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JACC March 20, 2018


Volume 71, Issue 11

Prevention
THE SGLT2 INHIBITOR EMPAGLIFLOZIN DOES NOT EXHIBIT PRO THROMBOTIC EFFECTS
Poster Contributions
Poster Hall, Hall A/B
Sunday, March 11, 2018, 9:45 a.m.-10:30 a.m.

Session Title: The Not So Sweet Truth: Latest Insights in Insulin Resistance and Diabetes For Preventive Cardiology
Abstract Category: 14. Heart Failure and Cardiomyopathies: Therapy
Presentation Number: 1212-433

Authors: Carlos G. Santos-Gallego, Mohammad Zafar, Rodolfo San Antonio, Juan Antonio Requena Ibanez, Maria Belen Picatoste Botija,
Kiyotake Ishikawa, Shin Watanabe, Roger Hajjar, Valentin Fuster, Juan Badimon, Icahn School of Medicine at Mount Sinai, New York, NY,
USA
Background: SGLT2 inhibitor empagliflozin (EMPA) reduces CV death by 40% and heart failure by 35%. Of note, there is no decrease
in myocardial infarction or stroke. In fact, there is a numerical increase in stroke rate in the EMPA-treated group (a non-significant trend,
p=0.12). The reduction in volemia and the hemoconcetration induced by EMPA may both potentially induce a prothrombotic state,
which could explain the numerical increase in strokes. Therefore, we aimed to study the effects of chronic EMPA treatment on platelet
aggregation and thrombus kinetics
Methods: HF was induced in 16 pigs by 2-hour balloon occlusion of proximal LAD in order to mimic the clinical profile of a patient taking
EMPA. Animals were randomized to daily treatment with EMPA 10mg PO or placebo. Thrombogenicity assays were performed baseline
(before MI) and 2 month post-MI. Platelet aggregation was studied with Multiplate impedance aggregometry using ADP and collagen as
agonists. Thrombus kinetics were assessed using rotational thromboelastography (ROTEM)
Results: Both groups exhibited similar initial ischemic injury (MI size 42±3% vs 42±2%, p=NS; LVEF, p=NS). There was no difference in
platelet aggregation or in thrombus kinetics between both groups either baseline or at 2-month (Table)
Conclusion: Chronic EMPA treatment does not enhance platelet aggregation nor modifies thrombus kinetics in our porcine model. The
non-significant stroke increase seems to be related to play of chance rather than to a real prothrombotic effect