What question did this study set out to answer?

This review aims to clarify the two-way relationship between atrial fibrillation and acute myocardial infarction, including their shared risk factors and pathophysiological mechanisms.

March 2, 2026Open Access

Atrial fibrillation and acute myocardial infarction: a Two-Way relationship

Q: What is the clinical evidence from this study?

Study design: Review. Population: Patients with atrial fibrillation and/or acute myocardial infarction at risk of new-onset atrial fibrillation or myocardial infarction. Primary outcome: Incidence of acute myocardial infarction in AF patients and incidence of new-onset atrial fibrillation (NOAF) in AMI patients (increased risk of NOAF by 60%-77% in AMI patients; statin use associated with reduced NOAF incidence; semaglutide reduced NOAF incidence by about 20%-50%; SGLT2 inhibitors reduced AF risk with RR 0.62 (95% CI 0.44-0.87), 95% CI RR 0.44-0.87 for SGLT2i).

Resultado clave

Semaglutide reduced new-onset atrial fibrillation incidence by 20%-50% and SGLT2 inhibitors reduced atrial fibrillation risk by 38% (RR 0.62) in cardiovascular patients.

Puntos clave

This review aims to clarify the two-way relationship between atrial fibrillation and acute myocardial infarction, including their shared risk factors and pathophysiological mechanisms.
Examined epidemiology and pathophysiology of atrial fibrillation and coronary artery disease
Discussed risk stratification for patients with both conditions
Analyzed management strategies for atrial fibrillation in acute myocardial infarction scenarios
Patients with atrial fibrillation face higher risks of developing coronary artery disease and acute myocardial infarction.
Acute myocardial infarction can lead to new-onset atrial fibrillation, with varying implications for patient outcomes based on the timing of onset.
Early new-onset atrial fibrillation indicates a better outcome, while late onset is associated with worse outcomes.

PICO

Población

Patients with atrial fibrillation and/or acute myocardial infarction at risk of new-onset atrial fibrillation or myocardial infarction

Resultado principal

Incidence of acute myocardial infarction in AF patients and incidence of new-onset atrial fibrillation (NOAF) in AMI patients — increased risk of NOAF by 60%-77% in AMI patients; statin use associated with reduced NOAF incidence; semaglutide reduced NOAF incidence by about 20%-50%; SGLT2 inhibitors reduced AF risk with RR 0.62 (95% CI 0.44-0.87) (RR 0.44-0.87 for SGLT2i)

Resultado numérico

Estimación del efecto: increased risk of NOAF by 60%-77% in AMI patients; statin use associated with reduced NOAF incidence; semaglutide reduced NOAF incidence by about 20%-50%; SGLT2 inhibitors reduced AF risk with RR 0.62 (95% CI 0.44-0.87) (95% CI RR 0.44-0.87 for SGLT2i)

Tasa de eventos absoluta: 10% vs 2.3%

Limitaciones

Lack of randomized controlled trials specifically addressing the effect of direct oral anticoagulants on myocardial infarction risk in AF patients.
Most studies are observational or meta-analyses; underlying biological mechanisms for early vs late NOAF primarily inferred from indirect clinical data.
Heterogeneity in definition and timing of NOAF across studies.
Limited evidence on AF-CARE score compared to ABC pathway; further studies needed.
Suboptimal prescription of statins and renin-angiotensin inhibitors in AF patients despite evidence of benefit.
Lack of strong evidence for pharmacological prevention of AF relapses post-AMI.
No direct trial evidence on antithrombotic strategies optimally balancing ischemic and bleeding risk in AMI patients with NOAF.

Resumen

Atrial fibrillation (AF) and coronary artery disease (CAD) are among the most frequent cardiovascular diseases and leading causes of morbidity/mortality worldwide. The concomitant presence of AF and CAD is relatively common, as the association is supported not only by shared atherosclerotic risk factors, but also by a pathophysiological link. Patients with a history of AF have been described as at increased risk of CAD, in particular acute myocardial infarction (AMI), through several mechanisms, such as increased oxidative stress, systemic inflammation, increased platelet aggregation. On the other hand, up to 10% of patients with AMI are at risk of developing new-onset atrial fibrillation (NOAF). In the past, any type of NOAF during AMI was considered identical and equally associated with a worse outcome. More recently, increasing evidence supports the pathophysiological and nosological difference between early NOAF (occurring within the first 24 h after the index event and associated with atrial ischaemia, oxidative stress and a better outcome) and late NOAF (occurring after 24 h and correlated with increased left atrial pressures, deterioration of haemodynamic status, elevated left ventricular filling pressures and a worse outcome). In this review, we summarise the available evidence on the epidemiology, pathophysiology, risk stratification, and management of the complex two-way relationship between AF and CAD.

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