A Randomized Comparison of Antiplatelet and Anticoagulant Therapy after the Placement of Coronary-Artery Stents
Albert Schömig, M.D., Franz-Josef Neumann, M.D., Adnan Kastrati, M.D., Helmut Schühlen, M.D., Rudolf Blasini, M.D., Martin Hadamitzky, M.D., Hanna Walter, M.D., Eva-Maria Zitzmann-Roth, M.D., Gert Richardt, M.D., Eckhard Alt, M.D., Claus Schmitt, M.D., and Kurt Ulm, Ph.D.
Background The clinical benefit of coronary-artery stentingperformed in conjunction with coronary angioplasty is limitedby the risk of thrombotic occlusion of the stent as well ashemorrhagic and vascular complications of intensive anticoagulation.We compared antiplatelet therapy with conventional anticoagulanttherapy with respect to clinical outcomes 30 days after coronary-arterystenting.
Methods After successful placement of Palmaz–Schatz coronary-arterystents, 257 patients were randomly assigned to receive antiplatelettherapy (ticlopidine plus aspirin) and 260 to receive anticoagulanttherapy (intravenous heparin, phenprocoumon, and aspirin). Theprimary cardiac end point was a composite measure reflectingdeath from cardiac causes or the occurrence of myocardial infarction,aortocoronary bypass surgery, or repeated angioplasty. The primarynoncardiac end point comprised death from noncardiac causes,cerebrovascular accident, severe hemorrhage, and peripheralvascular events.
Results Of the patients assigned to antiplatelet therapy, 1.6percent reached a primary cardiac end point, as did 6.2 percentof those assigned to anticoagulant therapy (relative risk, 0.25;95 percent confidence interval, 0.06 to 0.77). With antiplatelettherapy, there was an 82 percent lower risk of myocardial infarctionthan in the anticoagulant-therapy group, and a 78 percent lowerneed for repeated interventions. Occlusion of the stented vesseloccurred in 0.8 percent of the antiplatelet-therapy group andin 5.4 percent of the anticoagulant-therapy group (relativerisk, 0.14; 95 percent confidence interval, 0.02 to 0.62). Aprimary noncardiac end point was reached by 1.2 percent of theantiplatelet-therapy group and 12.3 percent of the anticoagulant-therapygroup (relative risk, 0.09; 95 percent confidence interval,0.02 to 0.31). Hemorrhagic complications occurred only in theanticoagulant-therapy group (in 6.5 percent). An 87 percentreduction in the risk of peripheral vascular events was observedwith antiplatelet therapy.
Conclusions As compared with conventional anticoagulant therapy,combined antiplatelet therapy after the placement of coronary-arterystents reduces the incidence of both cardiac events and hemorrhagicand vascular complications.
Intracoronary stenting is an accepted treatment for vessel closureafter percutaneous transluminal coronary angioplasty (PTCA).1,2,3Moreover, as compared with balloon angioplasty, elective stentplacement reduces the rate of restenosis.4,5 However, thromboticocclusion of the stent, as well as hemorrhagic and peripheralvascular complications due to the intensive anticoagulationrecommended for the first few weeks after the procedure, seriouslylimits the benefits of intracoronary stenting.6,7 Recent studieswith intravascular ultrasonography or coated stents suggestthat anticoagulant therapy may be dispensable.8,9 We recentlyidentified a high level of surface expression of the induciblefibrinogen receptor on platelets as a strong independent predictorof thrombosis in the stented vessel, whereas monitoring of anticoagulationwas not predictive.10 These findings suggest that effectiveinhibition of platelet function may be superior to anticoagulanttherapy in preventing occlusion of the stent.
We therefore conducted the Intracoronary Stenting and AntithromboticRegimen trial, a prospective, randomized study designed to comparethe early outcome of patients treated with two different antithromboticregimens after the placement of coronary-artery stents: combinedantiplatelet therapy with ticlopidine plus aspirin, and conventionalanticoagulant therapy with intravenous heparin, phenprocoumon(a coumarin derivative), and aspirin.
