Practical Issues on the Use of Enoxaparin in Elective and Emergent Percutaneous Coronary Intervention

ABSTRACT: Unfractionated heparin (UFH) has been the standard choice of adjunctive antithrombotic therapy during elective percutaneous coronary intervention (PCI). Evidence is emerging that intravenous (IV) enoxaparin may offer similar benefits to UFH in terms of ischemic events or death, but with the benefit of reduced major bleeding risk. In addition, enoxaparin has pharmacological and practical advantages that can simplify patient management. This review considers the current evidence for IV enoxaparin in the management of patients requiring elective PCI, as well as practical aspects of patient management.


J INVASIVE CARDIOL 2008;20:482–489

Unfractionated heparin (UFH) has been the standard for adjunctive antithrombotic therapy during percutaneous coronary intervention (PCI). However, because of its limitations, such as unpredictable pharmacokinetics, the need for frequent laboratory monitoring of the anticoagulant effects and the potential to stimulate platelet aggregation,1 alternative treatments have been explored. Among the alternatives tested by large randomized trials in the setting of nonurgent PCI are the direct thrombin inhibitor bivalirudin,2 the factor-Xa inhibitor fondaparinux3 and the low-molecular-weight heparin (LMWH) enoxaparin.4

Conventionally, enoxaparin has been administered by the subcutaneous (SC) route in most clinical settings. In non-ST-segment elevation myocardial infarction (NSTEMI), six large-scale randomized trials compared the efficacy of SC enoxaparin with intravenous (IV) UFH, with 17–47% of patients undergoing urgent PCI. A meta-analysis of 21,946 patients, which included these six trials, demonstrated that SC enoxaparin (1 mg/kg every 12 hours [q12hr]) is more effective than IV UFH in preventing myocardial infarction (MI) or death (10.1% vs. 11.0%, respectively; odds ratio [OR] 0.91; 95% confidence interval [CI] 0.83–0.99), with no difference in the incidence of major bleeding (4.7% vs. 4.5%, respectively; OR 1.04; 95% CI 0.89–1.30).5 The most recent of these six trials, the Superior Yield of the New strategy of Enoxaparin, Revascularization and Glycoprotein IIb/IIIa inhibitors (SYNERGY) trial, demonstrated no difference in the efficacy of enoxaparin 1.0 mg/kg q12hr SC compared with IV UFH in the prevention of death or nonfatal MI (14.0% vs. 14.5%, respectively; p = 0.40), with an increased rate of thrombolysis in myocardial infarction (TIMI) major bleeding (9.1% vs. 7.6%; p = 0.008).6 In addition, a large randomized, double-dummy trial in patients receiving fibrinolysis for ST-segment elevation MI (STEMI) demonstrated that enoxaparin (initial IV bolus 30 mg followed by 1.0 mg/kg q12hr SC) is more effective than IV UFH in preventing death, reinfarction or urgent revascularization (11.7% vs. 14.5%, respectively; p < 0.001), with an increased rate of major bleeding (2.1% vs. 1.4%, respectively; p < 0.001).7

In nonurgent PCI, emerging data suggest potential advantages of IV-administered enoxaparin across a range of doses that allow for greater flexibility in individual patient case management. In particular, the Safety and Efficacy of Enoxaparin in Percutaneous Coronary Intervention: An International Randomized Evaluation (STEEPLE) trial showed that IV enoxaparin in elective PCI had a better safety profile than UFH, with similar rates of ischemic events or death, and has practical advantages that simplify patient management.4

An evaluation of the relative clinical profiles of these antithrombotic drugs is beyond the scope of this review. This paper provides the physician who is looking to use enoxaparin in nonurgent PCI with a discussion on practical issues such as its IV administration and dosing, and the transition of patients already receiving SC enoxaparin to IV enoxaparin.

