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<title>Therapeutic Advances in Cardiovascular Disease current issue</title>
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<prism:coverDisplayDate>October 2008</prism:coverDisplayDate>
<prism:publicationName>Therapeutic Advances in Cardiovascular Disease</prism:publicationName>
<prism:issn>1753-9447</prism:issn>
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<title>Therapeutic Advances in Cardiovascular Disease</title>
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<title><![CDATA[Review: Prevention of coronary heart disease in women]]></title>
<link>http://tak.sagepub.com/cgi/content/abstract/2/5/321?rss=1</link>
<description><![CDATA[<p><b>Objective</b> Coronary heart disease (CHD) mortality is higher in women than in men and misdiagnosis of CHD in women is one of the reasons for this, with differences in the presentation of CHD between men and women being a cause for the misdiagnosis. This review discusses the need for evidence-based guidelines to diagnose and treat CHD in women.</p><p><b>Methods</b> Reviews, randomized controlled trials, and other studies pertinent to the topic were obtained using electronic search strategies, such as MEDLINE and Cochran Library, as well as manual selection. Sources selected were limited to those that discussed CHD, with specific emphasis placed on sources that focused on CHD in women. Selected studies were then assessed for quality of data and relevance via analysis of the study's methodology, results, and data. Results of selected studies were then stratified using a rating system devised to determine the quality of results using the scientific evidence provided for them. The references of the selected studies were then used to obtain and analyze additional studies in the same manner.</p><p><b>Results</b> Control of lifestyle factors such as smoking, physical activity, diet, and weight are all necessary in women to control CHD, as is the maintenance of healthy lipid levels and blood pressure. Angiotensin-converting enzyme inhibitors and antiplatelets can help aid lifestyle changes in CHD management for women while hormone therapy and vitamin E have no proven benefits in CHD management.</p><p><b>Conclusions</b> New gender- and evidence-based guidelines for the prevention of CHD in women need to be developed and adopted by physicians so that prevention, diagnosis, and treatment of CHD is made more effective.</p>]]></description>
<dc:creator><![CDATA[Rohit Seth Loomba,  , Arora, R.]]></dc:creator>
<dc:date>2008-09-22</dc:date>
<dc:identifier>info:doi/10.1177/1753944708093511</dc:identifier>
<dc:title><![CDATA[Review: Prevention of coronary heart disease in women]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>2</prism:volume>
<prism:endingPage>327</prism:endingPage>
<prism:publicationDate>2008-10-01</prism:publicationDate>
<prism:startingPage>321</prism:startingPage>
<prism:section>Article</prism:section>
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<item rdf:about="http://tak.sagepub.com/cgi/content/abstract/2/5/329?rss=1">
<title><![CDATA[Review: Hypercholesterolemia-associated endothelial progenitor cell dysfunction]]></title>
<link>http://tak.sagepub.com/cgi/content/abstract/2/5/329?rss=1</link>
<description><![CDATA[<p>Hypercholesterolemia has been associated with increased cardiovascular risk by contributing to mechanical endothelial injury and dysfunction. There is evidence that chronic exposure to increased plasma cholesterol levels might also impair the repair of lipoprotein-mediated endothelial injury, possibly by reducing the availability and function of circulating endothelial progenitors. This review summarizes current knowledge about the mechanisms of lipoprotein-mediated endothelial injury and endothelial progenitor cell assisted vascular repair; the influence of hypercholesterolemia on endothelial progenitor cell dysfunction will be also addressed.</p>]]></description>
<dc:creator><![CDATA[Pirro, M., Bagaglia, F., Paoletti, L., Razzi, R., Mannarino, M. R.]]></dc:creator>
<dc:date>2008-09-22</dc:date>
<dc:identifier>info:doi/10.1177/1753944708094769</dc:identifier>
<dc:title><![CDATA[Review: Hypercholesterolemia-associated endothelial progenitor cell dysfunction]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>2</prism:volume>
