ABC | Volume 113, Nº5, November 2019

Original Article Congo et al. New-Onset atrial fibrillation in STEMI Arq Bras Cardiol. 2019; 113(5):948-957 Table 8 – Independent predictors of new onset atrial fibrillation All Group 1 – No AF Group 2 – New onset AF p Swan-Ganz catheter 0.6 0.4 3.6 p < 0.001 Intra-aortic balloon pump 1.2 1.1 2.7 p = 0.012 Invasive mechanical ventilation 3.5 3.2 9.0 p < 0.001 Transvenous cardiac pacing 3.6 3.1 11.2 p < 0.001 STEMI: ST-segment elevation myocardial infarction beta‑blockers may have a protective role, which is in line with previous studies. 1,19,20 No difference was found regarding statin therapy, unlike what was suggested in previous studies. 21 New-onset AF was associated with higher incidence of complications, namely stroke, heart failure, cardiogenic shock, arrhythmias, cardiac arrest, mechanical complications and major bleeding, and in-hospital mortality, but was not found as an independent predictor of mortality, suggesting that new-onset AF complicating STEMI may simply be an indicator of poor overall clinical status, which is consistent with previous studies. 5,22 Studies on critically ill patients also suggest new-onset AF is an indicator of clinical severity and poorer prognosis. 4,23-25 Age, prior stroke, inferior STEMI and complete AV block were found as independent predictors of new-onset AF. Age and prior stroke reflect patients with more comorbidities. A systematic review by Schmitt et al. 1 of 20 publications also found that new-onset AF is more likely to complicate AMI in older patients. 1 Anatomic atrial abnormalities with aging, such as atrial fibrosis and smooth muscle cell proliferation, may provide anatomic substrate for the multiple wavelet re-entry mechanism of AF. 26 Logistic regression analysis showed that inferior STEMI was an independent predictor of new-onset AF in our population. Kyriakidis et al. 27 found that all patients that developed supraventricular arrhythmia had inferior STEMI and right and left atrial ischemia, and concluded that ischemia of the sinus node due to coronary occlusion proximal to the origin of the sinus node artery was probably one of the underlying causes of atrial fibrillation. 27 According to Tjandrawidjaja et al., 28 the compromised anatomy of the principal coronary atrial branches is associated with the development of atrial arrhythmia. 28 The GUSTO III study found that the development of AF could be due to other post-AMI complications occurring before AF, such as complete AV block. 26 An association between complete AV block and incidence of AF has also been reported previously, particularly in AH type of AV block, due to lesions observed in the atrial muscles including the internodal tracts. 29 The main question of long-termmanagement of new‑onset AF in STEMI and whether to start anticoagulation therapy in these patients remains unanswered, as there is not enough data. In our population, only one in five patients was discharged on oral anticoagulation. Follow-up data on these patients is needed to assess long-term complications. According to some studies, new-onset AF in the acute setting may indicate a propensity to develop arrhythmia again, potentially because of associated comorbidities or other predisposing factors. 3 In our population, the therapeutic strategy seems to have been based on the notion that new‑onset AF in STEMI could represent a transient complication of acute coronary syndrome, as suggested by some studies that have shown that in patients with coronary artery disease, atrial ischemia independently promotes the formation of a substrate for AF and that atrial impulse conduction abnormalities were abolished after reperfusion was achieved with either thrombolysis or primary percutaneous coronary intervention (PCI). 8,30,31 Study limitations Although data have been prospectively acquired, the main limitations of this study derive from its retrospective design, which limits some available data. Another limitation is that some patients diagnosed with new‑onset AF may in fact have previous yet undiagnosed paroxysmal AF, which may lead to an overestimated incidence. These patients may also represent a different subtype of patients, compared to actual new-onset AF due to the ischemic event. Conclusions This study reflects a very large registry of new-onset AF in patients hospitalized for STEMI. It shows that in a modern revascularization era, AF is still a frequent complication of acute myocardial infarction. It can be reduced by early reperfusion independently of reperfusion strategy. These registry data confirm the high mortality and morbidity associated with AF, which may suggest the importance of identifying this subgroup of STEMI patients. Age, prior stroke, inferior STEMI and complete AV block were found as independent predictors of new-onset AF in the setting of STEMI. Furthermore, data indicates that only a minority of patients receive oral anticoagulants at discharge. Although the incidence has decreased, we can still expect AF to remain a frequent and worrisome complication of AMI. Further studies answering questions such as how to reduce the risk of AF development, whether the use of new generation drug‑eluting stents and modern antithrombotic strategies aimed at better reperfusion will reduce the incidence of new-onset AF during AMI and how to determine the optimal use of oral anticoagulation therapy in combination with antiplatelet therapy in this setting. 955