Efficacy and Safety of IV Enoxaparin in Elective PCI

Small-scale studies and meta-analysis. A number of small-scale feasibility studies have shown that single IV bolus injections of enoxaparin are feasible in the management of patients undergoing elective PCI, with or without concomitant glycoprotein (GP) IIb/IIIa inhibitors. Table 1 provides a summary of studies that examined the efficacy and safety profile of IV enoxaparin at a range of doses from 0.5 mg/kg to 1.0 mg/kg.8–11 An earlier descriptive dose-ranging study evaluated higher doses of enoxaparin (1.5 mg/kg and 1.25 mg/kg) when used alone, or 1.0 mg/kg in combination with GP IIb/IIIa inhibitors.12 Small studies have also compared a range of IV bolus doses of enoxaparin with the use of IV UFH in patients undergoing PCI, although none of these studies were powered to detect significant differences (Table 2).4,12–18

In a recent meta-analysis of these and other small-scale studies, LMWH (81% enoxaparin) was found to be potentially more effective than UFH in terms of the combined endpoint of death, MI or urgent revascularization (5.8% vs. 7.6%, respectively; p = 0.03) and was associated with reduced rates of major bleeding (0.6% vs. 1.8%, respectively; p = 0.0001).19 Despite the accumulated evidence, there was a need for a large randomized clinical trial evaluating the use of IV enoxaparin in the setting of elective PCI. In addition, it was necessary to explore the effects of different doses in this scenario.

The STEEPLE trial. The most recent and largest-scale evidence to show that IV enoxaparin offers an attractive alternative to IV UFH during elective PCI has come from the multicenter STEEPLE trial.4 STEEPLE involved 3,528 patients requiring nonurgent PCI who were randomized to one of three treatment arms: enoxaparin 0.5 mg/kg IV; enoxaparin 0.75 mg/kg IV; or IV UFH (70–100 IU without GP IIb/IIIa inhibitors, or 50–70 IU with GP IIb/IIIa inhibitors). Previous trials had evaluated single IV doses of enoxaparin of 0.5 mg/kg,8,11 0.75 mg/kg,9,16–18 or 1 mg/kg.9, 10,13–15 The meta-analysis of randomized studies reported that the 0.5 mg/kg dose resulted in fewer efficacy endpoints and bleeding events compared with the 0.75 mg/kg dose.19 Consequently, both the 0.5 mg/kg and the 0.75 mg/kg doses were investigated in the STEEPLE trial.19 The use of concomitant GP IIb/IIIa inhibitors was allowed in any treatment arm at the discretion of the physician.

The trial data safety and monitoring committee recommended that enrollment be discontinued in the enoxaparin 0.5 mg/kg arm based on global differences in all-cause mortality between the three treatment groups. As a result of this, enrollment in this arm was discontinued just short of full study completion, but did not affect the power of the study. However, at the end of the study, it must be stressed that data analysis showed no significant mortality difference in the group of patients treated with enoxaparin 0.5 mg/kg (10 patients [1.0%]) compared with enoxaparin 0.75 mg/kg (3 patients [0.2%]; p = 0.06), or compared with UFH (5 patients [0.4%]; p = 0.07). Four deaths in the 0.5 mg/kg group were considered to be possibly related to treatment.

The primary endpoint of protocol-defined noncoronary artery bypass graft-related major or minor bleeding at 48 hours occurred less frequently with enoxaparin 0.5 mg/kg than with UFH (5.9% vs. 8.5%, respectively; p = 0.01), but the difference did not reach statistical significance at a dose of 0.75 mg/kg (6.5% vs. 8.5%, respectively; p = 0.051). Major bleeding occurred less frequently in both the 0.5 mg/kg and 0.75 mg/kg enoxaparin groups compared with UFH (1.2% and 1.2% vs. 2.8%, respectively; p = 0.004 and p = 0.007). This reduction in major bleeding events was achieved without any increase in ischemic events. The rate of death, nonfatal MI, or urgent revascularization was not significantly different between groups (6.2% and 6.8% vs. 5.8%, respectively; p = 0.51 and p = 0.30) (Table 2).

