<?xml version="1.0" encoding="UTF-8"?>

<rdf:RDF
   xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"
   xmlns:rdfs="http://www.w3.org/2000/01/rdf-schema#"
   xmlns="http://purl.org/rss/1.0/"
   xmlns:dc="http://purl.org/dc/elements/1.1/"
   xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/"
   xmlns:dcterms="http://purl.org/dc/terms/"

>
<channel rdf:about="http://www.citeulike.org/about">
<pubDate>Thu, 21 Aug 2008 15:06:17 BST</pubDate>


	<title>CiteULike: Tag cardiovascular</title>
	<description>CiteULike: Tag cardiovascular</description>


	<link>http://www.citeulike.org/tag/cardiovascular</link>
	<dc:publisher>CiteULike.org</dc:publisher>
	<dc:language>en-gb</dc:language>
	<dc:rights>Copyright &#169; 2004-2008 citeulike.org</dc:rights>
	<items>
    <rdf:Seq>
        <rdf:li rdf:resource="http://www.citeulike.org/user/xtizon/article/742046"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/xtizon/article/742045"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/wilbur/article/2393101"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/waffle168/article/1094452"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/tsjipko/article/3023930"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/tsjipko/article/2808320"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/tsjipko/article/2808314"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/tmansi/article/1593532"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/sigir/article/1644171"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/shupsy/article/1428874"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/shupsy/article/2427177"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/shupsy/article/2427171"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/shupsy/article/2031553"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/shupsy/article/1644622"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/shupsy/article/1927721"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/shupsy/article/1857296"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/shrikant/article/174802"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/rsimkus/article/2941858"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2120384"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2120360"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2120342"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2120323"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2120304"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2195425"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2177670"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/306045"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2538928"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/1091594"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/370344"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2141373"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2152634"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2124291"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2142478"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2181869"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2563984"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2285790"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2541073"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/524134"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2541027"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2712686"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2204386"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2184667"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2177707"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2204810"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2161653"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/1024708"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2587026"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2161560"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/2206206"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/Prodiana/article/1029155"/>

	</rdf:Seq>
	</items>
	</channel>


<item rdf:about="http://www.citeulike.org/user/xtizon/article/742046">
    <title>Shape Statistics Variational Approach for the Outer Contour Segmentation of Left Ventricle MR Images</title>
    <link>http://www.citeulike.org/user/xtizon/article/742046</link>
    <description>&lt;i&gt;Information Technology in Biomedicine, IEEE Transactions on, Vol. 10, No. 3. (2006), pp. 588-597.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Segmentation of left ventricles is one of the important research topics in cardiac magnetic resonance (MR) imaging. The segmentation precision influences the authenticity of ventricular motion reconstruction. In left ventricle MR images, the weak and broken boundary increases the difficulty of segmenting the outer contour precisely. In this paper, we present an improved shape statistics variational approach for the outer contour segmentation of left ventricle MR images. We use the Mumford&#8211;Shah model in an object feature space and incorporate the shape statistics and an edge image to the variational framework. The introduction of shape statistics can improve the segmentation with broken boundaries. The edge image can enhance the weak boundary and thus improve the segmentation precision. The generation of the object feature image, which has homogenous &#8220;intensities&#8221; in the left ventricle, facilitates the application of the Mumford&#8211;Shah model. A comparison of mean absolute distance analysis between different contours generated with our algorithm and that generated by hand demonstrated that our method can achieve a higher segmentation precision and a better stability than various approaches. It is a semiautomatic way for the segmentation of the outer contour of the left ventricle in clinical applications.</description>
    <dc:title>Shape Statistics Variational Approach for the Outer Contour Segmentation of Left Ventricle MR Images</dc:title>

    <dc:creator>Q Chen</dc:creator>
    <dc:creator>ZM Zhou</dc:creator>
    <dc:creator>M Tang</dc:creator>
    <dc:creator>PA Heng</dc:creator>
    <dc:creator>DS Xia</dc:creator>
    <dc:source>Information Technology in Biomedicine, IEEE Transactions on, Vol. 10, No. 3. (2006), pp. 588-597.</dc:source>
    <dc:date>2006-07-06T12:52:02-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Information Technology in Biomedicine, IEEE Transactions on</prism:publicationName>
    <prism:volume>10</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>588</prism:startingPage>
    <prism:endingPage>597</prism:endingPage>
    <prism:category>cardiovascular</prism:category>
    <prism:category>heart</prism:category>
    <prism:category>mri</prism:category>
    <prism:category>segmentation</prism:category>
    <prism:category>shape</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xtizon/article/742045">
    <title>First-Pass Contrast-Enhanced Myocardial Perfusion MRI Using a Maximum Up-Slope Parametric Map</title>
    <link>http://www.citeulike.org/user/xtizon/article/742045</link>
    <description>&lt;i&gt;Information Technology in Biomedicine, IEEE Transactions on, Vol. 10, No. 3. (2006), pp. 574-580.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Magnetic resonance first-pass perfusion imaging offers a noninvasive method for the rapid, accurate, and reproducible assessment of cardiac function without ionizing radiation. Quantitative or semiquantitative analysis of changes in signal intensity (SI) over the whole image sequence yields a more efficient analysis than direct visual inspection. In this paper, a method to generate maximum up-slope myocardial perfusion maps is presented. The maximum up-slope is defined by comparison of the SI variations using frame-to-frame analysis. A map of first-pass transit of the contrast agent is constructed pixel by pixel using a linear curve fitting model. The proposed method was evaluated using data from eight subjects. The data from the parametric maps agreed well with those obtained from traditional, manually derived region-of-interest methods as shown through ANOVA. The straightforward implementation and increase in image analysis efficiency resulting from this method suggests that it may be useful for clinical practice.</description>
    <dc:title>First-Pass Contrast-Enhanced Myocardial Perfusion MRI Using a Maximum Up-Slope Parametric Map</dc:title>