Methods
Selection of Patients
The study population consisted of patients in whom intracoronarystents were successfully placed after PTCA at our institution.The indications for stenting were extensive coronary-arterydissection after PTCA, complete vessel closure, residual stenosisof 30 percent or more of the vessel diameter, and lesions invenous bypass grafts. All patients in whom stenting was successful(i.e., in whom the stent was placed at the desired positionand there was less than 30 percent residual stenosis) who gavetheir written, informed consent to participate in the studywere eligible for randomization, if they had no contraindicationsto the use of aspirin, ticlopidine, or phenprocoumon and noabsolute indication for anticoagulant therapy. We excluded patientsin whom stenting was intended primarily as a bridge to aortocoronarybypass grafting, who had cardiogenic shock, or who had neededmechanical ventilation before undergoing PTCA. All eligiblepatients were randomly assigned to a treatment group, by meansof sealed envelopes, immediately after the intervention. Therandomization sequence was specified before the study began.The study was carried out according to the principles of theDeclaration of Helsinki and was approved by our institutionalethics committee.
Placement of Coronary Stents
Stents were implanted as previously described.3 Before undergoingPTCA, patients received heparin (15,000 units) and aspirin (500mg) intravenously. Conventional rapid-exchange balloon catheterswere used for angioplasty (Express, Scimed, Verviers, Belgium).The 7-mm or the articulated 15-mm standard Palmaz–Schatzstent (Johnson and Johnson, Warren, N.J.) was folded by handonto the angioplasty balloon. Balloon catheters for the deploymentof stents were chosen with the intention of using a slightlyoversized balloon. In addition, relatively noncompliant ballooncatheters (High Energy, Boston Scientific, Hilden, Germany)were used in most of the patients for higher-pressure dilation.If necessary, multiple stents were used for complete coverageof the area of dissection. Intravascular ultrasonography wasnot used routinely.
The arterial sheath was removed when the partial-thromboplastintime fell below 60 seconds, typically within three hours afterthe procedure. After manual compression of the groin, carriedout as long as necessary for local hemostasis (at least 30 minutes),a pressure bandage was applied. No other specific devices topromote hemostasis were used.
Antiplatelet and Anticoagulant Regimens
Immediately after the application of the pressure bandage, acontinuous heparin infusion, adjusted to achieve a partial-thromboplastintime of 80 to 100 seconds, was started in all patients. In patientsassigned to antiplatelet therapy, heparin was discontinued 12hours after stent placement. Ticlopidine therapy (250 mg twicea day; Tiklyd, Sanofi–Winthrop, Munich, Germany) was startedimmediately after the procedure and continued for four weeks.In patients assigned to anticoagulant therapy, phenprocoumontherapy (Marcumar, Hoffmann–LaRoche, Granzach-Wyhlen,Germany) was initiated immediately after placement of the stentand continued for four weeks. The heparin infusion was continuedfor 5 to 10 days, until a stable degree of oral anticoagulationwas achieved. The target international normalized ratio (INR)was between 3.5 and 4.5, a range selected on the basis of ourprevious experience.3 The partial-thromboplastin time and INRwere monitored twice daily. All patients in both groups receivedaspirin (100 mg twice a day) throughout the study.
Angiographic Analysis
Coronary angiography was performed with a digital angiographicsystem (Hicor, Siemens, Erlangen, Germany). Qualitative andquantitative analysis was performed at a digital angiographicwork station (AWOS, Siemens) by operators who were unaware ofthe study groups to which the patients were assigned.
Follow-Up
All patients remained in the hospital for at least 10 days toensure identical observation after the stenting procedure. Completeblood counts and enzyme measurements were performed three timeseach week. Electrocardiograms were recorded daily. Duplex ultrasonographyof the groin was performed routinely by operators unaware ofthe patients' antithrombotic regimens. Coronary angiographywas repeated in patients with suspected myocardial ischemia.All patients were seen as outpatients one month after discharge.
