Open Access Medical Books


Edited by Armen Yuri Gasparyan .
504 pages . 

Our understanding of the implications of cardiovascular risk factors has greatly 
improved over the past two decades. It has been postulated that numerous risk factors 
and markers of inflammation and immune response trigger pathologic changes in the 
vascular wall from early life, leading to atherosclerotic cardiovascular disease in later 
life [1]. It has also been widely recognized that no single risk factor causes 
atherosclerotic disease, and that the likelihood of the disease depends on a 
multifactorial genetic and environmental background. The complex nature of risk 
factors and their interdependence implies the need of multidirectional preventive 
measures, which should be monitored and assessed with the use of multiple 
demographic, clinical, genetic and laboratory parameters.
Over the past decades, the dominating concept of cardiovascular prevention has been 
based on the initial results of the landmark Framingham Heart Study, which linked 
the burden of cardiovascular disease with a combination of traditional risk factors, 
such as age, sex, arterial hypertension, hyperlipidemia, smoking, obesity, diabetes, and 
sedentary lifestyle. The study led to the validation and wide-spread use of the 
Framingham Risk Score, which is an indispensable tool for stratifying cardiovascular 
risk and treatment by clinicians and deploying strategies for community-based 
primary preventive measures by health administrators [2, 3].
The decades-long application of the Framingham Risk Score in different populations 
worldwide has also revealed its inherent limitations and led to the development of 
several alternative tools (e.g., SCORE [Systematic Coronary Risk Evaluation], 
Reynolds Risk Score, QRISK [QRESEARCH Cardiovascular Risk Algorithm]) [4].
Though the new tools have addressed some problems, none of these has been 
universally accepted, raising concerns over ethnicity, psychosocial background, 
comorbidities, drug therapies, and validity of biomarkers incorporated in the risk 
scores. For example, a recent large study showed that currently available risk scores 
do not provide precise estimates of cardiovascular risk in patients with rheumatoid 
arthritis [5], leaving the issue of risk-score-based cardiovascular prevention in this 
particular population uncertain. The guidance based on cardiovascular risk scores in 
patients with inflammatory disorders may either underestimate, which is more likely, 
or overestimate the real risk. Given the results of statistical analyses in large cohorts, 
an attempt was made to correct values of risk scores in patients with rheumatoid 
arthritis by using a 1.5 multiplier [6]. In practice, however, the latter approach was not 
regarded as realistic [7], necessitating more research into cardiovascular 
pathophysiology and therapies in inflammatory disorders.
There are still many uncertainties over the interaction between traditional and novel 
risk factors leading to premature cardiovascular morbidity and mortality in the 
general population and in patients with diseases predisposing to vascular damage and 
accelerated atherothrombosis. Systemic inflammation has long been regarded as a 
crucial factor of premature cardiovascular disease. Initial evidence for this stems from 
the Physicians’ Health Study [8], which highlighted the significance of subclinical 
inflammation and slight elevation of C-reactive protein (CRP) level undetectable by 
conventional laboratory tests. A more recent large trial, the Justification for Use of statins 
in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER), reaffirmed that 
the suppression of low-grade inflammation (CRP just above 2 mg/l) can bring benefits in 
terms of primary cardiovascular prevention in the general population [9]. The JUPITER 
study also proved that the greatest cardiovascular risk reduction as a result of 
antiinflammatory therapy with rosuvastatin is expected in subjects with the highest 
levels of CRP. Whether the same or even greater risk reduction can be derived in highand 
low-grade inflammatory disorders and whether statins can occupy their niche in the 
combined treatment of the patients are still a matter of debate, which may be resolved 
once the results of specifically designed and powered trials become available [10-12].
Several lines of evidence, mainly derived from retrospective cohort studies, suggest 
that systemic inflammation drives atherogenesis in cohorts of patients with systemic 
lupus erythematosus (SLE) and rheumatoid arthritis (RA). The exposure to high-grade 
inflammation is a crucial pathogenic factor in these patients, justifying aggressive 
antiinflammatory treatment, which, in turn, proved to reduce atherosclerotic burden 
among other disease-modifying effects [13-15]. The link between inflammation and 
atherosclerotic cardiovascular disease, however, is not universally evident across 
cohorts of patients with inflammatory disorders [16]. A recent systematic review on 
vascular function in RA revealed discrepancies across numerous cross-sectional and 
longitudinal studies, and questioned the direct link between rheumatoid inflammation 
and vasculopathy [17]. Moreover, numerous studies of varying levels of evidence 
suggested the lack of association between persistent low-grade inflammation and 
atherosclerotic vascular disease in patients with systemic vasculitides, including those 
with Wegener granulomatosis [18] and Behçet disease (BD) [19], the latter viewed as a 
model of venous thrombosis [20]. Obviously, the reported discrepancies indicate the 
complexity of atherogenic pathways and warrant further research into novel 
cardiovascular risk markers ......