    <dc:creator>C Ruan</dc:creator>
    <dc:creator>S Yang</dc:creator>
    <dc:creator>GD Clarke</dc:creator>
    <dc:creator>MR Amurao</dc:creator>
    <dc:creator>SR Partyka</dc:creator>
    <dc:creator>YC Bradley</dc:creator>
    <dc:creator>K Cusi</dc:creator>
    <dc:source>Information Technology in Biomedicine, IEEE Transactions on, Vol. 10, No. 3. (2006), pp. 574-580.</dc:source>
    <dc:date>2006-07-06T12:50:58-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Information Technology in Biomedicine, IEEE Transactions on</prism:publicationName>
    <prism:volume>10</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>574</prism:startingPage>
    <prism:endingPage>580</prism:endingPage>
    <prism:category>cardiovascular</prism:category>
    <prism:category>heart</prism:category>
    <prism:category>mri</prism:category>
    <prism:category>perfusion</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/wilbur/article/2393101">
    <title>C-Reactive Protein, Inflammatory Conditions, and Cardiovascular Disease Risk</title>
    <link>http://www.citeulike.org/user/wilbur/article/2393101</link>
    <description>&lt;i&gt;The American Journal of Medicine, Vol. 120, No. 12. (December 2007), pp. 1054-1062.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Background It is uncertain to what extent high C-reactive protein (CRP) concentrations reflect the presence of inflammatory conditions in the community.Methods We evaluated 3782 Framingham Offspring Study participants (mean age 55 years; 52% women) free of baseline cardiovascular disease. Logistic regression models examined the prevalence of common inflammatory conditions by CRP categories, while a separate matched case-referent analysis evaluated the prevalence of uncommon inflammatory conditions. Cox models were used to assess the influence of common inflammatory conditions on relations between CRP and incident cardiovascular disease.Results Common inflammatory conditions were reported by nearly half of the participants; these individuals were more likely to have markedly high CRP concentrations (&#62;10 mg/L, P for trend = .001). In multivariable models, there were increased odds of having at least one common inflammatory condition with CRP concentrations of 1-3.0, 3.01-10, and &#62;10 mg/L, compared with the referent category (&#60;1 mg/L); the respective odds ratios with 95% confidence intervals were 1.41 (1.07-1.86), 1.45 (1.07-1.98), and 1.64 (1.09-2.47) in men, and 1.08 (0.82-1.43), 1.07 (0.80-1.44), and 1.38 (0.97-1.96) in women. In case-referent analyses, uncommon inflammatory conditions were more common in individuals with CRP &#62;10 mg/L compared with those with CRP &#60;1 mg/L (12.1% vs 6.6%; P = .0001). In multivariable models, higher CRP categories were not associated with incident cardiovascular disease, and with additional adjustment for inflammatory conditions, results remained unchanged.Conclusion There is high prevalence of common and uncommon inflammatory conditions in individuals with high CRP concentrations. Higher CRP concentrations should be interpreted with caution in cardiovascular disease risk assessment.</description>
    <dc:title>C-Reactive Protein, Inflammatory Conditions, and Cardiovascular Disease Risk</dc:title>

    <dc:creator>Ravi Dhingra</dc:creator>
    <dc:creator>Philimon Gona</dc:creator>
    <dc:creator>Byung-Ho Nam</dc:creator>
    <dc:creator>D'Agostino</dc:creator>
    <dc:creator>Peter Wilson</dc:creator>
    <dc:creator>Emelia Benjamin</dc:creator>
    <dc:creator>Christopher O'Donnell</dc:creator>
    <dc:identifier>doi:10.1016/j.amjmed.2007.08.037</dc:identifier>
    <dc:source>The American Journal of Medicine, Vol. 120, No. 12. (December 2007), pp. 1054-1062.</dc:source>
    <dc:date>2008-02-18T09:26:46-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>The American Journal of Medicine</prism:publicationName>
    <prism:volume>120</prism:volume>
    <prism:number>12</prism:number>
    <prism:startingPage>1054</prism:startingPage>
    <prism:endingPage>1062</prism:endingPage>
    <prism:category>cardiovascular</prism:category>
    <prism:category>disease</prism:category>
    <prism:category>inflammatory</prism:category>
    <prism:category>protein</prism:category>
    <prism:category>risk</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/waffle168/article/1094452">
    <title>Improving women's quality of care for cardiovascular disease and diabetes: the feasibility and desirability of stratified reporting of objective performance measures.</title>
    <link>http://www.citeulike.org/user/waffle168/article/1094452</link>
    <description>&lt;i&gt;Womens Health Issues, Vol. 13, No. 4. (g 2003), pp. 150-157.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Despite growing recognition of significant morbidity and mortality among women from cardiovascular disease, management of primary and secondary cardiac risk factors continues to be suboptimal for many women. Although there is a good deal of room to improve the care for cardiovascular disease and diabetes in men, existing gender differences in performance suggest much can be gained by specifically assessing and monitoring quality of care for these conditions in women. In this paper, we describe recent work showing gender differences in quality of ambulatory care in managed care plans with some plans having substantial gender differences on widely used measures of the quality of primary and secondary prevention of cardiac disease. We then discuss potential benefits of and barriers to routine reporting of objective measures of the quality of care, such as Health Plan Employer Data and Information Set (HEDIS) measures, by health plans.</description>
    <dc:title>Improving women's quality of care for cardiovascular disease and diabetes: the feasibility and desirability of stratified reporting of objective performance measures.</dc:title>

