762 research outputs found

    Myocardial infarction and coronary care units

    Get PDF

    Editor-in-Chief's Picks From 2014: Part One

    Get PDF
    As I spent countless hours pouring over hundreds of manuscripts to select those that rose to the top over the past year, I became incredibly excited about being part of a Journal that produces such wonderfully rich and diverse content each year. I have personally selected the papers (both original investigations and review articles) from 13 distinct specialties for your review. There are approximately 150 articles selected across this 2-part series, which represents less than 3% of the papers submitted to JACC in 2014. In order to present the full breadth of this important research in a consumable fashion, we will present these manuscripts over the course of 2 issues of JACC.Part One includes the sections: Congenital Heart Disease, Coronary Disease & Interventions, Genetics, Omics, & Tissue Regeneration, CV Prevention & Health Promotion, Cardiac Failure, and Cardiomyopathies (1–70). Part Two includes the sections: Hypertension, Imaging, Metabolic Disorders & Lipids, Neurovascular & Neurodegenerative Disorders, Rhythm Disorders, Valvular Heart Disease, and Vascular Medicine

    A First Dilemma in Cardiovascular Medicine Adherence Versus Personalized Therapy

    Get PDF

    Unraveling the Complexities of Statistical Presentation Why it Is Important

    Get PDF

    A Second Dilemma in Cardiovascular Medicine Personalized Medicine Versus Personal Interaction With the Patient

    Get PDF

    Imaging of atherosclerosis: magnetic resonance imaging

    Get PDF
    Atherosclerosis and its thrombotic complications are the major cause of morbidity and mortality in the industrialized countries. Despite advances in our understanding of the pathophysiology, pathogenesis, and new treatment modalities, the absence of an adequate non-invasive imaging tool for early detection limits both the prevention and treatment of patients with various degrees and anatomical localizations of atherothrombotic disease. An ideal clinical imaging modality for atherosclerotic vascular disease should be safe, inexpensive, non-invasive or minimally invasive, accurate, and reproducible, and the results should correlate with the extent of atherosclerotic disease and have high predictive values for future clinical events. High-resolution magnetic resonance imaging (MRI) has emerged as the most promising technique for studying atherothrombotic disease in humans in vivo. Most importantly, MRI allows for the characterization of plaque composition, i.e. the discrimination of lipid core, fibrosis, calcification, and intraplaque haemorrhage deposits. Magnetic resonance imaging also allows for the detection of arterial thrombi and in defining thrombus age. Magnetic resonance imaging has been used to monitor plaque progression and regression in several animal models of atherosclerosis and in humans. Emerging MRI techniques capable of imaging biological processes, including inflammation, neovascularization, and mechanical forces, may aid in advancing our understanding of the atherothrombotic disease. Advances in diagnosis do prosper provided they march hand-in-hand with advances in treatment. We stand at the threshold of accurate non-invasive assessment of atherosclerosis. Thus, MRI opens new strategies ranging from screening of high-risk patients for early detection and treatment as well as monitoring of the target lesions for pharmacological intervention. Identification of subclinical atherosclerosis and early treatment initiation has the potential to surpass conventional risk factor assessment and management in terms of overall impact on cardiovascular morbidity and mortality. Such strategy is currently under clinical investigatio

    Role of platelet activation and fibrin formation in thrombogenesis

    Get PDF
    Further progress in the search for more effective but safe antithrombotic agents is coupled to an improved understanding of the factors involved in arterial and venous thrombogenesis. Although arterial thrombosis is initiated by formation of a layer of platelets on modified endothelium or subendothelial constituents and subsequent recruitment of passing-by platelets, this phenomenon is not sufficient to lead to a full thrombus. Further growth of such a platelet mass depends, to a large extent, on the presence of free thrombin. Thrombin is mainly generated by activation of factor XI on the platelet contact with collagen. In addition, thrombin leads to formation of fibrin, which maintains the stability of the arterial platelet thrombus and is the main component of the venous thrombus. The search for agents that inhibit platelet activation and thrombin formation is, therefore, a logical endeavor
    • 

    corecore