<prism:endingPage>339</prism:endingPage>
<prism:publicationDate>2008-10-01</prism:publicationDate>
<prism:startingPage>329</prism:startingPage>
<prism:section>Article</prism:section>
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<item rdf:about="http://tak.sagepub.com/cgi/content/abstract/2/5/341?rss=1">
<title><![CDATA[Review: Cardiogenic potential of endothelial progenitor cells]]></title>
<link>http://tak.sagepub.com/cgi/content/abstract/2/5/341?rss=1</link>
<description><![CDATA[<p>Transplantation of endothelial progenitor cells (EPCs) are one of the promising                 strategies to recover the capillary flow in ischaemic diseases such as ischaemic                 heart disease and peripheral artery disease (PAD) in the leg. However, our previous                 and another group's works suggested the scarcity of the number of EPCs in peripheral                 blood might cause insufficient effect for the ischaemic diseases. There are several                 strategies to overcome this issue, such as (1) <I>in vivo</I> EPC expansion; (2) <I>ex vivo</I>                 EPC expansion; (3) local (not systemic) EPC injection; and (4) modification of EPC                 by gene transfer. Recent publications from our own and other groups have reported                 the possibility of cardiogenic potential of EPCs. We would like to focus on the                 strategies of EPC transplantation and cardiomyogenesis of EPCs in this review.</p>]]></description>
<dc:creator><![CDATA[Murasawa, S., Asahara, T.]]></dc:creator>
<dc:date>2008-09-22</dc:date>
<dc:identifier>info:doi/10.1177/1753944708096283</dc:identifier>
<dc:title><![CDATA[Review: Cardiogenic potential of endothelial progenitor cells]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>2</prism:volume>
<prism:endingPage>348</prism:endingPage>
<prism:publicationDate>2008-10-01</prism:publicationDate>
<prism:startingPage>341</prism:startingPage>
<prism:section>Article</prism:section>
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<item rdf:about="http://tak.sagepub.com/cgi/content/abstract/2/5/349?rss=1">
<title><![CDATA[Review: Systemic and uteroplacental renin--angiotensin system in normal and pre-eclamptic pregnancies]]></title>
<link>http://tak.sagepub.com/cgi/content/abstract/2/5/349?rss=1</link>
<description><![CDATA[<p>Pregnancy is characterized by an increase in many of the different components of the circulating renin&mdash;angiotensin system (RAS). However, the physiological mechanisms of stimulated RAS activity during pregnancy are unknown. Even less understood is how this system may be altered in pre-eclampsia, a hypertensive disorder of pregnancy. Additional studies have shown the presence of a local tissue specific RAS in the uteroplacental unit of normal and pre-eclamptic pregnancies. Differences in normal pregnant and pre-eclamptic RAS component regulation may provide insight into the mechanisms responsible for the clinical pathological features of pre-eclampsia. Specifically, this review summarizes the key findings in the circulating and uteroplacental RAS in normal and pre-eclamptic pregnancies.</p>]]></description>
<dc:creator><![CDATA[Anton, L., Brosnihan, K. B.]]></dc:creator>
<dc:date>2008-09-22</dc:date>
<dc:identifier>info:doi/10.1177/1753944708094529</dc:identifier>
<dc:title><![CDATA[Review: Systemic and uteroplacental renin--angiotensin system in normal and pre-eclamptic pregnancies]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>2</prism:volume>
<prism:endingPage>362</prism:endingPage>
<prism:publicationDate>2008-10-01</prism:publicationDate>
<prism:startingPage>349</prism:startingPage>
<prism:section>Article</prism:section>
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<title><![CDATA[Review: Genetics of diabetic nephropathy]]></title>
<link>http://tak.sagepub.com/cgi/content/abstract/2/5/363?rss=1</link>
