RESUMEN
Acute myocardial infarction in a young patient is a nebulous entity, but in the absence of traditional cardiovascular risk factors, particular attention must be paid to thrombotic disorders and hypercoagulable states. A 28-year-old male presented with worsening substernal chest pain for 36 hours. He was recently diagnosed with systemic lupus erythematosus (SLE) with active class II lupus nephritis. With an initial electrocardiogram revealing ischemic changes, and an elevated troponin I, a concern was raised for myocardial infarction. Transthoracic echocardiography revealed a severely reduced ejection fraction of 25%, and a subsequent emergent left heart catheterization revealed a complete, massive thrombotic occlusion of the proximal left anterior descending artery, requiring aspiration thrombectomy. After extensive workup for hypercoagulable states, he was found to have elevated anticardiolipin IgG and IgM antibodies on two occasions, twelve weeks apart. The patient was managed with triple anticoagulation with aspirin, clopidogrel, and warfarin for one month, followed by dual anticoagulation with clopidogrel and warfarin with a targetted international normalized ratio (INR) of 2.0 - 3.0. The management of acute coronary syndrome caused by antiphospholipid syndrome (APS) is highly individualized and driven by clinician gestalt owing to the lack of a standardized consensus. While systemic thrombolysis, primary percutaneous coronary intervention (PCI), and coronary artery bypass grafting all have their utility, only a very small handful of case reports exist on the benefits of each. This particular case serves to showcase an instance where a patient was successfully managed with PCI with dual antiplatelet therapy. Further prospective randomized controlled trials are necessary to determine the optimal management of this rarely encountered patient population.
RESUMEN
Background Vorapaxar as an adjunct to dual antiplatelet therapy (DAPT) reduces thrombotic events in patients with prior myocardial infarction at the expense of increased bleeding. Withdrawal of aspirin has emerged as a bleeding reduction strategy. The pharmacodynamic effects of vorapaxar with potent P2Y12 inhibitors as well as the impact of dropping aspirin is unexplored and represented the aim of the VORA-PRATIC (Vorapaxar Therapy in Patients With Prior Myocardial Infarction Treated With Newer Generation P2Y12 Receptor Inhibitors Prasugrel and Ticagrelor) study. Methods and Results Post-myocardial infarction patients (n=130) on standard DAPT (aspirin+prasugrel or ticagrelor) were randomized to 1 of 3 arms: (1) triple therapy: aspirin+prasugrel/ticagrelor+vorapaxar; (2) dual therapy (drop aspirin): prasugrel/ticagrelor+vorapaxar; (3) DAPT: aspirin+prasugrel/ticagrelor. Pharmacodynamic assessments were performed at 3 time points (baseline and 7 and 30 days). Vorapaxar reduced CAT (collagen-ADP-TRAP)-induced platelet aggregation, a marker of platelet-mediated global thrombogenicity (triple therapy versus DAPT at 30 days: mean difference=-27; 95% CI,-35 to -19; P<0.001; primary end point). This effect was attenuated but still significant in the absence of aspirin (dual therapy versus DAPT at 30 days: mean difference=-15; 95% CI,-23 to -7; P<0.001; between-group comparisons, P<0.05). Vorapaxar abolished TRAP-induced aggregation (P<0.001), without affecting thrombin generation and clot strength. There were no differences in markers of P2Y12 reactivity. Markers sensitive to aspirin-induced effects increased (P<0.001) in the dual-therapy arm. Conclusions In post-myocardial infarction patients treated with potent P2Y12 inhibitors, vorapaxar reduces platelet-driven global thrombogenicity, an effect that persisted, albeit attenuated, in the absence of aspirin and without affecting markers of P2Y12 reactivity or clot kinetics. The clinical implications of these PD observations warrant future investigation. Registration URL: https://www.cliniâcaltrâials.gov. Unique identifier: NCT02545933.