    <dc:creator>CE Bird</dc:creator>
    <dc:creator>A Fremont</dc:creator>
    <dc:creator>S Wickstrom</dc:creator>
    <dc:creator>AS Bierman</dc:creator>
    <dc:creator>E McGlynn</dc:creator>
    <dc:source>Womens Health Issues, Vol. 13, No. 4. (g 2003), pp. 150-157.</dc:source>
    <dc:date>2007-02-08T09:25:16-00:00</dc:date>
    <prism:publicationYear>2003</prism:publicationYear>
    <prism:publicationName>Womens Health Issues</prism:publicationName>
    <prism:issn>1049-3867</prism:issn>
    <prism:volume>13</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>150</prism:startingPage>
    <prism:endingPage>157</prism:endingPage>
    <prism:category>cardiovascular</prism:category>
    <prism:category>data</prism:category>
    <prism:category>diabetes</prism:category>
    <prism:category>quality</prism:category>
    <prism:category>reporting</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/tsjipko/article/3023930">
    <title>Caveolae and endothelial dysfunction: filling the caves in cardiovascular disease.</title>
    <link>http://www.citeulike.org/user/tsjipko/article/3023930</link>
    <description>&lt;i&gt;European journal of pharmacology, Vol. 585, No. 2-3. (13 May 2008), pp. 256-260.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Discovery in the early 1990s of caveolin-1, the structural protein responsible for maintaining the ohm shape of caveolae, greatly enhanced investigations to elucidate the role of these little caves in the plasma membrane. Perhaps one of the most important realizations concerning caveolae and caveolin is that these elements play an important functional role in the modulation of cell signal transduction pathways, including those involved in endothelial nitric oxide synthase (eNOS) function. Their role was confirmed by studies with caveolin-1 knockout mice which lack caveolae and display abnormal endothelial function responses. One limitation of these knockout models, however, is that absence of the caveolin protein not only results in the lack of caveolae as a structure but also in the lack of interaction/modulation of enzymes/molecules (e.g. eNOS) to which caveolin binds (whether in- or outside caveolae). In contrast to caveolin knockout models, recent experimental findings suggest that in certain cardiovascular diseases caveolin may dissociate from caveolae to the cytosol, hence decreasing the number of caveolae without a change in the total amount of caveolin. Therefore, as the importance of defining the role of caveolins both in caveolae and in cellular regions is being highlighted, it seems also important at the same time to further define the role of caveolae per se being present in the plasma membrane as a structural entity. The objective of this review is to make an explorative tour on the role of caveolae in vascular endothelial function based on existing literature together with some preliminary experimental findings. Evidence and arguments are put forward that alterations in endothelial caveolae do occur in cardiovascular disease and may contribute to the observed endothelial dysfunction in these conditions.</description>
    <dc:title>Caveolae and endothelial dysfunction: filling the caves in cardiovascular disease.</dc:title>

    <dc:creator>Y Xu</dc:creator>
    <dc:creator>H Buikema</dc:creator>
    <dc:creator>WH van Gilst</dc:creator>
    <dc:creator>RH Henning</dc:creator>
    <dc:identifier>doi:10.1016/j.ejphar.2008.02.086</dc:identifier>
    <dc:source>European journal of pharmacology, Vol. 585, No. 2-3. (13 May 2008), pp. 256-260.</dc:source>
    <dc:date>2008-07-21T09:30:28-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>European journal of pharmacology</prism:publicationName>
    <prism:issn>0014-2999</prism:issn>
    <prism:volume>585</prism:volume>
    <prism:number>2-3</prism:number>
    <prism:startingPage>256</prism:startingPage>
    <prism:endingPage>260</prism:endingPage>
    <prism:category>calcium</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>caveolae</prism:category>
    <prism:category>caveolin-1</prism:category>
    <prism:category>cholesterol</prism:category>
    <prism:category>disease</prism:category>
    <prism:category>dysfunction</prism:category>
    <prism:category>enos</prism:category>
    <prism:category>in_vivo</prism:category>
    <prism:category>no</prism:category>
    <prism:category>review</prism:category>
    <prism:category>signaling</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/tsjipko/article/2808320">
    <title>Scaling laws of vascular trees: of form and function</title>
    <link>http://www.citeulike.org/user/tsjipko/article/2808320</link>
    <description>&lt;i&gt;Am J Physiol Heart Circ Physiol, Vol. 290, No. 2. (1 February 2006), pp. H894-903.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The branching pattern and vascular geometry of biological tree structure are complex. Here we show that the design of all vascular trees for which there exist morphometric data in the literature (e.g., coronary, pulmonary; vessels of various skeletal muscles, mesentery, omentum, and conjunctiva) obeys a set of scaling laws that are based on the hypothesis that the cost of construction of the tree structure and operation of fluid conduction is minimized. The laws consist of scaling relationships between 1) length and vascular volume of the tree, 2) lumen diameter and blood flow rate in each branch, and 3) diameter and length of vessel branches. The exponent of the diameter-flow rate relation is not necessarily equal to 3.0 as required by Murray's law but depends on the ratio of metabolic to viscous power dissipation of the tree of interest. The major significance of the present analysis is to show that the design of various vascular trees of different organs and species can be deduced on the basis of the minimum energy hypothesis and conservation of energy under steady-state conditions. The present study reveals the similarity of nature's scaling laws that dictate the design of various vascular trees and the underlying physical and physiological principles. 10.1152/ajpheart.00579.2005</description>
    <dc:title>Scaling laws of vascular trees: of form and function</dc:title>

    <dc:creator>Ghassan Kassab</dc:creator>
    <dc:identifier>doi:10.1152/ajpheart.00579.2005</dc:identifier>
    <dc:source>Am J Physiol Heart Circ Physiol, Vol. 290, No. 2. (1 February 2006), pp. H894-903.</dc:source>
    <dc:date>2008-05-17T22:09:59-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Am J Physiol Heart Circ Physiol</prism:publicationName>
    <prism:volume>290</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>H894</prism:startingPage>
    <prism:endingPage>903</prism:endingPage>
    <prism:category>branching</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>computation</prism:category>
    <prism:category>murrays_law</prism:category>
    <prism:category>scaling</prism:category>
    <prism:category>theory</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/tsjipko/article/2808314">
    <title>A General Model for the Origin of Allometric Scaling Laws in Biology</title>
    <link>http://www.citeulike.org/user/tsjipko/article/2808314</link>
    <description>&lt;i&gt;Science, Vol. 276, No. 5309. (4 April 1997), pp. 122-126.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;10.1126/science.276.5309.122</description>
    <dc:title>A General Model for the Origin of Allometric Scaling Laws in Biology</dc:title>

