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Featured Commentaries from August - September 2007
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Lectin-like Oxidized Low-density Lipoprotein Receptor-1 (LOX-1): a New Promising Target for Therapy of Atherosclerosis-related Diseases
Authors: Changping Hu, Abhijit Dandapat, and Jawahar L. Mehta
Atherogenesis is a complex process initiated by endothelial dysfunction. This early step is followed by deposition of oxidized lipids in monocytes/macrophages, smooth muscle cell proliferation and migration, and an intense inflammatory reaction. Rupture of the soft inflamed atherosclerotic plaque results in exposure of sub-endothelial collagen to platelets and occlusion of the artery. Production of reactive oxygen species (ROS) is also increased in atherosclerotic arteries well beyond the capability of endogenous antioxidants to inactivate them [1].
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Psychosocial Stress Factors and the Metabolic Syndrome: Evidence for Their Relationship and the Role of Cortisol
Authors: Nicole Vogelzangs, M.Sc. and Brenda Penninx, Ph.D.
Cardiovascular disease (CVD) and diabetes are among the most common life-threatening diseases causing distress and disability [1]. In the recent history of psychosomatic research, psychosocial stress factors have repeatedly been found to be risk factors for CVD and diabetes. For instance, depression and anxiety have been shown to increase the risk of new CVD events, new coronary heart disease (CHD) events, cardiac mortality [2-4], and diabetes [5]. In addition to these psychiatric diagnoses, lack of emotional support and experience of major stressful life events have also been shown to subsequently increase the risk of CVD, CHD, and diabetes [6,7].
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Clinical Significance of Statin Induced HDL-C Increase
Authors:
Vasilios G. Athyros, Asterios Karagiannis , and Dimitri P. Mikhailidis
Apo-B100-containing lipoproteins and especially low-density lipoprotein cholesterol (LDL-C) are directly implicated in the formation and progression of atherosclerotic plaques and eventually to the pathogenesis of cardiovascular events. A large body of evidence supports a central role for lowering levels of LDL-C in the prevention of cardiovascular disease (CVD). Thus, the National Cholesterol Educational Program (NCEP) guidelines almost exclusively target LDL-C [1] and we now have the entire range of LDL-C targets for primary and secondary CVD prevention. Moreover, the available powerful statins and the dual inhibition strategy (statin plus ezetimibe) provide the means to attain these targets. However, if we want even larger CVD event reductions we have to investigate other lipid targets, besides LDL-C, that might provide additional clinical benefit.
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Childhood Overweight, Obesity, and Metabolic Syndrome in Developing Countries
Authors:
Roya Kelishadi, M.D
The potential increase in chronic disease is escalating much more rapidly in low- and middle-income than high-income countries. According to the World Health organization (WHO) estimates, by the year 2020, chronic diseases will account for approximately three-quarters of all death in the developing world [1]. Obesity is a major risk factor for chronic diseases and plays a central role in the metabolic syndrome (MetS), and as a result, an increased risk of atherosclerotic cardiovascular diseases.
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Metabolic Risk Factor Clustering and Cardiovascular Mortality: Important Role of Glucose Tolerance on CVD Mortality
Authors:
Aya Kadota, M.D.
Prevention of cardiovascular disease (CVD) is a worldwide major healthcare burden since it impairs our activities of daily living and quality of life. The World Health Organization (WHO) states that individual risk factors for CVD convey great CVD risk. Furthermore, even though each one of these risk factors alone is not serious, the risk becomes more “powerful” when they are combined [1]. Metabolic syndrome is the concept of clustering metabolic risk factors comprising insulin resistance, abdominal fat distribution, dyslipidemia, hypertension, and so on [2-5].
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Diabetes and Plaque Destabilization: Role of Ubiquitin Proteasome Activity Deregulation
Authors:
Raffaele Marfella, M.D., Ph.D. and Giuseppe Paolisso, M.D., Ph.D.
In middle-aged patients, the seven-year incidence of myocardial infarction among patients without diabetes who had pre-existing CHD was similar to that among patients with diabetes who did not have CHD, suggesting that type 2 diabetes may confer the same degree of risk as pre-existing CHD [1]. The issue of the association between diabetes and CHD is likely to become more important for two reasons. First, the incidence of type 2 diabetes is increasing among both high-risk populations and low-risk populations [2].
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Autoantibodies Recognizing Specific Antigens in Oxidized LDL - Do They Have a Protective Role?
Authors:
Gunilla Nordin Fredrikson and Jan Nilsson
During the last ten to fifteen years there has been a dramatic shift in the way we look on at mechanisms involved in the pathogenesis of atherosclerosis. From being regarded as a result of passive lipid accumulation and activation of smooth muscle cell proliferation, atherosclerosis is now seen as a degenerative inflammatory disease involving multiple aspects of both innate and adaptive immunity. This has focused attention on the immune system as a possible novel target in prevention and treatment of ischemic heart disease and stroke.
