 闭塞样本较小，M1 和 M2闭塞的数据被汇总起来并进行多元 logistic 回归分析

以此来确定 90 天良好结局的独立预测变量。对血管

再通状态分层后进行临床特点、并发症和结局的比较。

组与组之间差异的比较采用 95% CI。如果这

个区间不包含 0，组之间的差异在 P=0.05 时被认为

是有意义的。虽然这是一个回顾性的亚组分析，但

所考虑的两个组的样本大小应该是在两组间结局比

较上至少具有 80% 的效能检出 28% 的绝对差异和

50% 的效能检出 20% 的绝对差异。单因素分析确定

90 天的良好结局的独立预测变量，其中所有 Wald χ2 P<0.2 变量都将纳入多元 logistic 回归模型去确定

90 天良好结局的预测变量。该模型按前进 / 后退逐

步回归的方法来建立，且基于 χ2 的统计值，变量为

0.05 时进入模型而在 0.10 时离开该模型。在主要效

用的模型建立后，任何有意义的双向交互条件存在

的假设使用似然比 χ2(G2) 统计进行检测。最终的模

型由 Hosmer 和 Lemeshow 检验进行拟合度的检测。

P<0.05 认为有统计学意义。本文中的统计分析是使

用 SAS 软件来完成的。(8.2 版本；SAS 公司 )

结果MCA卒中患者的人口学特征

在 MERCI 和多中心 MERCI 试验中，对 178例经血管造影确定为 MCA 闭塞的患者进行了治

疗。其中 80 例患者来自 MERCI 试验，98 例来自

多中心 MERCI 试验。平均年龄 69.0 岁 (SD 15.7)，103(57.9%) 为女性患者。平均基线 NIHSS 分数

是 18.8 分 (SD 5.8)，范围为 9 至 40 分。队列中

27(15.2%) 例患者接受了 IV tPA 治疗并在进行机械

取栓前均未再通；剩余的 151 例患者则不适合接受

IV tPA 治疗。患者从卒中起病至器械进入动脉的平

均时间为 4.3 小时 (SD 1.6)，范围为 0.7 至 10.8 小时。

178 例患者中，84.3%(n=150) 表现为单独 MCA M1 闭塞或 M1/M2 合并的闭塞，15.7%(n=28) 表现

为单独 MCA M2 闭塞。在 150 例 MCA M1 闭塞患

者中，73 例来自 MERCI 试验，77 例来自多中心

MERCI 试验。在 28 例 MCA M2 闭塞患者中，7 例

来自 MERCI 试验，21 例来自多中心 MERCI 试验。

各组患者的基线特征 ( 年龄、性别、NIHSS 分数、

起病至进入动脉的时间以及联合 tPA 的使用 ) 均没

24

Stroke May 2010

有统计学差异。MCA M1 闭塞患者可能更易患冠状

动脉病，且凝血酶原时间更短，收缩压更低 ( 表 1)。在 M1 组中，最常使用 X6 和 L5 装置 ( 均为 44.7%)，X5(34.0%) 和 X4(6.7%) 的使用则较少。在 M2 组中，

最常用的是 L5 装置 (53.6%)，紧接着是 X6(28.6%)，之后是 X5(25.0%)，未使用 X4。两组中，7% 的患

者在评定其基线 NIHSS 分数时应用了镇静剂。尽管

与 M1 组 (52.5%) 相比，M2 组 (73.1%) 患者存在明

显更高比例的严重或完全性失语，但两组中 NIHSS的运动评分部分无统计学差异。

血管再通率

经 Merci 治疗后的即时血管再通率 (TIMI II/III血流分级 ) 在 MCA M1 组与单独 M2 组中分别为

46.0% 和 71.4%( 表 2)。包括接受联合治疗的患者在

内，单独 MCA M2 组的最终血管再通率高于 MCA M1组 (82.1% vs. 60.0%)。另外，相对于MCA M1闭塞，

单独 MCA M2 闭塞所需的疏通次数更少 (2.1 vs. 3.1)并具有平均操作时间更短的趋势 (1.6 vs. 1.8 小时 )。

良好结局和死亡率

尽管单独 MCA M2 闭塞组的良好结局与 MCA

M1 闭塞组相比，从数字上看具有较高的比例 (40.7% vs. 33.3%)，但两组 90 天良好临床结局 (mRS ≦ 2) 并无统计学差异 ( 表 2)。一般来说，远端动脉闭塞预

