Routine use of fondaparinux in acute coronary syndromes: a 2-year multicenter experience

François Schiele1, Nicolas Meneveau, Marie France Seronde

  • 1Department of Cardiology, University Hospital Jean-Minjoz, Besançon, France. francois.schiele@univ-fcomte.fr

American Heart Journal
|February 16, 2010
PubMed

Insights

Fondaparinux use increased in acute coronary syndrome patients from 2006-2007. Fondaparinux showed lower adjusted mortality than unfractionated heparin (UFH) and similar outcomes to enoxaparin.

Area of Science:

  • Cardiology
  • Pharmacology
  • Clinical Medicine

Background:

  • Fondaparinux recently approved for acute coronary syndromes (ACS).
  • Anticoagulant use patterns in ACS patients require investigation.
  • Understanding treatment shifts is crucial for patient outcomes.

Purpose of the Study:

  • To describe changes in anticoagulant use (UFH, enoxaparin, fondaparinux) in ACS patients between 2006-2007.
  • To compare 30-day mortality and major bleeding rates based on initial and final anticoagulant therapy.

Main Methods:

  • Multicenter registry analysis of 2,874 ACS patients.
  • Comparison of monthly anticoagulant use rates (UFH, enoxaparin, fondaparinux).
  • Assessment of initial, final, and switched anticoagulation strategies.

Main Results:

  • Fondaparinux use increased significantly, replacing enoxaparin and switching from UFH.
  • Patients receiving UFH were older, had more comorbidities, and higher risk.
  • Adjusted 30-day mortality and combined endpoint rates were higher with UFH compared to fondaparinux or enoxaparin.

Conclusions:

  • Fondaparinux use surged in ACS patients between 2006-2007.
  • Fondaparinux demonstrated lower adjusted mortality than UFH.
  • Outcomes for enoxaparin and fondaparinux were comparable in ACS patients.
Abstract

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...
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...
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...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
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...