Tag Archives: ACS

European Society of Cardiology (ESC) guidelines recommend low-density lipoprotein (LDL) below 1.4 mmol/L in patients post ACS, which differs from UK National Institute for Health and Care Excellence (NICE) guideline recommendations of 1.8 mmol/L and 1.4 mmol/L in very-high-risk patients only.6,7 The fifth European survey of Cardiovascular Disease prevention and Diabetes (EUROASPIRE V) survey showed that only 30% of post-ACS patients had low-density lipoprotein cholesterol (LDL-C) levels <1.8 mmol/L one year after discharge.8 The ACS EuroPath survey showed a considerable lack of physicians’ compliance with guidelines in managing lipid low

The COMBO™ dual therapy stent REDUCE (Short-term Dual Anti Platelet Therapy in Patients with ACS Treated with the COMBO Dual-therapy Stent), a physician-initiated, prospective, multi-centre, randomised study, was conducted in 36 hospitals in Europe and Asia, enrolling a total of 1,496 ACS patients. The study was designed to demonstrate non-inferiority of a strategy of short-term (three months) dual antiplatelet therapy (DAPT) compared to standard 12-month DAPT in patients with ACS treated with a dual-therapy stent. The stent used in the study COMBO™ (OrbusNeich) is a sirolimus-eluting stent with an abluminal biodegradable polymer matrix,

Definition of ACS Acute coronary syndromes (ACS) include unstable angina and acute myocardial infarction (AMI). AMI is classified according to those patients with electrocardiographic ST-segment elevation, ST-elevation myocardial infarction (STEMI) and those without electrocardiographic ST-segment elevation, non-ST-elevation myocardial infarction (NSTEMI).1 The requirement for a diagnosis of AMI in the universal definition is the detection of troponin release from injured cardiac myocytes with at least one value >99th centile of the upper reference limit.1 Diagnosis is confirmed only if this is associated with at least one of: symptoms of

Background Thrombus formation in the coronary tree is the principal cause of acute coronary syndromes (ACS).1 Following plaque rupture or erosion, platelets adhere to exposed ligands (collagen, von Willebrand factor [vWF]) under high-flow conditions and this leads to platelet activation. Following platelet adhesion and activation, multiple agonists are secreted, including thromboxane A2 (TXA2) and adenosine diphosphate (ADP). TXA2 further activates platelets and ADP amplifies and sustains platelets’ activation, particularly through platelet P2Y12 receptors.2 In view of the pivotal role of platelets in arterial thrombosis, blocking TXA2 pro

*citation from Havelock Ellis ‘Impressions and Comments’ Introduction Rivaroxaban is an oral direct factor Xa inhibitor belonging to the novel oral anticoagulants (NOACs) class. Concerning efficacy and tolerability, it has been reported to be more effective than enoxaparin in preventing venous thromboembolism in patients undergoing orthopaedic surgery,1,2 and was non-inferior to enoxaparin followed by warfarin in a study involving patients with established venous thrombosis.3 Its good bioavailability, rapid-action and a half-life of 5–13 h,4 associated with a highly reproducible anticoagulant activity and the same rate of bleeding compl

Summary Oral anticoagulation has been restricted to vitamin K antagonists (VKAs) for more than 50 years. Starting in the last decade of the past century, central coagulation factors such as thrombin and factor Xa were explored as potential targets for the development of novel oral anticoagulants (NOACs). This led to the successful development and approval of a novel class of direct oral anticoagulants targeting factor Xa. Rivaroxaban was the first of the novel class of agents named ‘xabans’ that are direct oral factor Xa inhibitors. Since its initial approval for thromboembolic prophylaxis after hip and knee surgery in 2008, rivaroxaban a