The 1-year results of the STEEPLE trial demonstrated low mortality rates, which were similar between patients receiving enoxaparin 0.5 mg/kg or 0.75 mg/kg and UFH (2.3% and 2.2% vs. 1.9%, respectively; p = 0.41 and p = 0.72). Ischemic events up to 30 days after PCI were the strongest independent predictor of 1-year mortality. Other independent predictors included major bleeding up to 48 hours post-PCI and high-risk patient characteristics.20

Bleeding Complications

The STEEPLE trial demonstrated that enoxaparin reduced the relative risk of major bleeds by 57% compared with UFH, with comparable reductions in ischemic events between the two drugs.4 Minimizing bleeding is increasingly seen as a major objective of antithrombotic therapy during PCI. Alongside reductions in death, MI and repeated revascularizations, major bleeding was a key outcome measure in major clinical studies such as the Randomized Evaluation in PCI Linking Angiomax to Reduced Clinical Events (REPLACE)-2 trial, the Fifth Organization to Assess Strategies in Acute Ischemic Syndromes (OASIS-5) study and STEEPLE.2,4,21 The patient undergoing nonurgent PCI is typically at the lower end of the spectrum for risk of ischemic events, which makes bleeding events in such patients relatively more important.

A recent meta-analysis of thirteen trials including 7,318 patients showed that the use of IV LMWH during PCI is associated with a significant reduction in major bleeding events compared with UFH, without compromising outcomes on hard ischemic endpoints. In this study, a total of 4,201 patients (57.4%) received LMWH, and 3,117 patients (42.6%) received UFH. IV LMWH use was associated with a significant reduction in the risk of major bleeding compared with UFH (OR 0.57; 95% CI 0.40–0.82). A trend toward a reduction in minor bleeding was also observed among LMWH-treated patients (OR 0.75; 95% CI, 0.47–1.20). Similar efficacy was observed between LMWH and UFH regarding the double endpoint of death or MI (OR 0.99; 95% CI 0.79–1.24). There were no significant differences in the incidence of the individual endpoints of death, MI and urgent revascularization between patients receiving LMWH and those receiving UFH.22

Practical Advantages of Enoxaparin over UFH in Elective PCI

Anticoagulant levels. The unpredictable pharmacodynamics of UFH makes it essential to monitor anticoagulant activity to ensure it is within therapeutic range.1 The pharmacodynamic profile of LMWHs, such as enoxaparin, are more predictable and laboratory monitoring of anticoagulant effects is generally not required, simplifying patient management.1

Moreover, more patients achieve target anticoagulation levels when receiving enoxaparin than when given UFH. For enoxaparin, it has been reported that 93% of patients achieved anti-Xa activity above the lower limit of 0.5 IU/mL,23 whereas 70% of patients administered UFH achieved a target aPTT above 60 seconds (sec).24 In a direct comparison in the STEEPLE trial, 78.8% and 91.7% of patients in the 0.5 mg/kg and 0.75 mg/kg enoxaparin treatment arms, respectively, achieved a target anti-Xa activity level of 0.5–1.8 IU/mL. A significantly lower percentage of UFH patients, 19.7%, reached their predefined activated clotting time (ACT) targets of 300–350 sec if no GP IIb/IIIa inhibitor was given, or 200–300 sec for patients also receiving GP IIb/IIIa therapy (p < 0.001 for both comparisons).4 Thus, enoxaparin achieves target anticoagulation levels more reliably than UFH.

Additionally, of patients in the STEEPLE trial receiving UFH, 16.5% received at least one additional bolus because of a low ACT, whereas at least one additional bolus of enoxaparin was administered during a prolonged procedure (> 2 hours) in 0.6% of patients receiving 0.5 mg/kg enoxaparin, and 0.2% of patients receiving 0.75 mg/kg of enoxaparin.