Events and End Points
This study was designed to assess the incidence of two typesof clinical events — cardiac events, and vascular andbleeding events — in the 30 days after placement of thestent. We defined two summary variables for the primary clinicalend points, cardiac and noncardiac, since these two types ofevents may reflect different responses to the two antithromboticregimens.
A primary cardiac end point was defined as death due to cardiaccauses or the occurrence of myocardial infarction, aortocoronarybypass surgery, or repeated PTCA of the stented vessel, whicheveroccurred first. All deaths were considered due to cardiac causesunless an autopsy established a noncardiac cause. The diagnosisof acute myocardial infarction was based on typical chest painlasting more than 30 minutes, abnormal Q waves not present onthe base-line electrocardiogram, or an increase in the creatinekinase concentration to twice the upper limit of normal, witha concomitant rise in the creatine kinase MB isoenzyme. Thediagnosis of recurrent myocardial infarction was also basedon an increase of more than 30 percent in the creatine kinaseconcentration.
A primary noncardiac end point was defined as death from anynoncardiac cause or the occurrence of cerebrovascular accidentor a severe peripheral vascular or hemorrhagic event. A diagnosisof cerebrovascular accident was made only when prolonged neurologicdeficit was present. Severe peripheral vascular events werepseudoaneurysms or arteriovenous fistulas at the access siterequiring surgery or prolonged, ultrasound-guided compression.11The diagnosis was always based on color-coded duplex ultrasonographyperformed by physicians blinded to the patient's study-groupassignment. Severe hemorrhagic events were defined as bleedingcomplications requiring surgery or transfusion, or bleedingassociated with objective signs of organ dysfunction. Bloodtransfusion was considered indicated at hemoglobin concentrationsbelow 8 g per deciliter.
We also defined two secondary end points: a combined clinicalend point comprising all cardiac and noncardiac events, andthe angiographic end point of occlusion in the stented vessel.
Statistical Analysis
All data were analyzed on an intention-to-treat basis. The prospectivelydetermined sample size was confirmed in a scheduled interimanalysis at six months. Discrete variables, expressed as counts,were compared by means of Fisher's exact test.12 Continuousdata, expressed as means ±SD, were analyzed with unpaired,two-tailed t-tests. The main analysis focused on comparisonsof the two groups with respect to the primary cardiac and noncardiacend points. In a second step, the two groups were compared withrespect to secondary end points. Finally, data were analyzedwith Fisher's exact test, and relative risks with 95 percentconfidence intervals were computed for antiplatelet therapyas compared with conventional anticoagulant therapy.12,13 Cumulative-event-ratecurves were used for graphic presentation of the differencesbetween the groups and of the time course of events. Differenceswere considered to be statistically significant when the P valueswere less than 0.05.
Results
Characteristics of the Patients
Among 626 consecutive patients who underwent stent implantationat our institution from October 1994 through September 1995,517 patients were eligible for enrollment and consented to berandomly assigned to treatment; 257 patients were assigned toantiplatelet therapy and 260 to anticoagulant therapy. No patientwas excluded after randomization. As Table 1 shows, there wereno significant differences between the groups in base-line characteristics.
Table 1. Base-Line Clinical Characteristics of the Patients, According to Study Group.
The angiographic and procedural data are summarized in Table 2.There was no significant difference between the groups withrespect to the distribution of target vessels, characteristicsof the target lesions, or luminal and balloon diameters.
Table 2. Angiographic and Procedural Characteristics, According to Study Group.