期有更好的结局，但在本系列中，左侧 M2 闭塞占

67.9% 而左侧的 M1 闭塞只有 47.3%( 有认为左侧大脑

半球梗死患者长期预后差，而本组M2闭塞左侧更多)。两组 90 天的死亡率也无统计学差异，然而，从

数字上看，单独 MCA M2 闭塞组比 MCA M1 闭塞

组低 (25.9% vs. 32.9% ；表 2)。

出血并发症

两组颅内出血率无统计学差异 (M1 组 36.7% vs. M2 组 42.9%)。同样，两组的症状性出血率也无统

计学差异 (M2 组 3.6% vs. M1 组 6.7%)。从数字上看，

M2 闭塞患者的有临床上严重操作相关不良反应比

M1 闭塞更低 (3.6% vs. 5.3%)。

多元Logistic回归分析

与先前的 MERCI 试验分析相似，年龄、基线

NIHSS 和操作后的血管再通状态均为 90 天良好临床

结局的预测因素。具体结果见表 3。最终的血管再通

状态是良好结局最强的独立预测因素 (OR 为 30.91)。

表 1　不同闭塞位置患者的特征总数 MCA M1 MCA M2 (n=178) (n=150) (n=28) P*年龄中位数，年 (IQR) 73.0(60.0-80.0)(178) 73.0(60.0-80.0)(150) 71.5(61.5-81.0)(28) 0.94女性 57.9%(103/178) 56.0%(84/150) 67.9%(19/28) 0.30高血压 77.5%(138/178) 77.3%(116/150) 78.6%(22/28) >0.99糖尿病 24.8%(44/177) 25.0%(37/149) 24.9%(7/28) 0.99血脂异常 34.8%(57/164) 34.1%(47/138) 38.5%(10/26) 0.67冠状动脉病 39.7%(69/174) 43.2%(63/146) 21.4%(6/28) 0.04充血性心力衰竭 21.6%(38/176) 22.3%(33/148) 17.9%(5/28) 0.59吸烟 18.4%(30/163) 19.6%(27/138) 12.0%(3/25) 0.35房颤 44.1%(78/177) 41.6%(62/149) 57.1%(16/28) 0.15血液系统疾病 6.3%(11/174) 6.2%(9/146) 7.1%(2/28) 0.85周围血管疾病 12.1%(21/173) 13.1%(19/145) 7.1%(2/28) 0.35血糖，mg/dL 134.2±51.4(176) 134.6±51.8(149) 132.1±49.9(27) 0.82凝血酶原时间，秒 13.4±4.4(170) 13.1±3.2(143) 15.1±8.1 (27) 0.03活化部分凝血激酶时间，秒 30.1±17.8(160) 30.2±19.1(134) 29.3±8.6(26) 0.8国际标准化比值 1.21±0.49(174) 1.18±0.42(148) 1.34±0.8(26) 0.13血小板 ( 计数 ) 240.4±77.2(175) 238.4±77.5(148) 251.4±75.4(27) 0.42收缩压中位数，mmHg(IQR) 150.0(131-165)(176) 147.0(130-163)(149) 157.0(132-176)(27) 0.08舒张压中位数，mmHg(IQR) 75.5(64-85)(176) 74.0(62-84)(149) 80.0(68-91)(27) 0.09基线 NIHSS，中位数 (IQR) 18.0(14-23)(178) 18.0(15-23)(150) 17.0(14-22)(28) 0.56左侧 MCA 闭塞 50.6%(90/178) 47.3%(71/150) 67.9%(19/28) 0.06起病至腹股沟穿刺时间中位数，小时 (IQR) 4.3(3.2-5.4)(177) 4.3(3.2-5.5)(149) 4.7(3.7-5.3)(28) 0.35Merci 前静脉 tPA 失败 15.2%(27/178) 14.0%(21/150) 21.4%(6/28) 0.33动脉溶栓治疗 32.0%(57/178) 30.7%(46/150) 39.3%(11/28) 0.38静脉或动脉溶栓治疗 41.6%(74/178) 40.0%(60/150) 50.0%(14/28) 0.33静脉和动脉溶栓治疗 5.6%(10/178) 4.7%(7/150) 10.7%(3/28) 0.19白种人 84.8%(151/178) 82.7%(121/150) 96.4%(27/28) 0.05*P 值：连续变量采用两样本 Wilcoxon 检验，分类变量采用 Fisher 精确检验计算。