Sheath removal. Another reported advantage of IV enoxaparin over IV UFH is that the use of enoxaparin 0.5 mg/kg allows immediate (or at least within an hour) sheath removal after PCI.4,8,25 When IV UFH is used as anticoagulant therapy in PCI, sheath removal must be delayed until such time as the ACT reaches a maximum of 150–180 sec to avoid high bleeding risks.26 This requires ongoing assessment of ACT and means that, generally, sheaths remain in place for 4–6 hours after PCI with UFH.27,28

In a study involving 53 patients with stable coronary disease undergoing elective PCI, immediate sheath removal by manual compression was successful and without bleeding complications immediately post PCI in 96% of patients pre-treated with aspirin and clopidogrel and given a single IV dose of 0.5 mg/kg enoxaparin 10 minutes before PCI.25 In the STEEPLE study, the median time-to-sheath removal was 54 minutes with enoxaparin 0.5 mg/kg, 194 minutes with enoxaparin 0.75 mg/kg, and 144 minutes with UFH. This represents a significantly shorter time-to-sheath removal in patients who received enoxaparin 0.5 mg/kg (p < 0.001).4

The ability to remove sheaths immediately after PCI both simplifies the practicalities of the procedure and has clinical benefits such as reduced bleeding risk and improved comfort for the patient.27,29 Bleeding risk in the form of oozing as a result of high residual anticoagulation is elevated shortly after PCI and diminishes over time, but with time, the bleeding risk in the form of large-sized access site hematomas increases.27

Dosing of Enoxaparin in Nonurgent PCI

An initial experience using the monitoring of anti-Xa activity levels documented that enoxaparin (1 mg/kg q12hr SC) for at least 48 hours achieved anti-Xa levels > 0.5 IU/mL in 97.6% of studied patients.30 Although the target for LMWH anticoagulant activity in PCI has not been clearly established, anti-Xa activity levels ranging from 0.5–1.8 IU/mL have been targeted in studies involving the administration of IV enoxaparin for PCI such as the Pharmacokinetics of Enoxaparin in PCI (PEPCI) study,31 the Evaluating Enoxaparin Clotting Times (ELECT) study,32 the TIMI-11A study,33 and STEEPLE.4 The need to achieve an anti-Xa activity level of at least 0.5 IU/mL was shown in a study of 803 unstable angina/NSTEMI patients that demonstrated a 3-fold increase in mortality in patients with anti-Xa activity levels < 0.5 IU/mL compared with the patients in a target range of 0.5–1.2 IU/mL (p = 0.004). Anti-Xa activity up to 1.8 IU/mL did not predict major bleeding complications.23 As target anti-Xa activity levels are reliably reached with enoxaparin,4 monitoring the anti-Xa level is generally not necessary.

However, there are instances where monitoring could be beneficial or helpful, particularly when SC enoxaparin has been used previously. In clinical practice, some patients may have received < 3 SC doses of enoxaparin, or there might be uncertainty regarding the number or timing of the last dose received. Monitoring has shown that at least 3–4 SC doses30,34 are required prior to PCI if only SC enoxaparin was given. If in doubt, a 0.3 mg/kg IV booster dose, added to the previous SC doses, would ensure adequate anticoagulation for PCI.32,34–36

SC and IV administration. The route of administration affects the onset and duration of activity of enoxaparin, with IV dosing offering a more rapid onset and termination of action and SC administration providing a more sustained anticoagulant effect. In the setting of PCI, IV injection has the advantage of rapidly achieving an anticoagulant effect for the duration of the procedure and not protracting beyond the time when antithrombotic activity is required.

Enoxaparin activity, as measured by anti-Xa levels, achieves peak effect within 10 minutes of an IV injection, irrespective of whether patients are receiving additional medications including GP IIb/IIIa inhibitors and clopidogrel.8,25,34,37 Levels of anti-Xa activity remain within the target range for the appropriate time required for typical PCI procedures. Following enoxaparin 0.75 mg/kg IV, anti-Xa activity decreases to below therapeutic levels (< 0.5 IU/mL) around 3–4 hours after injection.37,38 For an enoxaparin dose of 0.5 mg/kg IV, the time to subtherapeutic levels is shortened to 1–2 hours, and following administration of a 1.0 mg/kg dose, this time is prolonged to 4 hours.25,38