Cardiac Events
The clinical outcomes during the first 30 days after implantationof the stents are summarized in Table 3. Table 4 lists the cardiacevents individually. A primary cardiac end point was reachedby 16 patients in the anticoagulant-therapy group (6.2 percent),as compared with 4 in the antiplatelet therapy group (1.6 percent).This difference resulted from a decrease of 82 percent in theincidence of myocardial infarction and a 78 percent lower rateof reintervention (coronary-artery bypass grafting or repeatedPTCA) among patients assigned to antiplatelet therapy.
Table 4. Individual Cardiac Events and Occlusions of Stented Vessels.
As shown in Figure 1, all cardiac events among patients assignedto antiplatelet therapy occurred within the first week. Amongthose who received anticoagulant therapy, cardiac events occurredup to day 26; most of them occurred after day 3. During thefirst three days after stenting, the rate of cardiac eventswas similar in the two groups.
Figure 1. Cumulative Incidence of Cardiac and Noncardiac Events in the Study Groups.
A cardiac event was defined as death due to cardiac causes or the occurrence of myocardial infarction, bypass surgery, or repeated balloon angioplasty, whichever occurred first. A noncardiac event was defined as death due to noncardiac causes or the occurrence of cerebrovascular accident or severe hemorrhagic and peripheral vascular complications, whichever occurred first.
Noncardiac Events
As Table 3 shows, there were significantly fewer noncardiacevents in the antiplatelet-therapy group than in the group thatreceived anticoagulant therapy (P<0.001); there were no severehemorrhagic events in the antiplatelet-therapy group (P<0.001)and fewer peripheral vascular events (P = 0.001). One patientreceiving antiplatelet therapy had an ischemic stroke confirmedby computed tomography. Severe hemorrhagic events occurred duringall phases of anticoagulant therapy: four during heparin treatmentbefore oral anticoagulation became effective, five during theperiod of overlap between intravenous and oral therapy, andeight after the withdrawal of heparin. The bleeding was gastrointestinalin three patients, urogenital in three, in the respiratory tractin two, retroperitoneal in three, in the groin in five, andin both the gastrointestinal tract and the groin in one. Asto reversible organ dysfunction associated with bleeding, threepatients had renal dysfunction, three had neurologic symptomsdue to compression of a nerve by a retroperitoneal or groinhematoma, and one had pulmonary bleeding with respiratory insufficiency.Twelve patients receiving anticoagulant therapy required bloodtransfusion, and two required surgery (one for gastric bleedingand one for groin complications). All pseudoaneurysms and thearteriovenous fistula were successfully treated with ultrasound-guidedcompression. The cumulative rate of noncardiac events is shownin Figure 1. All noncardiac events in the patients receivingantiplatelet therapy occurred within the first four days afterstenting. Such events occurred up to 28 days after stentingin those assigned to anticoagulant therapy.
Secondary End Points
The cumulative rate of any cardiac or noncardiac event (thecombined clinical end point) was significantly lower among thepatients assigned to antiplatelet therapy than among those inthe anticoagulant-therapy group; the reduction in risk was 84percent (Table 3). The cumulative rate of clinical events isshown in Figure 2. Among the patients given antiplatelet therapy,the last event occurred on day 7, whereas among those givenanticoagulant therapy, complications continued to occur throughoutthe 30-day follow-up period.
Figure 2. Cumulative Incidence of Any Cardiac or Noncardiac Event, Whichever Occurred First.
The dotted lines represent 95 percent confidence intervals.
The angiographic end point of occlusion of the stented vesseloccurred in 14 patients assigned to anticoagulant therapy and2 patients assigned to antiplatelet therapy. Progressive dissectionwith subsequent vessel closure outside the stented segment occurredin three patients within the first three days. Thrombotic occlusionof the stent occurred in 13 patients assigned to anticoagulanttherapy and in none of the patients assigned to antiplatelettherapy. The association of occlusion of the stented vesselwith other cardiac events is shown in Table 4. The median intervalbetween implantation and thrombosis in the stented vessel wasseven days. In 3 of the 13 patients who had thrombosis, anticoagulationwas inadequate within 12 hours before the event; anticoagulantagents had been purposely withheld in 1 patient because of pulmonarybleeding; in 1 patient the target partial-thromboplastin timehad not been reached 3 hours after removal of the sheath. Inthe third patient, the partial-thromboplastin time had droppedto 48 seconds during the period of overlapping heparin and phenprocoumontherapy while the INR was still below the therapeutic range.
