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International Atherosclerosis |
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Featured IAS Commentaries These Commentaries, including all information, text, graphics, images, and other material are for general educational purposes only and are not intended to be used for the purposes of providing medical treatment or attention or making medical or health-related decisions. These Commentaries are not a substitute or replacement for medical advice. If you are seeking medical advice, we encourage you to consult a physician or other medical professional. The views expressed in these Commentaries are those of the authors and are not necessarily those of IAS. COMMENTARIES POSTED IN MAY 2010
Site-Specific Athero-Susceptible Endothelial
Phenotype Shows Prominent Adaptive ER-Stress and Unfolded Protein
Responses in Vivo Atherosclerosis is not a diffuse disease;
it has been noted for centuries that lesion development is associated
with arterial curvatures, asymmetries, and branches where the
non-uniform arterial geometry generates patterns of blood flow
that are considerably more complex than elsewhere. Since it is
well established that endothelial cells are highly sensitive
to flow/shear stress, a biomechanical contribution to localized
susceptibility is likely. Athero-susceptible endothelium in vivo
expresses a different repertoire of cell phenotypes than that
in nearby protected locations [1]. Identification of important
differences in gene and protein expression and the mechanisms
responsible requires both global profiling and classic cell and
molecular approaches. Recently, the chronic activation of a common
signature of cellular stress in endothelium has emerged as a
potential underlying contributor to athero-susceptibility. Intravascular Ultrasound (IVUS) Attenuated Plaque. A Finding Not Limited to
Culprit Lesion Sites Intravascular ultrasound (IVUS) allows limited classification of atherosclerotic plaque morphology as echolucent (“lipid-rich”), echodense (“fibrous”), and echodense with shadowing (“calcified”) plaque [1]. Acoustic shadowing describes areas of signal void behind highly reflective or absorbent structures and is typically seen behind calcified plaque or dense fibrous plaques. However, recent observations at culprit lesions in patients with acute coronary syndromes have described acoustic shadowing behind large, echolucent plaques. This finding has been termed “attenuated plaque” and has been considered an IVUS characteristic of high-risk lesions [2-4]. However, the presence and frequency in stable, non-culprit lesion sites is incompletely known. Vascular Risk Factors, Endothelial Function, and Carotid Thickness in Patients
with Migraine: Relationship to Atherosclerosis Migraine is a common presenting complaint encountered in neurology and internal medicine clinics. The World Health Organization ranks migraine among the world’s most disabling medical illnesses as it creates a significant and chronic burden for patient during and between attacks in terms of pain and its effects on functional capacity and quality of life [1]. Migraine has a variable prevalence worldwide despite the unifying use of the new operational International Headache Society (IHS) criteria [2]. For example, in European and American studies, the one-year period prevalence of migraine in adults is estimated at 10-15% [3,4], while in Arab countries and Africa, it is estimated at 2.6-19% [5,6]. In a study of Egyptian school children in Assiut, the prevalence of migraine is 16.6% [7]. Predictive Role of Circulating Levels of C-Reactive Protein in Hypertensive
Subjects with Subclinical Carotid Lesions: beyond the Traditional Cardiovascular
Risk Factors Traditional risk factors (RFs) for atherosclerosis (ATS), such as age, blood pressure, smoke, cholesterol, high-density lipoprotein cholesterol, and diabetes mellitus, have been shown to be predictive of coronary and cerebrovascular disease in a large number of prospective observational studies [1-3]. Novel biomarkers have also been investigated as possible indicators of increased risk [4-6]. Ample evidence, indeed, suggested the pivotal causal role of inflammation [7] in the atherosclerotic process from endothelial dysfunction to plaque rupture and thrombosis. As a consequence, the various cytokines and cytokine-inducible inflammatory molecules are progressively becoming markers of ATS [8,9]. Atherothrombosis of the coronary and cerebral vessels could then be a disorder of inflammation and innate immunity, as well as a disorder of lipid accumulation [10]. Some data suggest important relationships between inflammation and traditional cardiovascular RFs: plasmatic reactants may play an integral role in either the biological mechanisms of these cardiovascular RFs or provide a marker of smouldering systemic vascular disease. The Role
of Oxidized Low-Density Lipoprotein/ß2-Glycoprotein I
Complexes in Autoimmune-Mediated Atherothrombosis Atherosclerotic cardiovascular disease is a frequent complication in autoimmunity. Patients with systemic autoimmune diseases, i.e. systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS), often develop severe atherothrombotic events involving both the venous and arterial vasculatures [1,2]. Antiphospholipid antibodies are thought to play a direct pathogenic role in the development of the thrombotic complications of APS [3,4]. Venous thromboembolism is common with an incidence of 60-75%; however, over one third of APS patients may develop arterial thrombosis (myocardial infarction, cerebrovascular accident, etc.) [5], suggesting a possible pro-atherogenic role of autoimmune inflammation and antiphospholipid antibodies in arterial thrombosis (atherothrombosis). Human Monocyte Heterogeneity and Cardiometabolic Risk Obesity and cardiovascular diseases are worldwide growing health issues with a closely intertwined pathophysiology. Caloric excess with consecutive obesity is associated with traditional and non-traditional cardiovascular risk factors, such as hypertension, dyslipidemia, and inflammation, leading in concert to the elevated cardiovascular risk of obese subjects [1]. The underlying mechanisms by which obesity confers its cardiovascular risk are nevertheless still poorly understood. Angiopoietin-2: Cause
or Effect of Endothelial Micro-Inflammation Some new cardiovascular (CV) risk markers (e.g. C-reactive protein) are powerful in the prediction of CV disease [2], endothelial dysfunction [3], or mortality [4] than established factors such as cholesterol. Furthermore, there is increasing evidence that some of these markers my also act as mediators directly contributing to the complex pathophysiology of atherosclerosis [5]. |
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