Atrial fibrillation complicating acute myocardial infarction: how should it be interpreted and how should it be treated and prevented?

Atrial fibrillation (AF) has been reported to complicate the course of acute myocardial infarction (AMI) in 6–21% of hospitalized patients. Possible precipitating factors of AF in this setting include atrial ischaemia or infarction, right ventricular infarction, pericardial inflammation, acute hypoxia or hypokalaemia, and haemodynamic impairment secondary to left ventricular (LV) dysfunction. Endogenous or exogenous catecholamines may also precipitate AF. These factors can be found alone or in combination, and may superimpose on predisposing diseases affecting cardiac anatomy and physiology, such as previous cardiomyopathy, valvular impairment, or chronic lung disease. Finally, AF in the setting of AMI has been reported to be associated with ageing, severely impaired LV function, presence of mitral regurgitation, or frequent ventricular arrhythmias plus right bundle branch block, and presence of left bundle branch block. Although most of these factors are claimed to be causative of AF, the intimate relationship between their presence and AF occurrence is not known. Despite the variability of factors and conditions associated with AF in clinical practice, patients developing this arrhythmia during AMI are usually reported as a uniform category. AF can cause haemodynamic instability because of the rapid ventricular rate, irregular ventricular filling, and/or loss of atrial contribution to cardiac output, ultimately leading to an increase in oxygen demand. If deterioration of the haemodynamic balance secondary to AF may intuitively affect pre-discharge outcome of AMI victims, less intuitive is the association between AF in the early phase of AMI and long-term outcome. Schmitt et al. report on a clinical review evaluating the incidence, clinical features, and prognostic implication of AF in AMI. Through this investigation, the authors provide a summary on clinically relevant items such as identification of clinical variables associated with the development of AF and their prognostic implications, incidence of in-hospital and post-discharge mortality in AF groups vs. the remaining population, causes of death, impact of AF on stroke risk, efficacy of anticoagulation strategies, and treatment of AF during AMI. Ageing, Killip class IV, heart rate at admission, and pre-existing AF were consistently found to be strong independent predictors in different trials; not unexpectedly, the prevalence of patients presenting with these parameters, except for ageing, appeared to decrease in most recent trials under the influence of early reperfusion therapies, and use of b-blockers, angiotensinconverting enzyme (ACE) inhibitors and angiotensin (AT) II inhibitors. Also LV hypertrophy, probably as an indicator of increased intracardiac pressure, was shown to be a significant predictor, whereas the ST-segment elevation myocardial infarction (STEMI) vs. non-ST-segment elevation myocardial infarction (NSTEMI) nature of myocardial damage did not appear to influence the propensity to develop in-hospital AF. The presence of AF during AMI carried an increased risk of developing in-hospital re-infarction, cardiogenic shock, heart failure, and asystole. Importantly, the presence of AF of new onset during AMI carried an increased risk of in-hospital, 30-day, 1-year, and 3-year mortality, whereas pre-existing AF did not appear to carry any such risk. 9 Increased risk included both sudden and non-sudden cardiac death. Some evidence was reported regarding the independent significance of short-lasting vs. long-lasting AF episodes. The independent value of AF as a predictor of mortality was not substantiated in all trials, which raises doubts about the impact of AF therapies on