After a SC injection of enoxaparin, the peak time to effective anticoagulation is delayed such that maximum anti-Xa activity levels are not seen until 3–5 hours after drug administration.39 Stable anticoagulation levels suitable for performing PCI can be reached after ≥ 3 SC injections of enoxaparin 1 mg/kg q12hr;34 and < 3 SC injections do not provide therapeutic levels to support PCI.34 Clinical data from the SYNERGY trial suggest that there may be an increased risk of death or MI associated with PCI performed within the first few hours after a single enoxaparin dose (1 mg/kg SC).6 After an adequate number of SC doses of enoxaparin (1 mg/kg q12hr for at least 48 hours), anti-Xa activity levels can remain therapeutic for at least 8 hours after the last injection.30

Thus, to support elective PCI, IV enoxaparin has pharmacokinetic advantages over therapy given by the SC route (Figure 1).36,38 SC enoxaparin is widely used in the treatment of acute coronary syndrome (ACS) patients, and it may therefore be necessary to transition patients on SC enoxaparin to IV enoxaparin. A booster dose of 0.3 mg/kg IV enoxaparin has been shown to achieve therapeutic anti-Xa activity levels for 2–6 hours, allowing PCI in ACS patients who had previously received only 1 SC dose of enoxaparin, or in patients who had received their last enoxaparin dose 8–12 hours before PCI.6,31,34–36,40 Patients who had received an initial 30 mg IV bolus of enoxaparin before a single SC dose (1 mg/kg) do not seem to require additional anticoagulation within 8 hours of SC enoxaparin.31,37

Choosing the dose for PCI. A number of IV enoxaparin doses have been studied. Target levels of anti-Xa activity appropriate for PCI procedures can be achieved in most patients following IV injection of 0.5 mg/kg enoxaparin. Data from clinical studies, including STEEPLE, have shown that 77–95% of patients reach target anti-Xa activity levels after receiving a 0.5 mg/kg bolus injection.4,8,25,38 In STEEPLE, 91.7% of patients achieved target anti-Xa activity levels during PCI with the higher dose of 0.75 mg/kg enoxaparin, and 78.8% with the 0.5 mg/kg dose.4 However, the use of higher doses of enoxaparin has been associated with an increased risk of initial overcoagulation. Population pharmacokinetic analyses using data from over 500 patients undergoing PCI predict that after a dose of enoxaparin 0.75 mg/kg, 48% of patients would achieve anti-Xa levels above 1.5 IU/mL, and 2.5% of patients receiving a dose of 0.5 mg/kg. The anticoagulant effects of a single 0.75 mg/kg dose would also persist for a mean 3.4 ± 1.1 hours, rather than 2.7 ± 0.9 hours for a dose of 0.5 mg/kg.38
A meta-analysis of clinical studies of IV enoxaparin in PCI indicates that use of an IV enoxaparin 0.5 mg/kg dose results in significantly fewer ischemic events, minor bleeding and all bleeding (although not major bleeding), compared with higher-dose bolus injections (Table 3).19 Such analyses are based on pooled data from heterogeneous study populations, but nevertheless provide some indication that the 0.5 mg/kg dose of enoxaparin can offer effective anticoagulant activity and clinical efficacy without undue bleeding risk in most patients undergoing PCI. While the STEEPLE study was not designed to compare the 2 doses of enoxaparin studied (0.5 and 0.75 mg/kg; Table 3), both doses were highly effective and were shown to be better than UFH in terms of major bleeding outcomes.4