Discontinuation of the Assigned Therapy
In the anticoagulant-therapy group, bleeding and peripheralvascular complications necessitated the discontinuation of anticoagulantsin 24 patients an average of 8.5 days after the intervention.The subsequent clinical course was uneventful in all but onepatient, who had subacute thrombosis in the stented vessel.In four patients assigned to antiplatelet therapy, ticlopidinewas discontinued without subsequent complications; one of thesepatients had an allergic skin reaction, and three had evidenceof substantial left ventricular thrombus on the echocardiogramand subsequently required full anticoagulation.
Discussion
Our prospective, randomized trial compared antiplatelet andanticoagulant therapy after the placement of intracoronary stentsin a large cohort of patients. The study population encompassedthe entire spectrum of symptomatic coronary artery disease,including patients with stable angina and acute ischemic syndromes,as well as a substantial number of patients with complex coronary-arterylesions. Our data show that, as compared with anticoagulanttherapy, antiplatelet therapy was associated with a lower rateof noncardiac events (including hemorrhagic and peripheral vascularcomplications), a lower rate of cardiac events (such as death,myocardial infarction, and the need for repeated interventions),and in particular, a lower incidence of thrombotic occlusionof the stented vessel. The incidence of severe hemorrhagic andperipheral vascular events was significantly lower with antiplatelettherapy, for a risk reduction of 91 percent. Our most notablefinding was the significantly lower rate of cardiac events inthe group that received antiplatelet therapy, which translatedinto a reduction of 75 percent in the risk of such events. Thisreduction was due to the significantly lower rates of myocardialinfarction and reintervention. Rates of cardiac events in bothgroups were similar to those of previously studied patientsgiven antiplatelet therapy (0 to 1.1 percent)8,15 and anticoagulanttherapy (5.9 to 6.9 percent).3,4,5
Our data show that the reduction in the incidence of cardiacevents with antiplatelet therapy can be attributed largely toa reduction in the frequency of thrombotic occlusion of thestented vessel. Several mechanisms may account for this outcome,including possible thrombogenic effects of phenprocoumon orheparin and antithrombotic effects of ticlopidine (since thepatients in both groups received aspirin). Phenprocoumon, likewarfarin, induces a decrease in the natural anticoagulants proteinC and protein S before the reduction in prothrombin occurs.16This factor is unlikely to have played a major part in our results,however, since most thrombotic occlusions of stents occurredeither during intravenous heparin treatment or in a later phaseof phenprocoumon therapy. The differences between the two regimensappear to be more readily explained by their differential effecton platelet function. Synergistically with aspirin, ticlopidineinterferes with platelet activation by strong agonists; it doesso by limiting exposure of fibrinogen receptors and plateletaggregation.17,18 In contrast, heparin stimulates fibrinogen-receptoractivation and -degranulation in platelets,19 and it may induceIgG antibodies that cause platelet activation and thrombocytopenia.20Evidence for this hypothesis comes from a recent study showingprogressive activation of platelets after coronary-artery stentingin patients who received anticoagulant agents; in patients givencombined antiplatelet therapy, on the contrary, the surfaceexpression of activated fibrinogen receptors decreased duringthe first few days after stenting.21 The latter finding is inaccord with the known delay in the onset of action of ticlopidine17and may explain the different rates of thrombotic occlusionof the stented vessels after day 3 in our study. Within thefirst two days, however, the rates of cardiac events did notdiffer significantly between the groups. In this early post-interventionperiod, subacute occlusion of the stented vessel is caused primarilyby residual dissection.
