C ardiovascular diseases still remain one of the greatest health challenges. While the incidence and case-fatality rate of acute myocardial infarction (AMI) have decreased with the development of medications and reperfusion therapy, the disease burden of complications has increased. 1) Arrhythmia in the setting of AMI is an adverse prognostic factor, and atrial fibrillation (AF), the most frequent supraventricular arrhythmia, is associated with the increased risk of short-term and longterm mortality.2,3) In addition, AMI patients with AF have more comorbidities as compared to patients in sinus rhythm, which relate to a higher re-infarction rate, higher stroke rate, and higher risk for heart failure. [4][5][6] The presence of AF requires anti-coagulant therapy for the prevention of strokes, although anticoagulant drug administration plus dual anti-platelet therapy after percutaneous coronary intervention would increase the risk of bleeding and a variety of clinical trials have been conducted to evaluate alternative regimens. 7,8) Hence, the prediction and prevention of atrial fibrillation as a complication of AMI could be a meaningful strategy. In patients with left ventricular dysfunction secondary to AMI, treatment with an angiotensinconverting-enzyme (ACE) inhibitor could reduce the incidence of AF in the chronic phase. 9) Carvedilol has been shown to suppress AF and atrial flutter in a similar patient population, according to a sub-analysis in the the CAPRI-CORN study.10) Additionally, atorvastatin significantly reduced the incidence of postoperative AF after elective cardiac surgery.11,12) However, there is limited evidence suggesting that upstream medical therapy reduces the incidence of AF as primary endpoint.13) It is deemed desirable to provide preventive therapy tailored to risk stratification with respect to new-onset AF associated with AMI.
Article p.64Zhang, et al. investigated the expression of Toll like receptors (TLRs) on the surface of peripheral blood mononuclear cells (PBMCs) in AMI patients. 14) They collected blood samples before any reperfusion therapy within two hours after AMI onset, and divided the clinical subjects into two groups: patients with new-onset AF in 1 month after AMI (AFMI group) or without (MI group). The results showed that the expressions of both TLR2 and TLR4 in PBMCs in the MI group were higher than that in healthy volunteers, and much higher in PBMCs in the AFMI group. Protein assay and flow cytometry analysis also showed a significant difference in TLR2 and TLR4 expression. With respect to the TLR adaptor proteins, myeloid differentiation factor 88 (MyD88) and TIR domain-containing protein-β antibody (TRIF-β), their protein levels were significantly higher in the AFMI group than in the MI group as well, indicating that the TLR2 and TLR4 pathway was surely augmented in PBMCs in the AFMI group. Of note, these differences were already found in the very rapid phase of AMI onset.Evidence to support the involvement of the inflammatory process in the pathophysiology of AF has...