Current data suggest that the selection of an appropriate dose of IV enoxaparin could be based on patient stratification. The majority of patients on the 0.5 mg/kg dose of enoxaparin will achieve the desired level of anticoagulant activity for the duration of PCI. The 0.5 mg/kg dose provides a sufficiently short duration of anticoagulant activity so the sheath can be removed immediately post procedure, allowing earlier patient ambulation and discharge. If, however, it is determined that a patient will require a longer procedure, a single bolus injection of enoxaparin 0.75 mg/kg IV may be chosen to provide appropriate anticoagulant activity. At the end of the procedure in the STEEPLE trial, 95.1% and 84.5% of patients on enoxaparin 0.75 mg/kg and 0.5 mg/kg, respectively, were within target range (anti-Xa activity 0.5–1.8 IU/mL) with 0.2% and 0.6%, respectively, receiving 1 additional bolus of enoxaparin during a prolonged (> 2-hour procedure).4 A dose of 0.3 mg/kg IV is sufficient to transition patients on SC enoxaparin to IV enoxaparin, if necessary.6,31,36,40 Table 4 summarizes dosing suggestions for using IV enoxaparin in patients undergoing PCI.

Switching between Enoxaparin and UFH

Many patients with ACS are receiving antithrombin therapy before nonurgent or elective PCI. Previously patients given SC enoxaparin might have been switched to IV UFH when undergoing PCI. However, recent data suggest there is the option to continue these patients on IV enoxaparin during invasive procedures. This is of particular importance, because data from the SYNERGY trial suggested that switching between anticoagulants has a negative impact on patient outcome.41

Consistent use of enoxaparin (1 mg/kg SC) in NSTEMI patients, rather than switching between anticoagulants, is associated with less mortality or MI, compared with UFH (13.3% vs. 15.9%, respectively; adjusted p = 0.041) and an increased rate of Global Utilization of Streptokinase and t-PA for Occluded coronary arteries (GUSTO) defined severe bleeding (2.9% vs. 2.1%, respectively; p = 0.0456).42 If there is a need to transition from one antithrombin agent to another, it is important to do it under a prespecified protocol (Table 4).

A prespecified subanalysis of the SYNERGY trial evaluating NSTEMI patients proceeding to PCI demonstrated that the rates of death or MI at 30 days were similar between patients randomized to enoxaparin and UFH (13.1% vs. 14.2%; p = 0.289), with an increased rate of TIMI-defined major bleeding (3.7% vs. 2.5%; p = 0.028). However, crossovers to the alternative drug occurred in 12.7% of patients assigned to enoxaparin and 3.0% of patients assigned to UFH.6

In STEEPLE, IV enoxaparin was associated with less bleeding than UFH, with similar rates of ischemic event or mortality. Although the STEEPLE study did not evaluate the effects of prior antithrombotic therapy on outcomes, as patients were new to antithrombotic therapy, extrapolation of the results of this study suggests that there should be no need to switch an ACS patient on SC enoxaparin to UFH in the event of an urgent or elective PCI.4

Indeed, in a subgroup analysis of the Enoxaparin and Thrombolysis Reperfusion for Acute myocardial infarction Treatment – TIMI 25 (ExTRACT-TIMI 25) trial of STEMI patients who continued treatment with the study drug during PCI, death or MI occurred less frequently in the enoxaparin group than in the UFH group (13.0% vs. 16.7%, respectively; p = 0.013). There was no difference in TIMI-defined major bleeding (1.8% vs. 2.4%, respectively; p = 0.33). Enoxaparin was given as an initial 30 mg IV dose followed by 1.0 mg/kg q12hr SC. For patients aged 75 years or older, the initial IV bolus was eliminated and the SC dose reduced to 0.75 mg/kg q12hr. In patients with a creatine clearance below 30 mL/minute, the SC dose was modified to 1.0 mg/kg every 24 hours. Patients on SC enoxaparin received an IV bolus of 0.3 mg/kg enoxaparin at the time of PCI, if the last SC dose was administered 8–12 hours earlier, while no additional enoxaparin was administered when the last SC dose was given within the preceding 8 hours.43

These data suggest that IV enoxaparin offers the option of seamlessly transitioning patients on SC enoxaparin to interventional management without the need for introducing a second anticoagulant in the cardiac catheterization laboratory.