    <dc:creator>Geofv West</dc:creator>
    <dc:creator>James Brown</dc:creator>
    <dc:creator>Brian Enquist</dc:creator>
    <dc:identifier>doi:10.1126/science.276.5309.122</dc:identifier>
    <dc:source>Science, Vol. 276, No. 5309. (4 April 1997), pp. 122-126.</dc:source>
    <dc:date>2008-05-17T22:05:08-00:00</dc:date>
    <prism:publicationYear>1997</prism:publicationYear>
    <prism:publicationName>Science</prism:publicationName>
    <prism:volume>276</prism:volume>
    <prism:number>5309</prism:number>
    <prism:startingPage>122</prism:startingPage>
    <prism:endingPage>126</prism:endingPage>
    <prism:category>allometric</prism:category>
    <prism:category>arterial</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>murrays_law</prism:category>
    <prism:category>scaling</prism:category>
    <prism:category>tree</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/tmansi/article/1593532">
    <title>Cardiovascular Simulation Toolbox</title>
    <link>http://www.citeulike.org/user/tmansi/article/1593532</link>
    <description>&lt;i&gt;Cardiovascular Engineering: An International Journal, Vol. 7, No. 2. (June 2007), pp. 81-88.&lt;/i&gt;</description>
    <dc:title>Cardiovascular Simulation Toolbox</dc:title>

    <dc:creator>Sheffer</dc:creator>
    <dc:creator>Liron</dc:creator>
    <dc:creator>Santamore</dc:creator>
    <dc:creator>William</dc:creator>
    <dc:creator>Barnea</dc:creator>
    <dc:creator>Ofer</dc:creator>
    <dc:identifier>doi:10.1007/s10558-007-9030-z</dc:identifier>
    <dc:source>Cardiovascular Engineering: An International Journal, Vol. 7, No. 2. (June 2007), pp. 81-88.</dc:source>
    <dc:date>2007-08-26T01:57:14-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Cardiovascular Engineering: An International Journal</prism:publicationName>
    <prism:issn>1567-8822</prism:issn>
    <prism:volume>7</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>81</prism:startingPage>
    <prism:endingPage>88</prism:endingPage>
    <prism:publisher>Springer</prism:publisher>
    <prism:category>cardiovascular</prism:category>
    <prism:category>matlab</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/sigir/article/1644171">
    <title>Cardiovascular response to stress</title>
    <link>http://www.citeulike.org/user/sigir/article/1644171</link>
    <description>&lt;i&gt;Physiol. Rev., Vol. 71, No. 1. (1 January 1991), pp. 305-330.&lt;/i&gt;</description>
    <dc:title>Cardiovascular response to stress</dc:title>

    <dc:creator>JA Herd</dc:creator>
    <dc:source>Physiol. Rev., Vol. 71, No. 1. (1 January 1991), pp. 305-330.</dc:source>
    <dc:date>2007-09-11T12:50:39-00:00</dc:date>
    <prism:publicationYear>1991</prism:publicationYear>
    <prism:publicationName>Physiol. Rev.</prism:publicationName>
    <prism:volume>71</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>305</prism:startingPage>
    <prism:endingPage>330</prism:endingPage>
    <prism:category>cardiovascular</prism:category>
    <prism:category>ngd</prism:category>
    <prism:category>psychophysiological</prism:category>
    <prism:category>stress</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/shupsy/article/1428874">
    <title>Methamphetamine and cardiovascular pathology: a review of the evidence</title>
    <link>http://www.citeulike.org/user/shupsy/article/1428874</link>
    <description>&lt;i&gt;Addiction, Vol. 0, No. 0. (0000), pp. ???-???.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;ABSTRACT Aims To examine the literature pertaining to the cardiovascular effects of methamphetamine and discuss the implications for methamphetamine users. Methods Relevant literature was identified through comprehensive MEDLINE and EMBASE searches. Findings and conclusions There is sufficient clinical and experimental evidence to suggest that methamphetamine can have adverse and potentially fatal effects on the cardiovascular system. The existing literature suggests that: (1) methamphetamine users are at elevated risk of cardiac pathology; (2) risk is not likely to be limited to the duration of their methamphetamine use, because of the chronic pathology associated with methamphetamine use; (3) the risk of cardiac pathology is greatest among chronic methamphetamine users; (4) pre-existing cardiac pathology, due to methamphetamine use or other factors, increases the risk of an acute cardiac event; and (5) methamphetamine use is likely to exacerbate the risk of cardiac pathology from other causes, and may therefore lead to premature mortality.</description>
    <dc:title>Methamphetamine and cardiovascular pathology: a review of the evidence</dc:title>

