[Antithrombotic treatment in acute coronary syndrome and atrial fibrillation]

H Darius1, G Görge2, M Spiecker3

  • 1Klinik für Kardiologie, Angiologie, Nephrologie und konservative Intensivmedizin, Vivantes Klinikum Neukölln, Rudower Str. 48, 12351, Berlin, Deutschland. harald.darius@vivantes.de.

Herz
|January 29, 2019
PubMed

Insights

Non-vitamin K oral anticoagulants plus a single antiplatelet agent are safer than triple therapy for patients with atrial fibrillation and acute coronary syndrome. This approach reduces bleeding complications without increasing stroke or cardiac ischemia risks.

Area of Science:

  • Cardiology
  • Pharmacology
  • Clinical Medicine

Background:

  • Increasing prevalence of atrial fibrillation (AF) and need for oral anticoagulation (OAC) in aging populations.
  • Rising incidence of patients requiring both OAC for stroke prevention and dual antiplatelet therapy (DAPT) after acute coronary syndrome (ACS) and/or percutaneous coronary intervention (PCI).
  • Traditional triple therapy (TT) for these patients has shown higher bleeding risks without proven efficacy benefits compared to other strategies.

Purpose of the Study:

  • To evaluate the efficacy and safety of non-vitamin K oral anticoagulants (NOACs) combined with antiplatelet therapy in patients with AF and ACS/PCI.
  • To compare NOAC-based strategies against traditional vitamin K antagonist (VKA) therapies and DAPT regimens.
  • To assess the bleeding risk and thrombotic events associated with different antithrombotic strategies.

Main Methods:

  • Review of prospective and randomized studies investigating all four approved NOACs for stroke prevention in AF.
  • Comparison of NOACs plus single antiplatelet therapy versus VKA plus single antiplatelet therapy, specifically excluding DAPT in some trials.
  • Analysis of published trial data (e.g., PIONEER AF-PCI, RE-DUAL PCI) and ongoing investigations (e.g., AUGUSTUS, ENTRUST-AF PCI).

Main Results:

  • NOAC plus a single antiplatelet agent demonstrates superiority over TT in terms of reduced bleeding complications.
  • No significant increase in stroke or cardiac ischemia events observed with NOAC plus single antiplatelet therapy compared to TT.
  • International guidelines now support NOAC plus single antiplatelet therapy for patients with high bleeding risk, deeming TT unnecessary for most.

Conclusions:

  • Triple therapy is no longer indicated for the majority of patients with AF who have undergone ACS or PCI.
  • Non-vitamin K oral anticoagulants combined with a single antiplatelet agent represent a safer and effective alternative to triple therapy.
  • Current evidence supports individualized antithrombotic strategies prioritizing bleeding risk reduction in AF patients with coronary indications.

Related Concept Videos

Acute Coronary Syndrome I: Introduction01:30

Acute Coronary Syndrome I: Introduction

Acute Coronary Syndrome (ACS) encompasses a spectrum of heart conditions caused by sudden obstruction of coronary arteries, typically resulting from the rupture of an atherosclerotic plaque and subsequent thrombus (blood clot) formation. This obstruction can lead to partial or complete blockage of blood flow, causing varying degrees of myocardial ischemia or infarction.ACS includes the following clinical entities:Unstable Angina (UA)Non-ST-Elevation Myocardial Infarction (NSTEMI)ST-Elevation...
958
Acute Coronary Syndrome V: Nursing Management01:26

Acute Coronary Syndrome V: Nursing Management

Nursing Assessment:Nursing management of acute coronary syndrome (ACS) involves taking the patient's history, focusing on primary complaints such as chest pain, dyspnea, and excessive sweating (diaphoresis), as well as other symptoms like back or jaw pain, nausea, vomiting, palpitations, dizziness, and fatigue. The nurse also reviews the patient's history of cardiac events, risk factors such as hypertension, diabetes, smoking, family history, and current medications.In the objective assessment,...
324
Acute Coronary Syndrome III: Diagnostic Studies01:30

Acute Coronary Syndrome III: Diagnostic Studies

Diagnosing acute coronary syndrome or ACS begins with a thorough patient history. Notable symptoms include central, crushing chest pain radiating to the left arm, neck, jaw, or back, along with shortness of breath, sweating (diaphoresis), nausea, vomiting, dizziness, and palpitations.It is crucial to note any history of cardiac illnesses and assess risk factors, including age, gender, smoking, hypertension, diabetes, hyperlipidemia, and a sedentary lifestyle.During physical examination, vital...
267
Acute Coronary Syndrome IV: Interprofessional Care01:28

Acute Coronary Syndrome IV: Interprofessional Care

IntroductionThe management of Acute Coronary Syndrome (ACS) aims to minimize myocardial damage, preserve myocardial function, and prevent complications.Initial ManagementInpatient management involves continuous cardiac monitoring, preferably in an ICU, focusing on blood pressure, serum sodium, potassium, and creatinine levels, and urine output. Ongoing pharmacologic management is crucial for stabilizing the patient.Supplemental Oxygen: Administer supplemental oxygen if oxygen saturation is...
286
Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations01:19

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the...
420
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining,...
11.9K