IQR ：四分位数间距。

25


血管再通与血管未再通患者的比较

在所有 MCA 闭塞的患者中，血管再通的比未

再通的患者具有更高比例的 90 天良好结局、更低的

死亡率和症状性出血、疏通次数更少和操作时间更

短 ( 表 4)。年龄、NIHSS 分数、危险因素和入院时

实验室检查结果等基线特征在最终血管再通与未再

通患者之间是相似的。

讨论本研究结果表明应用 Merci 装置进行机械取栓

后，MCA M1 闭塞或单独 M2 闭塞患者能达到较高的

血管再通率和良好的临床结局。单独 M2 闭塞患者的

血管再通率更高，并具有平均操作时间更短的趋势。

越来越多的证据显示血管再通率和良好临床

结局受血管闭塞位置的显著影响。IV 和 IA 溶栓的

研究发现，溶栓治疗对 MCA 闭塞比对 ICA 和基底

动脉闭塞更有效果 [9,11]。与先前的 MERCI 和多中

心 MERCI 试验分析相比，经机械取栓术治疗后的

MCA M1 组 60% 的血管再通率与 ICA 闭塞组 63%的血管再通率相似，低于椎基底动脉闭塞组 78% 的

血管再通率 [17,18]。而单独 MCA M2 闭塞 82% 的血管

再通率则明显高于其他位置的闭塞。

本研究中机械取栓治疗 MCA 闭塞后，63.5% 的

血管再通率高于其他试验中只用 IV 溶栓治疗的患

者。有研究报告，起病 6 小时内 18% 的 MCA 心源

性栓塞患者可出现由经颅多普勒超声确定的自发再

通 [19]。在 PROACT II 研究中，卒中起病后 6 到 8 小

时，大约 18% 的接受静脉肝素治疗后的急性 MCA闭塞安慰剂组患者，可发生经血管造影确定的自发

再通 [5]。另一项基于82例MCA主干闭塞患者的研究，

采用 TIMI 血流分级和 MR 血管造影确定自发血管再

通，其结果显示起病后 24 小时，IV 溶栓组比未溶

栓组具有更高的自发血管再通率 [20]。IV 溶栓组和未

溶栓组的局部和全部血管再通率 (TIMI II级和 III级 )分别为 38.5% 和 24%[20]。

尽管在已发表的 IV 溶栓试验数据中，MCA M1与单独 M2 闭塞的血管再通状态差异未予报道，但

本研究中单独 MCA M2 闭塞的血管再通优于 M1 闭

塞，与最近两篇 IV 溶栓研究一致 [9,10]。根据经颅多普

勒超声标准，MCA M2 与 M1 闭塞患者接受 IV tPA治疗后，2 小时的完全再通率分别为 44.2%(50/113)和 30%(49/163)[9]。另一项采用 CT 血管造影和 / 或经颅多普勒超声监测的研究，IV tPA 24 小时后 53%的M1闭塞患者 (n=32)和 68%的M2闭塞患者 (n=19)达到完全再通 [10]。对 IV tPA 后进行取栓治疗与只

进行取栓治疗的血管再通率比较超出了我们目前研

究的范围。取栓前的 IV tPA 治疗会软化凝块，促进

Merci 装置穿透凝块和取回。对不同位置动脉闭塞采

用 IV tPA 后再行机械取栓治疗，这种疗法产生的潜

在血管再通的益处应在以后的研究中进行探讨。

与 PROACT II 研究中接受治疗的 121 例患者

相比，本研究的中位基线 NIHSS 和平均年龄均高

于 PROACT II( 基线 NIHSS ：18 vs. 17 ；年龄：69岁 vs. 64 岁 )，但本组患者与其有相似的血管再通

率 (MERCI/ 多中心 MERCI 63.5% vs. PROACT II 66%)，90天良好结局 (34.5% vs. 40%)和死亡率 (31.8% vs. 25%)，以及更低的症状性出血 (6.2% vs. 10.0%)[5]。

最近的一项研究全面比较了 MERCI/ 多中心 MERCI

表 2　不同闭塞位置的血管再通和临床结局总数 MCA M1 MCA M2 (n=178) (n=150) (n=28) P*操作持续时间中位数，小时 (IQR) 1.6(0.3-4.7)(173) 1.7(0.3-4.7)(149) 1.5(0.8-2.8)(28) 0.19移除凝块尝试次数 2.96±1.56 3.12±1.55 2.11±1.31 0.001取回装置后 TIMI II/III 级血流 50.0%(89/178) 46.0%(69/150) 71.4%(20/28) 0.02最终 TIMI II/III 级血流 63.5%(113/178) 60.0%(90/150) 82.1%(23/28) 0.03临床上操作相关的严重不良反应 5.1%(9/178) 5.3%(8/150) 3.6%(1/28) >0.9924 小时 NIHSS 提高≥ 10 分 20.4%(33/162) 19.9%(27/136) 23.1%(6/26) 0.7990 天 mRS ≤ 2 34.5%(57/165) 33.3%(46/138) 40.7%(11/27) 0.5190 天死亡 31.8%(55/173) 32.9%(48/146) 25.9%(7/27) 0.65颅内出血 37.6%(67/178) 36.7%(55/150) 42.9%(12/28) 0.53无症状性出血 31.5%(56/178) 30.0%(45/150) 39.3%(11/28) 0.38症状性出血 6.2%(11/178) 6.7%(10/150) 3.6%(1/28) >0.99*P 值：连续变量采用两样本 Wilcoxon 检验，分类变量采用 Fisher 精确检验计算。