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Fish intake and QTc protection
Christina Chrysohoou, M.D., Ph.D.
The Mediterranean type of diet has been proved to have a significant ben ef icial impact on the progression of cardiovascular diseases. Fish is one of the main components of this diet; while many epidemiological studies and clinical trials have indicated its antioxidant and anti-inflammatory properties and its ben ef icial ef fects on the clinical outcome in patients with cardiovascular disease [1,2]. Furthermore, many studies have shown long-chain omega-3 polyunsaturated fatty acids (n-3 LC-PUFAs), which comprise the most important components of fish diet, may protect against heart disease mortality and morbidity.
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A Simple Demographic Model to Predict the Prevalence of Cardiometabolic Risk Factors
Authors: Richard E Scranton, M.D., MPH
Cardiometabolic risk (CMR) factors, including obesity, dyslipidemia, increased blood pressure, and insulin resistance, are health conditions known to increase the risk of cardiovascular disease [1,2]. The growing concern of errant weight coupled with prevalent metabolic derangements has raised awareness from all sectors of the healthcare society. How best to manage this unfortunate reality has also been of interest to public heath officials, ministries of health, and professional medical societies. Lifestyle modification is the commonly cited solution. Despite the bulging medical costs often attributed to this prevalent condition, many large employers fail to provide or cover lifestyle modification services [3].
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Oral Direct Thrombin Inhibitors and Atherosclerosis
Authors: Marc Husmann, M.D. and Matthias Barton, M.D.
Atherothrombosis is the most frequent cause of morbidity and mortality in the Western world and is present in all major vascular pathologies, which encompasses myocardial infarction, cerebrovascular disease, and peripheral arterial disease [1-6]. Plaque disruption and subsequent thrombus formation play a critical role in the clinical manifestations of atherothrombosis, such as myocardial infarction or stroke [7,8].
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Low Plasma RANTES Levels Are an Independent Predictor of Cardiac Mortality in Patients Referred for Coronary Angiography
Author:
Erdal Cavusoglu, M.D.
There is growing evidence which implicates inflammation in the initiation, progression, and complications of atherosclerosis [1,2]. Chemotactic chemokines, or chemokines, are a family of small secreted proteins that play a central role in the inflammatory process because of their ability to direct the migration of leukocytes to sites of vascular injury and inflammation, including developing atherosclerosis [3-6]. They are classified into 4 major groups, according to the arrangement of the conserved cysteine (C) residues in the mature proteins [7]. CC chemokines, which have the first 2 conserved cysteine residues adjacent to each other, constitute the largest family of chemokines. They tend to attract mononuclear cells and are found at sites of chronic inflammation [3].
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What Does It Take To Be a Syndrome? Need For a Thoughtful Consensus before Judging the Metabolic Syndrome
Author: Dhananjay Vaidya, Ph.D., M.P.H.
The metabolic syndrome was proposed as an entity ~20 years ago [1], however questions about the clinical utility of the concept continue to be raised. Some conclude from published data that the concept is not us ef ul [2,3], while others conclude that the data support its use [4]. This raises the doubt that experts may differ about what constitutes utility, but this issue has not been explicitly discussed by most commentators.
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Soy and Metabolic Syndrome
Author: Leila Azadbakht, Ph.D.
The metabolic syndrome is a heterogeneous condition accompanied by visceral adiposity, dyslipidemia, hypertension, and insulin resistance [1,2]. Elevated blood levels of inflammatory markers such as C-reactive protein (CRP), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-18 (IL-18), and tumor necrosis factor-a (TNF-a), and endothelial dysfunction are associated with features of the metabolic syndrome [3-7]. Fat accumulation, a serious problem in the metabolic syndrome, is correlated with systemic oxidative stress in humans [8,9]. Oxidative stress may play critical roles in the pathogenesis of various features of the metabolic syndrome, via impairment of glucose uptake in muscle and fat and reduction in insulin secretion [10].
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Could Adiponectin Reduce Atherosclerotic Plaque Sizes Via Paracirne Pathway in Blood Vessels?
Authors:
Chang-Jiang Li, Hui-Wen Sun, and Mei Zhang
Traditionally, adipose has been considered a simple energy storage tissue, but mounting evidence suggests that it can produce and secrete many bioactive substances, collectively r ef erred to as adipocytokines. One of these, adiponectin, has significant roles in regulating the metabolism of glucose and fatty acids and in protecting against atherosclerosis. Adiponectin is a collagen-like protein whose gene is located on human chromosome 3q27 and is named as apM 1 gene. The full-length of apM 1 gene is 17 kbp, which includes 3 exons and 2 introns. The full-length of apM 1 mRNA is 4,517 bp.