    <dc:creator>Sharlene Kaye</dc:creator>
    <dc:creator>Rebecca Mcketin</dc:creator>
    <dc:creator>Johan Duflou</dc:creator>
    <dc:creator>Shane Darke</dc:creator>
    <dc:identifier>doi:10.1111/j.1360-0443.2007.01874.x</dc:identifier>
    <dc:source>Addiction, Vol. 0, No. 0. (0000), pp. ???-???.</dc:source>
    <dc:date>2007-07-02T14:41:04-00:00</dc:date>
    <prism:publicationYear>0000</prism:publicationYear>
    <prism:publicationName>Addiction</prism:publicationName>
    <prism:volume>0</prism:volume>
    <prism:number>0</prism:number>
    <prism:startingPage>???</prism:startingPage>
    <prism:endingPage>???</prism:endingPage>
    <prism:category>cardiovascular</prism:category>
    <prism:category>comorbidity</prism:category>
    <prism:category>methamphetamine</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/shupsy/article/2427177">
    <title>Stimulant-drug therapy for attention-deficit disorder (with or without hyperactivity) and sudden cardiac death.</title>
    <link>http://www.citeulike.org/user/shupsy/article/2427177</link>
    <description>&lt;i&gt;Pediatrics, Vol. 119, No. 1. (January 2007), pp. 154-155.&lt;/i&gt;</description>
    <dc:title>Stimulant-drug therapy for attention-deficit disorder (with or without hyperactivity) and sudden cardiac death.</dc:title>

    <dc:creator>M Knight</dc:creator>
    <dc:identifier>doi:10.1542/peds.2006-2467</dc:identifier>
    <dc:source>Pediatrics, Vol. 119, No. 1. (January 2007), pp. 154-155.</dc:source>
    <dc:date>2008-02-25T21:31:15-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Pediatrics</prism:publicationName>
    <prism:issn>1098-4275</prism:issn>
    <prism:volume>119</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>154</prism:startingPage>
    <prism:endingPage>155</prism:endingPage>
    <prism:category>adhd</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>complications</prism:category>
    <prism:category>stimulants</prism:category>
    <prism:category>treatment</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/shupsy/article/2427171">
    <title>ADHD drugs and cardiovascular risk.</title>
    <link>http://www.citeulike.org/user/shupsy/article/2427171</link>
    <description>&lt;i&gt;New England Journal of Medicine, Vol. 354, No. 14. (6 April 2006), pp. 1445-1448.&lt;/i&gt;</description>
    <dc:title>ADHD drugs and cardiovascular risk.</dc:title>

    <dc:creator>SE Nissen</dc:creator>
    <dc:identifier>doi:10.1056/NEJMp068049</dc:identifier>
    <dc:source>New England Journal of Medicine, Vol. 354, No. 14. (6 April 2006), pp. 1445-1448.</dc:source>
    <dc:date>2008-02-25T21:29:24-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>New England Journal of Medicine</prism:publicationName>
    <prism:issn>1533-4406</prism:issn>
    <prism:volume>354</prism:volume>
    <prism:number>14</prism:number>
    <prism:startingPage>1445</prism:startingPage>
    <prism:endingPage>1448</prism:endingPage>
    <prism:category>adhd</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>complications</prism:category>
    <prism:category>stimulants</prism:category>
    <prism:category>treatment</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/shupsy/article/2031553">
    <title>Acute Myocardial Infarction Related to Methylphenidate for Adult Attention Deficit Disorder</title>
    <link>http://www.citeulike.org/user/shupsy/article/2031553</link>
    <description>&lt;i&gt;Journal of Emergency Medicine, Vol. In Press, Corrected Proof&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Adult Attention Deficit Disorder is increasingly diagnosed and treated. Psychostimulant medications, such as methylphenidate, are commonly prescribed for this condition, but the long-term safety of such medications in an adult population is unknown at present. Because these medications are closely related to amphetamines, it is expected that toxic side effects would be similar. We present the case of a 27-year-old man who suffered an acute myocardial infarction due to coronary vasospasm related to use of methylphenidate complicated by concomitant use of pseudoephedrine.</description>
    <dc:title>Acute Myocardial Infarction Related to Methylphenidate for Adult Attention Deficit Disorder</dc:title>

    <dc:creator>J Thompson</dc:creator>
    <dc:creator>JR Thompson</dc:creator>
    <dc:identifier>doi:10.1016/j.jemermed.2007.06.021</dc:identifier>
    <dc:source>Journal of Emergency Medicine, Vol. In Press, Corrected Proof</dc:source>
    <dc:date>2007-11-30T18:34:08-00:00</dc:date>
    <prism:publicationName>Journal of Emergency Medicine</prism:publicationName>
    <prism:volume>In Press, Corrected Proof</prism:volume>
    <prism:category>adhd</prism:category>
    <prism:category>adult</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>complications</prism:category>
    <prism:category>methylphenidate</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/shupsy/article/1644622">
    <title>Crack whips the heart: a review of the cardiovascular toxicity of cocaine.</title>
    <link>http://www.citeulike.org/user/shupsy/article/1644622</link>
    <description>&lt;i&gt;Am J Cardiol, Vol. 100, No. 6. (15 September 2007), pp. 1040-1043.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Cocaine is an extremely powerful reinforcing psychostimulant with highly addictive properties. Over the last few decades, cocaine addiction has attained epidemic proportions in North America, imposing a tremendous burden on society and the health care system. The cardiovascular complications of cocaine abuse are adrenergic mediated and range from cocaine-associated acute coronary syndromes to aortic dissection and sudden cardiac death. Concomitant alcohol and cigarette smoking exacerbate the cardiotoxicity of cocaine. This contemporary review discusses the spectrum of cardiac complications arising from cocaine use, operant pathophysiologic mechanisms and controversies surrounding the pharmacotherapy of cocaine-associated acute coronary syndromes.</description>
    <dc:title>Crack whips the heart: a review of the cardiovascular toxicity of cocaine.</dc:title>