表 3　90 天良好结局 (mRS 0-2) 的多变量预测因素 (M1 和M2 汇总 ) OR变量分类比较 [95% CI] P*最终血管再通是 vs. 否 30.91[7.82->99.99] <0.0001基线 NIHSS 分数连续 0.83[0.75-0.91] <0.0001年龄，年连续 0.96[0.93-0.99] 0.0073出血是 vs. 否 0.31[0.12-0.81] 0.0145似然比 χ2 检验：P=0.09( 结论：不能拒绝双向交互条件系数为 0 的

假设 )。Hosmer and Lemeshow 拟合度检验：P=0.83( 结论：不能拒

绝数据与模型相配的假设 )。

26

Stroke May 2010

和 PROACT 的数据 [21]。在对 MCA 闭塞患者使用尿

激酶 IA 溶栓治疗的研究中，血管造影显示有 57 例

患者为 MCA M1 闭塞，21 例为 M2 闭塞，22 例为

M3 或 M4 闭塞。与我们的研究相比，该研究报告

了更高的血管再通率 (76%)，更好的 90 天良好结局

(68%)，更低的死亡率 (10%) 以及相似的症状性出血

(7%)。该研究还显示良好的结局与入院时低的卒中

评分 (中位基线NIHSS，14)和更小的年龄 (平均年龄，

61 岁 ) 相关。

IA 溶栓研究中，MCA 卒中患者血管再通情况

由血管造影记录；然而，由 MCA M1 闭塞对单独

M2 闭塞分层的血管再通状态和临床结局并未在这些

随机临床试验中报告 [5,8]。在一个对卒中患者使用尿

激酶 IA 溶栓治疗的研究中，147 例 MCA M1 闭塞和

57 例 M2 闭塞患者的血管再通率 (TIMI II 级和 III 级 )分别为 77.6% 和 63.2%[11]。在该研究中，单独 M2 闭

塞与 M1 闭塞相比，具有更低的血管再通率，这与

我们研究的结果不同。目前尚不清楚这个差异是否

与 IA 溶栓和机械取栓不同的血管内治疗方式相关。

本研究也进一步证实了成功的血管再通与取栓

术后 90 天时得到良好的临床结局相关。我们发现，

在 M1 闭塞和单独 M2 闭塞中，成功的血管再通与

更高的效益风险比相关。单独 M2 闭塞患者比 M1闭塞患者有更好临床结局的倾向。单独 M2 闭塞的

这些有益作用也被一项 IV tPA 溶栓治疗患者的经颅

多普勒超声研究证实 [9]。卒中介入治疗试验 I 和 II的汇总数据显示单独 M2 闭塞患者其良好的临床结

局独立于血管再通状态之外，因为尽管存在不完全

的再通和再灌注，部分 M2 闭塞患者的仍获得良好

的临床结局 [6,7,23]。尚不清楚单独 M2 闭塞患者其良

好的临床结局倾向是否与更高的血管再通率或更小

的缺血区域相关联。可以推测 M2 与 M1 闭塞中，

更多的侧支循环是某一既定病人达到良好临床结局

的可能潜在因素。尽管 M2 组相比 M1 组，存在具

有更好结局的倾向，但这个差异可能因更高的左侧

M2 闭塞频率而抵消 (67.9% vs. 47.3%)。研究的纳入

标准要求必须具有高的基线 NIHSS 分数，因此优势

半球的 M2 闭塞更可能入组。

个例报告提出如果闭塞的 M2 分支无法经 IA 溶

栓开放，则可以用 microsnare 或 Attrater-18 装置进

行机械治疗而重新打开它们 [24,25]。然而，如今并不

推荐使用这些装置进行颅内大动脉血流的恢复。最

表 4　血管再通与未再通患者的比较血管再通血管未再通

(n=113) (n=65) P*年龄中位数，年 (IQR) 73.0(62.0-81.0)(113) 72.0(59-80.0)(65) 0.47女性 54.9%(62/1113) 63.1%(41/65) 0.34高血压 75.2%(85/113) 81.5%(53/65) 0.36糖尿病 28.6%(32/112) 18.5%(12/65) 0.15血脂异常 34.6%(37/107) 35.1%(20/57) >0.99冠状动脉病 45.5%(51/112) 29.0%(18/62) 0.04充血性心力衰竭 21.6%(24/111) 21.5%(14/65) >0.99吸烟 17.9%(19/106) 