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Platelet Hyperactivity: An Unrecognized Vascular Risk Factor in Patients with Metabolic Syndrome
Author: Victor Serebruany, M.D., Ph.D.
Vascular occlusive events, dependent on the location of the targeted vessel, including myocardial infarction, unstable angina, stroke, and peripheral vascular diseases, are the leading causes of death in developed countries. Coronary atherosclerosis is responsible for nearly 40% of all deaths in the U.S.A. [1], and nearly half of the mortality in the European Union [2]. The World Health Organization estimates that close to 17 million patients die around the globe each year of vascular disease and, by 2020, this number is projected to grow to 25 million annually [3]. In terms of years lost, vascular death will rise from fourth to first, while as a cause of premature death and disability, from fifth to first, thus becoming the leading cause of death in the world by 2020 [4]. As the cornerstone to the clinical complications of atherothrombosis, blood platelets are unquestionably involved in the pathophysiology of the thrombotic events [5,6]. This concept has been proven by the numerous large clinical trials of antiplatelet therapy that demonstrate significant benefit of moderate platelet inhibition with various pharmacological agents including aspirin [7], ticlopidine [8], or clopidogrel [9].
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Rationale and Use of Vascular Cell Adhesion Molecule - 1 (VCAM-1) as a Target for the Molecular Imaging of Vulnerable Plaque
Authors: Laurent M. Riou, Ph.D., Julien Dimastromatteo, M.S., Daniel Fagret, M.D., Ph.D., and Catherine Ghezzi, Ph.D.
Atherosclerotic cardiovascular diseases (CVD) are the leading cause of mortality worldwide, accounting for > 19.10 6 deaths annually [1,2]. Despite major advances in the treatment of CVD patients, a high proportion of CVD victims die suddenly while being apparently healthy, the great majority of these accidents due to the rupture or erosion of a vulnerable coronary atherosclerotic plaque. Indeed, an acute heart attack is the first symptom of atherosclerosis in as much as 50% of individuals with severe disease. This is due to the fact that risk stratification is currently based on the evaluation of the Framingham risk score in the United States or the Systemic Coronary Risk Evaluation (SCORE) in Europe and that most heart attacks occur in an intermediate-risk group to which the majority of the population pertains and in which risk factors are of low predictive power [3].
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Early Human Atherogenesis: Retention of Lipids in Intimal Thickenings Followed by Response of Macrophages
Author: Yutaka Nakashima, M.D., Ph.D.
Little is known as to how early human atherosclerosis develops. In the classic gross pathological study, Holman et al. showed that the fatty streak, a non-raised sudanophilic lesion, is the earliest lesion that appears in the aorta of children and adolescents and some fatty streaks convert into the advanced raised lesion in later life [1]. However, it is not clear how fatty streaks develop from normal arteries and covert into more advanced lesions. Based on microscopic findings, Virmani et al. defined the pathologic intimal thickening (PIT) as a preatheromatous lesion that is composed of extracellular lipid pools with an overlying layer of SMCs and lipid-laden macrophages [2].
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Vascular Risk Factors and Oxidative Stress as Independent Predictors of Asymptomatic Atherosclerosis in Adult Patients with Epilepsy
Authors: Sherifa A. Hamed, Enas A. Hamed, Ragaa Hamdy, and Toshitaka Nabeshima
Epilepsy is a frequent chronic medical problem [1]. In the last decade, several data are available about a number of vascular markers that are critically implicated in predisposition of atherosclerosis in patients with epilepsy [2]. However, there is still not enough information on the incidence of asymptomatic atherosclerosis among patients with epilepsy. We conducted our study in a relatively large number of adult epileptic patients (n = 225), untreated and treated with conventional antiepileptic drugs (AEDs), e.g. carbamazepine or CBZ, valproate or VPA, and combination therapy, with no manifest vascular disease or risk factors for atherosclerosis, to test the hypothesis that epileptic patients are at high risk for atherosclerosis.
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Resistin As an Inflammatory Marker in Subjects with Chronic Kidney Disease
Author: Subhashini Yaturu, M.D.
Cardiovascular disease (CVD) is the most common cause of mortality in patients with chronic kidney disease (CKD) and end-stage kidney disease (ESKD); subjects with CKD are considered as potential candidates for aggressive risk factor reduction. Recent studies show that even mild renal dysfunction is associated with an increased CVD risk. [1,2] Around 20 million adults in the United States have CKD, 8 million of whom are classified as having moderate or severe kidney disease. People with CKD have multiple metabolic abnormalities that may accelerate atherosclerosis, such as hypertension, insulin resistance, and dyslipidemia, along with other CKD-related risk factors.
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