Abstract

The incidence of atrial fibrillation (AF) in acute coronary syndrome (ACS) ranges from 2.3–23%. This difference in the incidence of AF is explained by the different ages of the patients in different studies and the different times of application of both reperfusion and drug therapies in acute myocardial infarction (AMI). About 6–8% of patients who underwent percutaneous intervention within AMI have an indication for oral anticoagulant therapy with vitamin K antagonists or new oral anticoagulants (NOAC).The use of oral anticoagulant therapy should be consistent with individual risk of bleeding as well as ischemic risk. Both HAS-BLED and CHA2DS2VASc scores are most commonly used for risk assessment. Except in patients with mechanical valves and antiphospholipid syndrome, NOACs have an advantage over vitamin K antagonists (VKAs). One of the advantages of NOACs is the use of fixed doses, where there is no need for successive INR controls, which increases the patient’s compliance in taking these drugs. The use of triple therapy in ACS is indicated in the case of patients with AF, mechanical valves as well as venous thromboembolism. The results of the studies showed that when choosing a P2Y12 receptor blocker, less potent P2Y12 blockers such as Clopidogrel should be chosen, due to the lower risk of bleeding. It has been proven that the presence of AF within AMI is associated with a higher degree of reinfarction, more frequent stroke, high incidence of heart failure, and there is a correlation with an increased risk of sudden cardiac death. With the appearance of AF in ACS, its rapid conversion into sinus rhythm is necessary, and in the last resort, good control of heart rate in order to avoid the occurrence of adverse clinical events.

Highlights

  • Atrial fibrillation is an atrial tachyarrhythmia characterized by uncoordinated atrial depolarization, with impaired mechanical function and variable, irregular ventricular frequency

  • It has been proven that the presence of atrial fibrillation (AF) within acute myocardial infarction (AMI) is associated with a higher degree of reinfarction, more frequent stroke, high incidence of heart failure, and there is a correlation with an increased risk of sudden cardiac death

  • The literature lists some of the mechanisms for the occurrence of AF within AMI: atrial ischemia, sinoatrial node ischemia, right ventricular ischemia, and left ventricular dysfunction, acute heart failure leading to atrial fibrillation and stimulating cardiomyocyte excitability, sympathetic dysfunction, endothelial dysfunction and systemic inflammation

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Summary

Introduction

Atrial fibrillation is an atrial tachyarrhythmia characterized by uncoordinated atrial depolarization, with impaired mechanical function and variable, irregular ventricular frequency. The incidence of AF in acute coronary syndrome, according to studies, ranges between 2.3–23% [1,3]. This difference in the incidence of AF is explained by the different ages of the patients within different studies and the different times of application of both reperfusion and drug therapies in AMI. The literature lists some of the mechanisms for the occurrence of AF within AMI: atrial ischemia, sinoatrial node ischemia, right ventricular ischemia, and left ventricular dysfunction, acute heart failure leading to atrial fibrillation and stimulating cardiomyocyte excitability, sympathetic dysfunction, endothelial dysfunction and systemic inflammation. The effect of AF on AMI occurrence is explained by the induction of coronary thromboembolism, which accounts for approximately 3% of all AMI [8]. The influence of inflammation in both AMI and AF affects the development and progression of coronary heart disease

Association of Atrial Fibrillation and AMI
Association of ACS Treatment with the Incidence of AF
Presence of Risk Factors for AF in AMI
Laboratory Parameters
AF Predictors in AMI
Echocardiographic Parameters
Heart Failure in AMI as a Predictor of AF Development
Influence of AF on Clinical Outcome within AMI
Prevention of Thromboembolic Complications in AMI Complicated AF
Findings
10. Conclusions
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