Atrial fibrillation (AF) is the most frequent arrhythmia worldwide and it is associated with increased risk of stroke, thromboembolism and mortality. 1 Nevertheless, these risks can be reduced by using oral anticoagulation (OAC), both Direct Oral Anticoagulants (DOACs) or Vitamin K Antagonists (VKAs). 2 Despite the increasing use of DOACs, VKAs (mainly warfarin and acenocoumarol) are still widely used for stroke prevention in AF in several countries. Notwithstanding, the efficacy and safety of VKAs depend upon the quality of anticoagulation control, as reflected by the average time in therapeutic range (TTR) of international normalised ratio (INR) 2.0-3.0.
Studies on older patients have established notable conceptual changes in the etiopathogenesis of acute coronary syndrome (ACS), but little is known about this disease in young patients (<45 years). Of special interest is thromboinflammation, key at onset, evolution and therapy of cardiovascular pathology. Therefore, we explored whether ACS at an early age is a thromboinflammatory disease by analyzing NETs and rs2431697 of miR-146a (a miRNA considered as a brake of TLR/NF-kB pathway), elements previously related to higher rates of recurrence in atrial fibrillation and sepsis. We included 359 ACS patients (<45 years) and classified them for specific analysis into G1 (collected during the hospitalization of the first event), G2 and G3 (retrospectively collected from patients with or without ACS recurrence, respectively). cfDNA and citH3–DNA were quantified, and rs2431697 was genotyped. Analysis in the overall cohort showed a moderate but significant correlation between cfDNA and citH3–DNA and Killip–Kimball score. In addition, patients with citH3–DNA > Q4 more frequently had a history of previous stroke (6.1% vs. 1.6%). In turn, rs2431697 did not confer increased risk for the onset of ACS, but T carriers had significantly higher levels of NET markers. By groups, we found that cfDNA levels were similarly higher in all patients, but citH3–DNA was especially higher in G1, suggesting that in plasma, this marker may be attenuated over time. Finally, patients from G2 with the worst markers (cfDNA and citH3–DNA > Q2 and T allele) had a two-fold increased risk of a new ischemic event at 2-year follow-up. In conclusion, our data confirm that ACS is younger onset with thromboinflammatory disease. In addition, these data consolidate rs2431697 as a silent proinflammatory factor predisposing to NETosis, and to a higher rate of adverse events in different cardiovascular diseases.
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