Armen Yuri Gasparyan and 
George D. Kitas
Department of Rheumatology, Clinical Research Unit,
Dudley Group NHS Foundation Trust
(A Teaching Trust of University of Birmingham),
Russell's Hall Hospital,
Dudley, West Midlands DY1 2HQ,
United Kingdom


Chapter 1 Cardiovascular Risk Investigation: When Should It Start? 1
Anabel Nunes Rodrigues, Gláucia Rodrigues de Abreu and Sônia Alves Gouvêa

Chapter 2 Early Identification of Cardiovascular 
Risk Factors in Adolescents and Follow-Up Intervention Strategies 17
Heather Lee Kilty and Dawn Prentice

Chapter 3 Novel and Traditional Cardiovascular 
Risk Factors in Adolescents 61
Alice P.S. Kong and Kai Chow Choi

Chapter 4 Cardiovascular Risk Factors in the Elderly 81
Melek Z. Ulucam

Chapter 5 Vascular Inflammation: A New Horizon 
in Cardiovascular Risk Assessment 103
Vinayak Hegde and Ishmael Ching

Chapter 6 Alterations in the Brainstem Preautonomic 
Circuitry May Contribute to Hypertension Associated with Metabolic Syndrome 141
Bradley J. Buck, Lauren K. Nolen, Lauren G. Koch, Steven L. Britton and Ilan A. Kerman

Chapter 7 Cardiometabolic Syndrome 161
Alkerwi Ala’a, Albert Adelin and Guillaume Michèle

Chapter 8 Relationship Between Cardiovascular Risk Factors 
and Periodontal Disease: Current Knowledge 193
Sergio Granados-Principal, Nuri El-Azem, Jose L. Quiles, Patricia Perez-Lopez, Adrian Gonzalez and MCarmen Ramirez-Tortosa

Chapter 9 Cardiovascular Risk Assessment 
in Diabetes and Chronic Kidney Diseases: A New Insight and Emerging Strategies 217
Ali Reza Khoshdel

Chapter 10 Non Invasive Assessment of Cardiovascular 
Risk Profile: The Role of the Ultrasound Markers 251
Marco Matteo Ciccone, Michele Gesualdo, Annapaola Zito, Cosimo Mandurino, Manuela Locorotondo and Pietro Scicchitano

Chapter 11 Endothelial Progenitor Cell Number: 
A Convergence of Cardiovascular Risk Factors 265
Michel R. Hoenig and Frank W. Sellke

Chapter 12 Nitric Oxide Signalling in
Vascular Control and Cardiovascular Risk 279
Annette Schmidt

Chapter 13 An Anti-Inflammatory Approach in 
the Therapeutic Choices for the Prevention of Atherosclerotic Events 301
Aldo Pende and Andrea Denegri

Chapter 14 Gender-Specific Aspects in the Clinical 
Presentation of Cardiovascular Disease 327
Chiara Leuzzi, Raffaella Marzullo, Emma Tarabini Castellani and Maria Grazia Modena

Chapter 15 The Role of Stress in a Pathogenesis of CHD 337
Taina Hintsa, Mirka Hintsanen, Tom Rosenström and Liisa Keltikangas-Järvinen

Chapter 16 Pulse Pressure and Target Organ Damage 365
Adel Berbari and Abdo Jurjus

Chapter 17 Low-Level Exposure to Lead as a Cardiovascular Risk Factor 387
Anna Skoczynska and Marta Skoczynska

Chapter 18 Obstructive Sleep Apnoea Syndrome 
as a Systemic Low-Grade Inflammatory Disorder 411
Carlos Zamarrón, Emilio Morete and Felix del Campo Matias

Chapter 19 New Cardiovascular Risk 
Factors and Physical Activity 433
Nicolás Terrados and Eduardo Iglesias-Gutiérrez

Chapter 20 Dietary Supplements and Cardiovascular Disease: What 
is the Evidence and What Should We Recommend? 449
Satoshi Kashiwagi and Paul L. Huang

Chapter 21 Mediterranean Diet and Cardiovascular Risk 465 
Javier Delgado-Lista, Ana I. Perez-Caballero, Pablo Perez-Martinez, Antonio Garcia-Rios, Jose Lopez-Miranda and Francisco Perez-Jimenez .

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Published by: younes younes - Thursday, January 31, 2013


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