    <dc:creator>L Afonso</dc:creator>
    <dc:creator>T Mohammad</dc:creator>
    <dc:creator>D Thatai</dc:creator>
    <dc:identifier>doi:10.1016/j.amjcard.2007.04.049</dc:identifier>
    <dc:source>Am J Cardiol, Vol. 100, No. 6. (15 September 2007), pp. 1040-1043.</dc:source>
    <dc:date>2007-09-11T15:29:10-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Am J Cardiol</prism:publicationName>
    <prism:issn>0002-9149</prism:issn>
    <prism:volume>100</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>1040</prism:startingPage>
    <prism:endingPage>1043</prism:endingPage>
    <prism:category>cardiovascular</prism:category>
    <prism:category>cocaine</prism:category>
    <prism:category>complications</prism:category>
    <prism:category>crack</prism:category>
    <prism:category>toxicity</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/shupsy/article/1927721">
    <title>Disulfiram effects on acute cocaine administration</title>
    <link>http://www.citeulike.org/user/shupsy/article/1927721</link>
    <description>&lt;i&gt;Drug and Alcohol Dependence, Vol. 52, No. 1. (1 September 1998), pp. 27-39.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Disulfiram (Antabuse) is being used in outpatient clinical trials to determine its efficacy as a treatment for cocaine dependence. This inpatient randomized, double-blind, placebo-controlled, within-subjects study was conducted to determine whether disulfiram (placebo, 250 or 500 mg/day) alters responses to acute intranasal cocaine (placebo, 1 or 2 mg/kg) administration. Effects of disulfiram on cocaine pharmacokinetics, physiological, and behavioral responses were determined. Disulfiram treatment increased plasma cocaine concentrations three to six times and significantly increased cocaine-associated cardiovascular responses, but did not significantly alter behavioral responses to cocaine. These interactions should be considered in the decision regarding disulfiram treatment in cocaine dependent patients.</description>
    <dc:title>Disulfiram effects on acute cocaine administration</dc:title>

    <dc:creator>EF Mccance-Katz</dc:creator>
    <dc:creator>TR Kosten</dc:creator>
    <dc:creator>P Jatlow</dc:creator>
    <dc:identifier>doi:10.1016/S0376-8716(98)00050-7</dc:identifier>
    <dc:source>Drug and Alcohol Dependence, Vol. 52, No. 1. (1 September 1998), pp. 27-39.</dc:source>
    <dc:date>2007-11-16T19:51:41-00:00</dc:date>
    <prism:publicationYear>1998</prism:publicationYear>
    <prism:publicationName>Drug and Alcohol Dependence</prism:publicationName>
    <prism:volume>52</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>27</prism:startingPage>
    <prism:endingPage>39</prism:endingPage>
    <prism:category>cardiovascular</prism:category>
    <prism:category>cocaethylene</prism:category>
    <prism:category>cocaine</prism:category>
    <prism:category>disulfiram</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/shupsy/article/1857296">
    <title>Cocaethylene is as cardiotoxic as cocaine but is less toxic than cocaine plus ethanol</title>
    <link>http://www.citeulike.org/user/shupsy/article/1857296</link>
    <description>&lt;i&gt;Life Sciences, Vol. 59, No. 8. (19 July 1996), pp. 615-627.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Cocaethylene is a pharmacologically active cocaine metabolite that is produced in the liver by the transesterification of cocaine only in the presence of ethanol. The acute cardiovascular effects of cocaethylene are not known. We compared the acute cardiovascular effects of cocaethylene with cocaine and with cocaine plus ethanol in 18 dogs. We administered cocaethylene 7.5 mg/kg to 6 dogs, cocaine 7.5 mg/kg to 6 dogs, and cocaine 7.5 mg/kg plus ethanol 1 gm/kg to 6 dogs. The dose of each drug was chosen to produce in dogs the concentrations of cocaethylene or cocaine that have been measured in patients who have experienced cardiotoxic reactions to cocaine or cocaine plus ethanol. Arterial, left ventricular (LV), pulmonary artery wedge pressures (PAWP), the maximum rate of LV pressure rise [(dP/dt)max] and fall [(dP/dt)min], and heart rate (HR) were continuously measured. Stroke volume was determined 3 times during the first hour after drug administration then hourly for four hours. The concentrations of cocaethylene and cocaine peaked in the serum at 3717 +/- 651 ng/ml and 4140 +/- 459 ng/ml, respectively, two minutes after each bolus. The median half-life of cocaethylene was 144.3 minutes whereas the median half-life of cocaine was 96.7 minutes (p &#60; 0.01). Cocaethylene maximally decreased (dP/dt)max by 44%, (dP/dt)min by 29%, and stroke volume by 28% (all p &#60; 0.01) and increased the PAWP by 50% (p &#60; 0.02) and the HR by 13% (p = NS) during the first hour. Cocaine maximally decreased (dP/dt)max by 40%, (dP/dt)min by 31%, and the stroke volume by 26% and increased the PAWP by 100% and the HR by 46% (all p &#60; 0.01) during the first hour. Ethanol plus cocaine maximally decreased (dP/dt)max by 68%, (dP/dt)min by 78% and the stroke volume by 49% and increased the PAWP by 118% and the HR by 74% (all p &#60; 0.01) during the first hour. In this last group, (dP/dt)max and stroke volume remained depressed by approximately 20% (p &#60; 0.01) for five hours. We conclude that cocaethylene is as toxic as cocaine to the myocardium but is less toxic than ethanol plus cocaine.</description>
    <dc:title>Cocaethylene is as cardiotoxic as cocaine but is less toxic than cocaine plus ethanol</dc:title>

    <dc:creator>Robert Henning</dc:creator>
    <dc:creator>Lance Wilson</dc:creator>
    <dc:identifier>doi:10.1016/0024-3205(96)00227-5</dc:identifier>
    <dc:source>Life Sciences, Vol. 59, No. 8. (19 July 1996), pp. 615-627.</dc:source>
    <dc:date>2007-11-02T20:36:01-00:00</dc:date>
    <prism:publicationYear>1996</prism:publicationYear>
    <prism:publicationName>Life Sciences</prism:publicationName>
    <prism:volume>59</prism:volume>
    <prism:number>8</prism:number>
    <prism:startingPage>615</prism:startingPage>
    <prism:endingPage>627</prism:endingPage>
    <prism:category>alcohol</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>cocaethylene</prism:category>
    <prism:category>cocaine</prism:category>
    <prism:category>complications</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/shrikant/article/174802">
    <title>CARDIOVASCULAR DISEASE: New use for cannabinoids</title>
    <link>http://www.citeulike.org/user/shrikant/article/174802</link>
    <description>&lt;i&gt;Nature Reviews Drug Discovery, Vol. 4, No. 5. (01 May 2005), pp. 374-374.&lt;/i&gt;</description>
    <dc:title>CARDIOVASCULAR DISEASE: New use for cannabinoids</dc:title>