<description><![CDATA[<p>Genetic susceptibility has been proposed as an important factor for the development and progression of diabetic nephropathy, and research efforts have been invested worldwide to identify the susceptibility gene for diabetic nephropathy. Although, several candidate genes were shown to be associated with the disease, the results were not always consistent; most of the genes conferring susceptibility to diabetic nephropathy remain to be identified. Recent development of the single nucleotide polymorphism (SNP) typing technology and collation of information on linkage disequilibrium in the human genome have facilitated genome-wide association studies (GWASs) for investigating novel disease-susceptibility genes across the entire human genome. GWASs are considered a powerful and promising approach and are expected to be useful for identifying convincing susceptibility genes for several common diseases; however, to date, these studies have not been able to completely cover the entire human genome.</p>]]></description>
<dc:creator><![CDATA[Maeda, S.]]></dc:creator>
<dc:date>2008-09-22</dc:date>
<dc:identifier>info:doi/10.1177/1753944708094768</dc:identifier>
<dc:title><![CDATA[Review: Genetics of diabetic nephropathy]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>2</prism:volume>
<prism:endingPage>371</prism:endingPage>
<prism:publicationDate>2008-10-01</prism:publicationDate>
<prism:startingPage>363</prism:startingPage>
<prism:section>Article</prism:section>
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<item rdf:about="http://tak.sagepub.com/cgi/content/abstract/2/5/373?rss=1">
<title><![CDATA[Review: New techniques for assessment of vascular function]]></title>
<link>http://tak.sagepub.com/cgi/content/abstract/2/5/373?rss=1</link>
<description><![CDATA[<p>The noninvasive measurement of hemodynamic variables associated with hypertension and cardiovascular disease processes needs to be recognized as a viable adjunct to clinical practice. This review traces the history of the inception and development of noninvasive measurement of hemodynamic variable. It then identifies well established, useful, and available devices, and then notes clinical studies verifying the clinical relevance of these measurements. Given the need to intervene earlier in the course of cardiovascular disease processes, tools are needed to assist the medical team to evaluate, prognosticate, and guide their patient's therapy correctly. It is the goal of this review to heighten the awareness and enhance and encourage the implementation of these devices in our armamentarium for the betterment of our patient's health.</p>]]></description>
<dc:creator><![CDATA[Smith, R. D., Levy, P. J.]]></dc:creator>
<dc:date>2008-09-22</dc:date>
<dc:identifier>info:doi/10.1177/1753944708091775</dc:identifier>
<dc:title><![CDATA[Review: New techniques for assessment of vascular function]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>2</prism:volume>
<prism:endingPage>385</prism:endingPage>
<prism:publicationDate>2008-10-01</prism:publicationDate>
<prism:startingPage>373</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://tak.sagepub.com/cgi/content/abstract/2/5/387?rss=1">
<title><![CDATA[Review: Recurrent stroke: where do we stand with the secondary prevention of noncardioembolic ischaemic strokes?]]></title>
<link>http://tak.sagepub.com/cgi/content/abstract/2/5/387?rss=1</link>
<description><![CDATA[<p>Strokes recur in 6&mdash;20% of the patients, most commonly within the first year; after a TIA or minor stroke; most recurrences will occur within the first 90 days. Our ability to identify patients at high risk is poor and most recurrent strokes cannot be explained by traditional risk factors. In 30&mdash;45% of the cases the second stroke will be of a different subtype. Moreover, patients are faced with other risks, like cardiac events and cognitive decline. With the population aging, the need for timely and effective secondary prevention strategies is more pressing than ever. This paper summarizes recent advances in pharmacological secondary prevention after a non-cardioembolic ischaemic stroke, and highlights critical questions still in need of answers.</p>]]></description>
<dc:creator><![CDATA[Talelli, P., Greenwood, R. J.]]></dc:creator>
<dc:date>2008-09-22</dc:date>
<dc:identifier>info:doi/10.1177/1753944708093411</dc:identifier>
<dc:title><![CDATA[Review: Recurrent stroke: where do we stand with the secondary prevention of noncardioembolic ischaemic strokes?]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>2</prism:volume>
<prism:endingPage>405</prism:endingPage>
<prism:publicationDate>2008-10-01</prism:publicationDate>
<prism:startingPage>387</prism:startingPage>
<prism:section>Article</prism:section>
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