Clinical Experience with Enoxaparin for PCI

Based on the literature of peer-reviewed data described earlier, a number of practical recommendations can be made on dosing of enoxaparin for PCI and sheath removal (Table 4). In addition, I would like to comment on the use of enoxaparin for PCI from our personal and institutional experience with more than 600 elective or emergent cases since December 1998.

There seems to be a difference in bleeding events depending on the case scenario or route of administration. In those patients receiving SC doses of enoxaparin and undergoing PCI there seems to be more bleeding than in those who receive a single IV dose of enoxaparin. In the case of SC dosing, it becomes even more important not to “stack” antithrombin therapies — i.e., adding a second drug on top of the received enoxaparin, as this leads to more bleeding without improving the prevention of ischemic events.

If enoxaparin is being used SC, it is important to adjust the dose in the elderly and those with severe renal insufficiency. In my practice, if the patient has an increased bleeding risk a single dose of 0.5 mg/kg is given. If the patient has such a high risk for bleeding that the physician would not use GP IIb/IIIa inhibitors, then neither UFH nor enoxaparin are used and other drugs like bivalirudin are used.
Although the dose of 0.5 mg/kg IV has been evaluated in previous studies, the most common and best-supported IV dose in terms of number of patients treated is 0.75 mg/kg IV. Single doses as high as 1.0 mg/kg IV have not been associated with more bleeding. As long as enoxaparin is given IV, there seems to be a very predictable response and PCI can be performed without the need for monitoring.

An important caveat for the use of IV enoxaparin is to make sure the IV line is working (not infiltrated) and to flush the dose with 10 cc of normal saline in order to ensure all enoxaparin is administered. In the Evaluating Enoxaparin Clotting Times (ELECT) study, some adverse events were related to the simple fact that the patient did not receive the enoxaparin due to IV line infiltration or to the fact that the dose was still inside a long IV tubing line.32

There is no single drug that fits all patients. The operator needs to weigh the ischemic and bleeding risks of the patient, any adjunctive pharmacotherapy being used and the level of comfort, when choosing the drug to support PCI. At least we can say with confidence that the IV use of enoxaparin for PCI (both elective and emergent) compared with IV UFH is associated with less bleeding, similar efficacy, does not require monitoring and expedites the procedure, as there is no need to stop to check an ACT. Thus, IV enoxaparin covers two important aspects: safety (less bleeding) and convenience (1 IV dose, no monitoring).

Summary

There are now data to support the use of IV enoxaparin in elective PCI as an effective antithrombin therapy with a good safety profile, which seems a preferable alternative to IV UFH. Enoxaparin has a number of practical benefits over UFH in this setting. Unlike UFH, enoxaparin does not require laboratory monitoring or dose titration to ensure that effective anticoagulation with adequate safety is achieved during PCI. Enoxaparin has been shown to be a suitable antithrombin drug at IV doses of 0.5 mg/kg and 0.75 mg/kg, with the 0.5 mg/kg dose offering the additional benefit of immediate sheath removal. With the advent of IV enoxaparin as a feasible alternative to UFH in PCI, it is no longer necessary to switch patients with ACS from enoxaparin-based management to UFH during PCI. Patients with ACS on SC enoxaparin can seamlessly transition from the medical management to the interventional management phase without the need for introducing a second anticoagulant in the cardiac catheterization laboratory. Appropriate dosing and use of enoxaparin have been shown to reduce bleeding risk while being as effective as IV UFH in elective PCI in the STEEPLE trial. It has also proved to be superior in reducing ischemic events or mortality without increased bleeding in PCI following thrombolysis in the ExTRACT-TIMI 25 trial. The accumulated evidence based on the results of the STEEPLE and ExTRACT-TIMI 25 trials should lead to guideline recommendations for the wider use of enoxaparin in PCI.

Acknowledgement. The author would like to thank Dr. John J. Warner for his critical review and valuable guidance and contribution to structure and content for the development of the manuscript. The author received editorial/writing support in the preparation of this manuscript which was funded by Sanofi-Aventis, Bridgwater, New Jersey.