Explore the vast range of titles available.

Myocardial ischaemia resulting from obstructive coronary artery disease is a major cause of morbidity and mortality in the developed world. Coronary artery bypass graft (CABG) surgery is the gold-standard treatment in many patients with complex multivessel coronary artery disease or left main disease. Despite substantial improvements in the outcome of patients undergoing CABG surgery in the past decade, graft patency remains the ‘Achilles’ heel’ of this procedure. Whereas the use of the left internal mammary artery as a conduit is associated with the highest 10-year patency rate (>90%), saphenous vein grafts — the most commonly used conduit in CABG surgery — fail in 40−50% of treated patients by 10 years after surgery. Vein graft disease (VGD) and failure result from complex pathophysiological processes that can lead to complete occlusion of the graft, affecting long-term clinical outcomes. Optimal harvesting techniques, intraoperative preservation strategies and intraoperative patency control have important roles in the prevention of VGD. In addition, several studies published in the past decade have reported similar mid-term patency rates between vein grafts and arterial grafts when veins are used as a composite graft based on the internal mammary artery. In this Review, we present the latest evidence on the utilization of saphenous vein grafts for CABG surgery and provide an overview of the current practices for the prevention of VGD and vein graft failure.Although saphenous vein grafts (SVGs) are the most commonly used conduit in coronary artery bypass graft surgery, vein graft failure (VGF) occurs in almost half of all patients with SVGs by 10 years after surgery. In this Review, Caliskan and colleagues discuss approaches to prevent saphenous VGF, including optimal harvesting techniques and intraoperative preservation strategies.

Andexanet alfa, a catalytically inactive decoy of factor Xa, successfully reversed the factor Xa inhibitory effects of rivaroxaban and apixaban in a small study involving patients with acute major bleeding. In randomized clinical trials, factor Xa inhibitors have been shown to be safe and effective for the treatment and prevention of venous thromboembolism and for stroke prevention in patients with atrial fibrillation. 1 – 4 However, factor Xa inhibitors have been associated with major and even fatal bleeding events. 1 – 4 Such episodes of acute major bleeding may be difficult to treat because there is no reversal agent. Andexanet alfa (andexanet) has been designed and developed specifically to reverse the effects of both direct and indirect factor Xa inhibitors. It is a recombinant, modified human factor Xa decoy protein that binds factor Xa . . .

In this placebo-controlled trial, 7119 patients were randomly assigned at 3 months after PCI to either receive ticagrelor alone or continue dual therapy with ticagrelor plus aspirin. The trial evaluated bleeding and ischemic end points at 1 year.

This trial compared standard therapy (dual antiplatelet therapy plus a vitamin K antagonist) with two regimens containing rivaroxaban plus antiplatelet therapy. The rivaroxaban groups had reduced rates of bleeding and similar efficacy in preventing cardiovascular events. Approximately 5 to 8% of patients who undergo percutaneous coronary intervention (PCI) have atrial fibrillation. 1 – 3 Dual antiplatelet therapy (DAPT) with a P2Y 12 inhibitor and aspirin is superior to oral anticoagulation with a vitamin K antagonist in reducing the risk of thrombosis in patients undergoing placement of a first-generation stent, 4 but oral anticoagulation is superior to DAPT in reducing the risk of ischemic stroke in patients with atrial fibrillation. 5 The treatment strategy for patients with atrial fibrillation who have received stents must balance the risk of stent thrombosis and ischemic stroke with the risk of bleeding. A common guideline-supported . . .

In a single-group trial, 352 patients with acute major bleeding while taking a factor Xa inhibitor were treated with andexanet. Andexanet markedly reduced anti–factor Xa activity, and 82% of the patients had excellent or good hemostatic efficacy at 12 hours.

In a randomized trial involving patients with high-risk vascular disease, the cholesteryl ester transfer protein inhibitor evacetrapib had favorable effects on established lipid biomarkers but was not associated with a lower rate of cardiovascular events than placebo. Pharmacologic reduction of the low-density lipoprotein (LDL) cholesterol level with statins substantially decreases the risks of death and complications from cardiovascular causes. 1 , 2 Considerable interest has focused on the identification of approaches that might further reduce cardiovascular-event rates among high-risk patients. 3 Epidemiologic studies have shown inverse associations between high-density lipoprotein (HDL) cholesterol levels and cardiovascular outcomes, 4 – 6 a correlation that persists despite treatment with statins. 7 Nevertheless, therapeutic interventions that raise the HDL cholesterol level have not been shown to reduce cardiovascular risk. Cholesteryl ester transfer protein (CETP) modulates the transfer of esterified cholesterol from HDL to apolipoprotein B–containing lipoproteins. 8 Two . . .

For many years, bleeding has been perceived as an unavoidable consequence of strategies aimed at reducing thrombotic complications in patients undergoing percutaneous coronary intervention (PCI). However, the paradigm has now shifted towards bleeding being recognized as a prognostically unfavourable event to the same extent as having a new or recurrent ischaemic or thrombotic complication. As such, in parallel with progress in device and drug development for PCI, there is clinical interest in developing strategies that maximize not only the efficacy but also the safety (for example, by minimizing bleeding) of any antithrombotic treatment or procedural aspect before, during or after PCI. In this Review, we discuss contemporary data and aspects of bleeding avoidance strategies in PCI, including risk stratification, timing of revascularization, pretreatment with antiplatelet agents, selection of vascular access, choice of coronary stents and antithrombotic treatment regimens.In this Review, Angiolillo and colleagues discuss the latest evidence and updates on bleeding avoidance strategies in patients undergoing percutaneous coronary intervention, including risk stratification, timing of revascularization, pretreatment with antiplatelet agents, selection of vascular access, choice of coronary stents and antithrombotic treatment regimens.

