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246 result(s) for "Goodman, Shaun"
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Initial Invasive or Conservative Strategy for Stable Coronary Disease
Patients with stable coronary disease were randomly assigned to an initial invasive strategy with angiography and revascularization if appropriate or to medical therapy alone. At 3.2 years, there was no significant difference between the groups with respect to the estimated rate of ischemic events. The findings were sensitive to the definition of myocardial infarction.
Effect of alirocumab, a monoclonal antibody to PCSK9, on long-term cardiovascular outcomes following acute coronary syndromes: Rationale and design of the ODYSSEY Outcomes trial
Following acute coronary syndrome (ACS), the risk for future cardiovascular events is high and is related to levels of low-density lipoprotein cholesterol (LDL-C) even within the setting of intensive statin treatment. Proprotein convertase subtilisin/kexin type 9 (PCSK9) regulates LDL receptor expression and circulating levels of LDL-C. Antibodies to PCSK9 can produce substantial and sustained reductions of LDL-C. The ODYSSEY Outcomes trial tests the hypothesis that treatment with alirocumab, a fully human monoclonal antibody to PCSK9, improves cardiovascular outcomes after ACS. This Phase 3 study will randomize approximately 18,000 patients to receive biweekly injections of alirocumab (75-150 mg) or matching placebo beginning 1 to 12 months after an index hospitalization for acute myocardial infarction or unstable angina. Qualifying patients are treated with atorvastatin 40 or 80 mg daily, rosuvastatin 20 or 40 mg daily, or the maximum tolerated and approved dose of one of these agents and fulfill one of the following criteria: LDL-C ≥ 70 mg/dL, non–high-density lipoprotein cholesterol ≥ 100 mg/dL, or apolipoprotein B ≥ 80 mg/dL. The primary efficacy measure is time to first occurrence of coronary heart disease death, acute myocardial infarction, hospitalization for unstable angina, or ischemic stroke. The trial is expected to continue until 1613 primary end point events have occurred with minimum follow-up of at least 2 years, providing 90% power to detect a 15% hazard reduction. Adverse events of special interest include allergic events and injection site reactions. Interim analyses are planned when approximately 50% and 75% of the targeted number of primary end points have occurred. ODYSSEY Outcomes will determine whether the addition of the PCSK9 antibody alirocumab to intensive statin therapy reduces cardiovascular morbidity and mortality after ACS.
Restrictive or Liberal Transfusion Strategy in Myocardial Infarction and Anemia
In patients with myocardial infarction and anemia, a liberal transfusion strategy led to fewer deaths and heart attacks than a restricted transfusion strategy, but the difference was of borderline significance.
Apolipoprotein A1 Infusions and Cardiovascular Outcomes after Acute Myocardial Infarction
In patients with acute MI, multivessel coronary artery disease, and other cardiovascular risk factors, CSL112 (human plasma–derived apolipoprotein A1) did not reduce the risk of MI, stroke, or death from cardiovascular causes.
Antithrombotic Therapy after Acute Coronary Syndrome or PCI in Atrial Fibrillation
The prevention of stroke and restenosis of coronary arteries in patients with atrial fibrillation who have an acute coronary syndrome or undergo percutaneous coronary intervention relies on antithrombotic therapy. In a two-by-two factorial, randomized trial, apixaban plus clopidogrel was more effective than a vitamin K antagonist, with or without aspirin.
Prehospital Ticagrelor in ST-Segment Elevation Myocardial Infarction
This study compared administration of the antiplatelet agent ticagrelor in the ambulance with administration in the cath lab in patients with ST-segment elevation MI. Prehospital administration did not improve coronary reperfusion before PCI but did reduce the risk of stent thrombosis. Effective antiplatelet therapy combining the inhibition of both thromboxane A 2 –dependent platelet aggregation and P2Y 12 receptors is necessary in patients undergoing percutaneous coronary intervention (PCI), particularly those with ST-segment elevation myocardial infarction (STEMI). Studies in this patient population have shown that the more intense P2Y 12 -receptor inhibition achieved with the use of prasugrel, ticagrelor, or cangrelor, as compared with clopidogrel, is associated with better clinical outcomes and a lower risk of stent thrombosis. 1 – 5 The benefit was obtained with in-hospital administration of these drugs, and it is not known whether earlier administration would be as safe and . . .
Empagliflozin after Acute Myocardial Infarction
Among patients hospitalized for acute myocardial infarction and at risk for heart failure, empagliflozin did not lead to a significantly lower risk of a first heart-failure hospitalization or death from any cause than placebo.
Asundexian versus Apixaban in Patients with Atrial Fibrillation
A randomized trial of the factor XIa inhibitor asundexian was stopped early owing to a higher incidence of stroke or systemic embolism than with apixaban therapy among patients with atrial fibrillation.
Abelacimab versus Rivaroxaban in Patients with Atrial Fibrillation
Abelacimab is a fully human monoclonal antibody that binds to the inactive form of factor XI and blocks its activation. The safety of abelacimab as compared with a direct oral anticoagulant in patients with atrial fibrillation is unknown. Patients with atrial fibrillation and a moderate-to-high risk of stroke were randomly assigned, in a 1:1:1 ratio, to receive subcutaneous injection of abelacimab (150 mg or 90 mg once monthly) administered in a blinded fashion or oral rivaroxaban (20 mg once daily) administered in an open-label fashion. The primary end point was major or clinically relevant nonmajor bleeding. A total of 1287 patients underwent randomization; the median age was 74 years, and 44% were women. At 3 months, the median reduction in free factor XI levels with abelacimab at a dose of 150 mg was 99% (interquartile range, 98 to 99) and with abelacimab at a dose of 90 mg was 97% (interquartile range, 51 to 99). The trial was stopped early on the recommendation of the independent data monitoring committee because of a greater-than-anticipated reduction in bleeding events with abelacimab. The incidence rate of major or clinically relevant nonmajor bleeding was 3.2 events per 100 person-years with 150-mg abelacimab and 2.6 events per 100 person-years with 90-mg abelacimab, as compared with 8.4 events per 100 person-years with rivaroxaban (hazard ratio for 150-mg abelacimab vs. rivaroxaban, 0.38 [95% confidence interval {CI}, 0.24 to 0.60]; hazard ratio for 90-mg abelacimab vs. rivaroxaban, 0.31 [95% CI, 0.19 to 0.51]; P<0.001 for both comparisons). The incidence and severity of adverse events appeared to be similar in the three groups. Among patients with atrial fibrillation who were at moderate-to-high risk for stroke, treatment with abelacimab resulted in markedly lower levels of free factor XI and fewer bleeding events than treatment with rivaroxaban. (Funded by Anthos Therapeutics; AZALEA-TIMI 71 ClinicalTrials.gov number, NCT04755283.).
Evacetrapib and Cardiovascular Outcomes in High-Risk Vascular Disease
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 . . .