19.3%(11/57) 0.84房颤 40.7%(46/113) 50.0%(32/64) 0.27血液系统疾病 6.4%(7/110) 6.3%(4/64) >0.99周围血管疾病 11.8%(13/110) 12.7%(8/63) >0.99血糖中位数，mg/dL(IQR) 119.0(105-146)(113) 118.0(103-143)(63) 0.56收缩压中位数，mmHg(IQR) 143.0(130-166)(112) 152.5(138-164)(64) 0.21舒张压中位数，mmHg(IQR) 74.0(63-82)(112) 77.0(65-89)(64) 0.23基线 NIHSS 中位数 (IQR) 17.0(14-22)(113) 19.0(15-23)(65) 0.18左侧 MCA 闭塞 52.2%(59/113) 47.7%(31/65) 0.64起病至腹股沟穿刺时间中位数，小时 (IQR) 4.1(3.1-5.3) 4.5(3.5-5.6) 0.19Merci 前静脉 tPA 失败 17.7%(20/113) 10.8%(7/65) 0.28动脉溶栓治疗 37.2%(42/113) 23.1%(15/65) 0.07静脉或动脉溶栓治疗 46.9%(53/113) 32.3%(21/65) 0.06白种人 85.8%(97/113) 83.1%(54/65) 0.67操作持续时间中位数，小时 (IQR) 1.6(1.0-2.1) 1.8(1.5-2.6) 0.002移除凝块尝试次数中位数 (IQR) 2.0(1-3) 4.0(3-5) <0.001操作并发症 8.0%(9/113) 16.9%(11/65) 0.09临床上操作相关的严重不良反应 2.7%(3/113) 9.2%(6/65) 0.0890 天 mRS ≤ 2 51.9%(54/104) 4.9%(3/61) <0.00190 天死亡 22.0%(24/109) 48.4%(31/64) <0.001症状性出血 2.7%(3/113) 12.3%(8/65) 0.02*P 值：连续变量采用两样本 Wilcoxon 检验，分类变量采用 Fisher 精确检验计算。


27


近，另一个可从缺血性卒中患者颅内大动脉中移出

凝块的治疗工具 -Penumbra 系统，已经获美国食品药

物监督管理局批准通过 [26]。这个血管内的血管再通

治疗也对卒中患者有益，但是它对于单独 M2 卒中及

M1 卒中的效果还未明确报道。另外，颅内放置自胀式

支架是对急性 MCA M1 闭塞的血管再通所做的替代选

择，但其在单独 MCA M2 卒中中的应用却很有限 [27]。

本研究存在一些局限。回顾性收集两个无对照

试验的研究数据并由此进行事后分析。纳入两个试

验的 M2 闭塞患者的样本量小于 M1 闭塞患者。由

于大部分 M2 闭塞患者来自于多中心 MERCI 试验，

因此 M2 闭塞组更好的结局可能是因为操作者从不

断增加的经验中所得知识的以及多中心 MERCI 中应

用的新一代 Merci Retriever 装置的合并的结果。病

例的选择可能存在偏倚。两组基线卒中的严重度是

类似的，这表明只有严重神经功能缺陷的 MCA M2闭塞患者才能被纳入这两个试验。MCA M2 闭塞组

可能纳入的患者有：基线时即有大面积缺血性病灶

的患者；已接受 IV tPA 治疗或伴无效再灌注自发诱

导再通的早期 MCA M1 或曾有过 ICA/MCA 串联状

或 ICA 终端闭塞的患者。这可能解释了类似的 3 月

临床结局而不只是组与组之间卒中的不平衡。最后，

不能从 MERCI 或多中心 MERCI 中获取基线抗血栓

的应用分布，也不能进行分析。

总之，MERCI 和多中心 MERCI 试验的汇总数

据回顾分析结果显示，单独 MCA M2 闭塞患者与

MCA M1 闭塞患者相比，可以从更高的血管再通率

中获益，而且对 Merci Retriever 装置进行再通要求

更少的疏通次数。此外，基于 MCA 闭塞患者汇总

数据的多变量分析，证明了最终的血管再通是操作

后 90 天良好结局最强的预测因素。

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