Dual antiplatelet therapy (DAPT) cessation increases the risk of adverse events after percutaneous coronary intervention (PCI). Whether risk changes over time, depends on the underlying reason for DAPT cessation, or both is unknown. We assessed associations between different modes of DAPT cessation and cardiovascular risk after PCI. The PARIS (patterns of non-adherence to anti-platelet regimens in stented patients) registry is a prospective observational study of patients undergoing PCI with stent implantation in 15 clinical sites in the USA and Europe between July 1, 2009, and Dec 2, 2010. Adult patients (aged 18 years or older) undergoing successful stent implantation in one or more native coronary artery and discharged on DAPT were eligible for enrolment. Patients were followed up at months 1, 6, 12, and 24 after implantation. Prespecified categories for DAPT cessation included physician-recommended discontinuation, brief interruption (for surgery), or disruption (non-compliance or because of bleeding). All adverse events and episodes of DAPT cessation were independently adjudicated. Using Cox models with time-varying covariates, we examined the effect of DAPT cessation on major adverse events (MACE [composite of cardiac death, definite or probable stent thrombosis, myocardial infarction, or target-lesion revascularisation]). Incidence rates for DAPT cessation and adverse events were calculated as Kaplan-Meier estimates of time to the first event. This study is registered with ClinicalTrials.gov, number NCT00998127. We enrolled 5031 patients undergoing PCI, including 5018 in the final study population. Over 2 years, the overall incidence of any DAPT cessation was 57·3%. Rate of any discontinuation was 40·8%, of interruption was 10·5%, and of disruption was 14·4%. The corresponding overall 2 year MACE rate was 11·5%, most of which (74%) occurred while patients were taking DAPT. Compared with those on DAPT, the adjusted hazard ratio (HR) for MACE due to interruption was 1·41 (95% CI 0·94–2·12; p=0·10) and to disruption was 1·50 (1·14–1.97; p=0·004). Within 7 days, 8–30 days, and more than 30 days after disruption, adjusted HRs were 7·04 (3·31–14·95), 2·17 (0·97–4·88), and 1·3 (0·97–1·76), respectively. By contrast with patients who remained on DAPT, those who discontinued had lower MACE risk (0·63 [0·46–0·86]). Results were similar after excluding patients receiving bare metal stents and using an alternative MACE definition that did not include target lesion revascularisation. In a real-world setting, for patients undergoing PCI and discharged on DAPT, cardiac events after DAPT cessation depend on the clinical circumstance and reason for cessation and attenuates over time. While most events after PCI occur in patients on DAPT, early risk for events due to disruption is substantial irrespective of stent type. Bristol-Myers Squibb and Sanofi-Aventis.

ST-segment elevation myocardial infarction (STEMI) is the most acute manifestation of coronary artery disease and is associated with great morbidity and mortality. A complete thrombotic occlusion developing from an atherosclerotic plaque in an epicardial coronary vessel is the cause of STEMI in the majority of cases. Early diagnosis and immediate reperfusion are the most effective ways to limit myocardial ischaemia and infarct size and thereby reduce the risk of post-STEMI complications and heart failure. Primary percutaneous coronary intervention (PCI) has become the preferred reperfusion strategy in patients with STEMI; if PCI cannot be performed within 120 minutes of STEMI diagnosis, fibrinolysis therapy should be administered to dissolve the occluding thrombus. The initiation of networks to provide around-the-clock cardiac catheterization availability and the generation of standard operating procedures within hospital systems have helped to reduce the time to reperfusion therapy. Together with new advances in antithrombotic therapy and preventive measures, these developments have resulted in a decrease in mortality from STEMI. However, a substantial amount of patients still experience recurrent cardiovascular events after STEMI. New insights have been gained regarding the pathophysiology of STEMI and feed into the development of new treatment strategies. ST-segment elevation myocardial infarction (STEMI) is an acute coronary syndrome in which transmural ischaemia (mostly caused by the formation of a thrombus on a ruptured atherosclerotic plaque) leads to cardiomyocyte death. STEMI is associated with considerable morbidity and mortality worldwide.

In patients with acute coronary syndromes, low doses of rivaroxaban were effective in reducing the primary end point of death from cardiovascular causes, myocardial infarction, or stroke. Rivaroxaban also reduced overall mortality, although there was more bleeding. After an acute coronary syndrome, patients remain at risk for recurrent cardiovascular events despite standard medical therapy, including long-term antiplatelet therapy with aspirin and an adenosine diphosphate–receptor inhibitor. This risk may be related in part to excess thrombin generation that persists beyond the acute presentation in such patients. 1 As a result, there has been interest in evaluating the role of oral anticoagulants after an acute coronary syndrome. Improved cardiovascular outcomes were reported for patients who were treated with the anticoagulant warfarin in addition to aspirin. 2 However, widespread use of long-term warfarin in such patients has been limited by challenges associated . . .