    <dc:creator>Peter Kirkpatrick</dc:creator>
    <dc:identifier>doi:10.1038/nrd1733</dc:identifier>
    <dc:source>Nature Reviews Drug Discovery, Vol. 4, No. 5. (01 May 2005), pp. 374-374.</dc:source>
    <dc:date>2005-04-29T23:08:15-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Nature Reviews Drug Discovery</prism:publicationName>
    <prism:issn>1474-1776</prism:issn>
    <prism:volume>4</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>374</prism:startingPage>
    <prism:endingPage>374</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>cardiovascular</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/rsimkus/article/2941858">
    <title>European guidelines on cardiovascular disease prevention in clinical practice: executive summary: Fourth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (Constituted by representatives of nine societies and by invited experts)</title>
    <link>http://www.citeulike.org/user/rsimkus/article/2941858</link>
    <description>&lt;i&gt;Eur Heart J (28 August 2007), ehm316.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;10.1093/eurheartj/ehm316</description>
    <dc:title>European guidelines on cardiovascular disease prevention in clinical practice: executive summary: Fourth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (Constituted by representatives of nine societies and by invited experts)</dc:title>

    <dc:creator>Authors/task Members</dc:creator>
    <dc:creator>Ian Graham</dc:creator>
    <dc:creator>Dan Atar</dc:creator>
    <dc:creator>Knut Borch-Johnsen</dc:creator>
    <dc:creator>Gudrun Boysen</dc:creator>
    <dc:creator>Gunilla Burell</dc:creator>
    <dc:creator>Renata Cifkova</dc:creator>
    <dc:creator>Jean Dallongeville</dc:creator>
    <dc:creator>Guy De Backer</dc:creator>
    <dc:creator>Shah Ebrahim</dc:creator>
    <dc:creator>Bjorn Gjelsvik</dc:creator>
    <dc:creator>Christoph Herrmann-Lingen</dc:creator>
    <dc:creator>Arno Hoes</dc:creator>
    <dc:creator>Steve Humphries</dc:creator>
    <dc:creator>Mike Knapton</dc:creator>
    <dc:creator>Joep Perk</dc:creator>
    <dc:creator>Silvia Priori</dc:creator>
    <dc:creator>Kalevi Pyorala</dc:creator>
    <dc:creator>Zeljko Reiner</dc:creator>
    <dc:creator>Luis Ruilope</dc:creator>
    <dc:creator>Susana Sans-Menendez</dc:creator>
    <dc:creator>Wilma Reimer</dc:creator>
    <dc:creator>Peter Weissberg</dc:creator>
    <dc:creator>David Wood</dc:creator>
    <dc:creator>John Yarnell</dc:creator>
    <dc:creator>Jose Zamorano</dc:creator>
    <dc:creator>Other</dc:creator>
    <dc:creator>Edmond Walma</dc:creator>
    <dc:creator>Tony Fitzgerald</dc:creator>
    <dc:creator>Marie Cooney</dc:creator>
    <dc:creator>Alexandra Dudina</dc:creator>
    <dc:creator>European</dc:creator>
    <dc:creator>Alec Vahanian</dc:creator>
    <dc:creator>John Camm</dc:creator>
    <dc:creator>Raffaele De Caterina</dc:creator>
    <dc:creator>Veronica Dean</dc:creator>
    <dc:creator>Kenneth Dickstein</dc:creator>
    <dc:creator>Christian Funck-Brentano</dc:creator>
    <dc:creator>Gerasimos Filippatos</dc:creator>
    <dc:creator>Irene Hellemans</dc:creator>
    <dc:creator>Steen Kristensen</dc:creator>
    <dc:creator>Keith Mcgregor</dc:creator>
    <dc:creator>Udo Sechtem</dc:creator>
    <dc:creator>Sigmund Silber</dc:creator>
    <dc:creator>Michal Tendera</dc:creator>
    <dc:creator>Petr Widimsky</dc:creator>
    <dc:creator>Jose Zamorano</dc:creator>
    <dc:creator>Document Reviewers:</dc:creator>
    <dc:creator>Irene Hellemans</dc:creator>
    <dc:creator>Attila Altiner</dc:creator>
    <dc:creator>Enzo Bonora</dc:creator>
    <dc:creator>Paul Durrington</dc:creator>
    <dc:creator>Robert Fagard</dc:creator>
    <dc:creator>Simona Giampaoli</dc:creator>
    <dc:creator>Harry Hemingway</dc:creator>
    <dc:creator>Jan Hakansson</dc:creator>
    <dc:creator>Sverre Kjeldsen</dc:creator>
    <dc:creator>Mogens Larsen</dc:creator>
    <dc:creator>Giuseppe Mancia</dc:creator>
    <dc:creator>Athanasios Manolis</dc:creator>
    <dc:creator>Kristina Orth-Gomer</dc:creator>
    <dc:creator>Terje Pedersen</dc:creator>
    <dc:creator>Mike Rayner</dc:creator>
    <dc:creator>Lars Ryden</dc:creator>
    <dc:creator>Mario Sammut</dc:creator>
    <dc:creator>Neil Schneiderman</dc:creator>
    <dc:creator>Anton Stalenhoef</dc:creator>
    <dc:creator>Lale Tokgozoglu</dc:creator>
    <dc:creator>Olov Wiklund</dc:creator>
    <dc:creator>Antonis Zampelas</dc:creator>
    <dc:identifier>doi:10.1093/eurheartj/ehm316</dc:identifier>
    <dc:source>Eur Heart J (28 August 2007), ehm316.</dc:source>
    <dc:date>2008-06-29T16:54:05-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Eur Heart J</prism:publicationName>
    <prism:startingPage>ehm316</prism:startingPage>
    <prism:category>cardiovascular</prism:category>
    <prism:category>clinical</prism:category>
    <prism:category>disease</prism:category>
    <prism:category>global</prism:category>
    <prism:category>guidelines</prism:category>
    <prism:category>practrice</prism:category>
    <prism:category>risk</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2120384">
    <title>Experimentally verified minimal cardiovascular system model for rapid diagnostic assistance</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2120384</link>
    <description>&lt;i&gt;Control Engineering Practice, Vol. 13, No. 9. (September 2005), pp. 1183-1193.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Characterising circulatory dysfunction and choosing a suitable treatment is often difficult and time consuming. This paper outlines a numerically stable minimal model of the human cardiovascular system (CVS) specifically aimed for rapid, on-site modelling to assist in diagnosis and treatment. A minimal number of governing equations and a realistic valve law are used to accurately capture trends in CVS dynamics. The model is shown to have long-term stability and consistency with non-specific initial conditions. Examples of model verification are shown for experimentally measured static and transient response data. The model is also verified to capture commonly seen changes in CVS function as a result of disease. These examples illustrate the power of the minimal model for capturing CVS dynamics in health and disease, while its simplicity enables its use as a clinical aid.</description>
    <dc:title>Experimentally verified minimal cardiovascular system model for rapid diagnostic assistance</dc:title>

