Physicians' Academy for Cardiovascular Education

Rivaroxaban reduces thrombotic events after STEMI

Literature - Mega JL, Braunwald E, Murphy SA, et al. - J Am Coll Cardiol. 2013;61:1853-9

Rivaroxaban in Patients Stabilized after a ST-Elevation Myocardial Infarction: Results from the ATLAS ACS 2-TIMI 51 Trial.

Mega JL, Braunwald E, Murphy SA, et al.
J Am Coll Cardiol. 2013;61:1853-9


Rates of morbidity and mortality after ST-segment elevation myocardial infarction (STEMI) decreased over time because of timely reperfusion and in-hospital treatment with anticoagulants and antiplatelet therapies .[1,2] However, during and after the acute STEMI event, a cumulative risk of death and ischemic events remains. [3]
In ATLAS ACS-2–TIMI-51 (Anti-Xa Therapy to Lower Cardiovascular Events in Addition to Standard Therapy in Subjects with Acute Coronary Syndrome–Thrombolysis In Myocardial Infarction-51), the
novel Xa inhibitor rivaroxaban reduced recurrent cardiovascular events across the spectrum of ACS. [4,5]
This analysis focused on the pre-specified subgroup of ST-elevation myocardial infarction (STEMI) patients, in whom anticoagulant therapy has been of particular interest.
7,817 patients in ATLAS ACS-2-TIMI 51 presented with a STEMI. After being stabilized (1 to 7 days), they underwent randomization to twice daily rivaroxaban 2.5 mg, rivaroxaban 5 mg, or placebo.

Main results

  • Among patients with a STEMI, rivaroxaban reduced the primary efficacy endpoint of cardiovascular death, myocardial infarction, or stroke (ischemic, hemorrhagic, or stroke of uncertain cause) versus placebo (ITT: 8.4% vs. 10.6%, HR: 0.81, 95% CI: 0.67 to 0.97, p = 0.019; mITT: 8.3% vs. 9.7%, HR: 0.85, 95% CI: 0.70 to 1.03, p = 0.09) (Fig. 1).
  • This reduction in the primary endpoint emerged within the first 30 days (ITT and mITT: 1.7% vs. 2.3%, HR: 0.71, 95% CI: 0.51 to 0.99, p = 0.042). The primary endpoint occurred while on treatment with dual antiplatelet therapies (ITT: 7.9% vs. 11.9%, HR; 0.78, 95% CI: 0.64 to 0.94, p = 0.010; mITT: 7.7% vs. 10.1%, HR; 0.82, 95% CI: 0.67 to 1.01, p = 0.061).
  • Both doses compared with placebo showed similar reductions in the primary efficacy endpoint, without significant differences (ITT: 8.7% vs. 8.2%, HR: 0.99, 95% CI: 0.80 to 1.24, p = 0.96; mITT: 8.8% vs. 7.9%, HR: 0.99, 95% CI: 0.79 to 1.25, p = 0.95, for the 2.5 and 5 mg dose, respectively)
  • Rivaroxaban 2.5 mg reduced cardiovascular death (ITT: 2.5% vs. 4.2%, p = 0.006; mITT: 2.2% vs. 3.9%, p = 0.006), which was not seen with 5 mg of rivaroxaban. This effect was consistent during treatment with dual antiplatelet therapy.
  • Rivaroxaban versus placebo increased non-coronary artery bypass grafting Thrombolysis In Myocardial Infarction major bleeding (2.2% vs. 0.6%, p < 0.001) and intracranial hemorrhage (0.6% vs. 0.1%, p = 0.015) without a significant increase in fatal bleeding (0.2% vs. 0.1%, p = 0.51).


The addition of rivaroxaban 2.5-mg twice daily dose may offer an effective strategy to reduce thrombotic events in patients following a STEMI.


  1. Roger VL, Go AS, Lloyd-Jones DM, et al. Heart disease and stroke statistics--2012 update: a report from the American Heart Association. Circulation 2012;125:e2–220.
  2. Nabel EG, Braunwald E. A tale of coronary artery disease and myocardial infarction. N Engl J Med 2012;366:54–63.
  3. Fox KA, Anderson FA, Jr., Goodman SG, et al. Time course of events in acute coronary syndromes: implications for clinical practice from the GRACE registry. Nat Clin Pract Cardiovasc Med 2008;5:580-9.
  4. Gibson CM, Mega JL, Burton P, et al. Rationale and design of the anti-Xa therapy to lower cardiovascular events in addition to standard therapy in subjects with acute coronary syndrome-thrombolysis in myocardial infarction 51 (ATLAS-ACS 2 TIMI 51) trial: a randomized, double-blind, placebo-controlled study to evaluate the efficacy and safety of rivaroxaban in subjects with acute coronary syndrome. Am Heart J 2011;161:815–21 e6.
  5. Mega JL, Braunwald E, Wiviott SD, et al. Rivaroxaban in patients with a recent acute coronary syndrome. N Engl J Med 2012;366:9 –19.
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