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

## TL;DR

This review explores the complex two-way relationship between atrial fibrillation and coronary artery disease, including how they influence each other and affect patient outcomes.

## Contribution

The paper highlights the distinction between early and late new-onset atrial fibrillation in acute myocardial infarction and their differing clinical implications.

## Key findings

- Patients with atrial fibrillation have an increased risk of acute myocardial infarction due to mechanisms like oxidative stress and inflammation.
- New-onset atrial fibrillation during acute myocardial infarction can be classified as early or late, with different pathophysiologies and outcomes.
- The review summarizes epidemiology, pathophysiology, and management strategies for the interplay between atrial fibrillation and coronary artery disease.

## Abstract

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.