Severe neutropenia has been noted in 0.8 percent of patientsreceiving long-term ticlopidine therapy; in all cases it hasoccurred in the second and third months of therapy and is fullyreversible after the discontinuation of ticlopidine.22 Althoughneutropenia developed in none of our patients, this complicationmay have been missed after discharge from the hospital whenblood-cell counts were not monitored in most patients. However,published data suggest that neutropenia would be of little clinicalimportance because of the short duration of therapy.22,23
Antiplatelet therapy after stenting has been advocated alongwith the use of intravascular ultrasonography and high balloonpressures.8 Our study was not intended to assess the specificrole of these procedural elements. Although high balloon pressureswere not required by the protocol, the mean values of 15.8 and16.0 atmospheres for the procedures in patients assigned toanticoagulant and antiplatelet therapy, respectively, comparewell with the recently reported value of 14.9 atmospheres.8We rarely performed ultrasound studies during the procedures.Although the outcome of patients in our study who received aspirinplus ticlopidine is similar to results reported previously withultrasound-guided stenting and antiplatelet therapy,8 this similaritydoes not rule out the possibility of further benefit with theaddition of ultrasound guidance.
The study protocol included a hospital stay of at least 10 daysafter the procedure. Such in-hospital surveillance of all patientsguaranteed a comprehensive assessment and detailed analysisof the time course of complications. In the anticoagulant-therapygroup, two additional complications occurred more than threeweeks after the procedure, whereas with antiplatelet therapy,only one additional event occurred later than day 4 after theprocedure. On the basis of these data, a shorter hospital staymay be safe for patients receiving antiplatelet therapy.
The fact that patients and physicians were not blinded to thetreatment assignment represents a further limitation of ourstudy. Consequently, bias on the part of investigators or patientscannot be fully excluded as a factor influencing managementafter stenting. However, bias in the angiographic analyses andin surveillance of the access site was precluded by blindingof the personnel who performed these assessments. As an addedmeasure to minimize investigator bias, definitions of eventswere specified in the protocol and based on objective criteria.
Although previous studies have established that the outcomeis more favorable after elective coronary-stent placement thanafter conventional balloon angioplasty,4,5 widespread clinicaluse of the technique has been limited by the risk of thromboticocclusion of the stented vessel and of complications of theanticoagulant regimen. Our results indicate that the risk–benefitratio for stenting may be substantially improved by the useof combined antiplatelet therapy. The marked decrease in thromboticstent occlusions with antiplatelet therapy implies that plateletshave a crucial role in the pathogenesis of this complication.
Supported in part by grants from Siemens Medical Systems, Scimed–BostonScientific, and Johnson and Johnson Interventional Systems.
Source Information
From the 1. Medizinische Klinik (A.S., F.-J.N., A.K., H.S., R.B., M.H., H.W., E.-M.Z.-R., G.R., E.A., C.S.), and the Institut für Medizinische Statistik und Epidemiologie (K.U.), Klinikum rechts der Isar, Technische Universität München, Munich, Germany.
Address reprint requests to Dr. Schömig at the 1. Medi-zinische Klinik der Technischen Universität München, Klinikum rechts der Isar, Ismaninger Strasse 22, 81675 Munich, Germany.
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-degranulation in platelets,19 and it may induce IgG antibodies that cause platelet activation and thrombocytopenia.20 Evidence for this hypothesis comes from a recent study showing progressive activation of platelets after coronary-artery stenting in patients who received anticoagulant agents; in patients given combined antiplatelet therapy, on the contrary, the surface expression of activated fibrinogen receptors decreased during the first few days after stenting.21 The latter finding is in accord with the known delay in the onset of action of ticlopidine17 and may explain the different rates of thrombotic occlusion of the stented vessels after day 3 in our study. Within the first two days, however, the rates of cardiac events did not differ significantly between the groups. In this early post-intervention period, subacute occlusion of the stented vessel is caused primarily by residual dissection. 
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