    <dc:creator>Bram Smith</dc:creator>
    <dc:creator>Geoffrey</dc:creator>
    <dc:creator>Geoffrey Shaw</dc:creator>
    <dc:creator>Roger Nokes</dc:creator>
    <dc:identifier>doi:10.1016/j.conengprac.2004.10.014</dc:identifier>
    <dc:source>Control Engineering Practice, Vol. 13, No. 9. (September 2005), pp. 1183-1193.</dc:source>
    <dc:date>2007-12-14T20:35:46-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Control Engineering Practice</prism:publicationName>
    <prism:volume>13</prism:volume>
    <prism:number>9</prism:number>
    <prism:startingPage>1183</prism:startingPage>
    <prism:endingPage>1193</prism:endingPage>
    <prism:category>cardiovascular</prism:category>
    <prism:category>physiological_model</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2120360">
    <title>Mathematical modeling of cardiovascular system dynamics using a lumped parameter method.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2120360</link>
    <description>&lt;i&gt;Jpn J Physiol, Vol. 54, No. 6. (December 2004), pp. 545-553.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;This work reviews the main aspects of cardiovascular system dynamics with an emphasis on modeling hemodynamic characteristics by the use of a lumped parameter approach. The methodological and physiological aspects of the circulation dynamics are summarized with the help of existing mathematical models. The main characteristics of the hemodynamic elements, such as the heart and arterial and venous systems, are first described. Distributed models of an arterial network are introduced, and their characteristics are compared with those of lumped parameter models. We also discuss the nonlinear characteristics of the pressure-volume relationship in veins. Then the control pathways that participate in feedback mechanisms (baroreceptors and cardiopulmonary receptors) are described to explain the interaction between hemodynamics and autonomic nerve control in the circulation. Based on a set-point model, the computational aspects of reflex control are explained.</description>
    <dc:title>Mathematical modeling of cardiovascular system dynamics using a lumped parameter method.</dc:title>

    <dc:creator>EB Shim</dc:creator>
    <dc:creator>JY Sah</dc:creator>
    <dc:creator>CH Youn</dc:creator>
    <dc:source>Jpn J Physiol, Vol. 54, No. 6. (December 2004), pp. 545-553.</dc:source>
    <dc:date>2007-12-14T20:27:18-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>Jpn J Physiol</prism:publicationName>
    <prism:issn>0021-521X</prism:issn>
    <prism:volume>54</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>545</prism:startingPage>
    <prism:endingPage>553</prism:endingPage>
    <prism:category>autonomic_ns</prism:category>
    <prism:category>baroreflex</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>feedback</prism:category>
    <prism:category>physiological_model</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2120342">
    <title>A human cardiopulmonary system model applied to the analysis of the Valsalva maneuver.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2120342</link>
    <description>&lt;i&gt;Am J Physiol Heart Circ Physiol, Vol. 281, No. 6. (December 2001)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Previous models combining the human cardiovascular and pulmonary systems have not addressed their strong dynamic interaction. They are primarily cardiovascular or pulmonary in their orientation and do not permit a full exploration of how the combined cardiopulmonary system responds to large amplitude forcing (e.g., by the Valsalva maneuver). To address this issue, we developed a new model that represents the important components of the cardiopulmonary system and their coupled interaction. Included in the model are descriptions of atrial and ventricular mechanics, hemodynamics of the systemic and pulmonic circulations, baroreflex control of arterial pressure, airway and lung mechanics, and gas transport at the alveolar-capillary membrane. Parameters of this combined model were adjusted to fit nominal data, yielding accurate and realistic pressure, volume, and flow waveforms. With the same set of parameters, the nominal model predicted the hemodynamic responses to the markedly increased intrathoracic (pleural) pressures during the Valsalva maneuver. In summary, this model accurately represents the cardiopulmonary system and can explain how the heart, lung, and autonomic tone interact during the Valsalva maneuver. It is likely that with further refinement it could describe various physiological states and help investigators to better understand the biophysics of cardiopulmonary disease. (Citado por 37)</description>
    <dc:title>A human cardiopulmonary system model applied to the analysis of the Valsalva maneuver.</dc:title>

    <dc:creator>K Lu</dc:creator>
    <dc:creator>JW Clark</dc:creator>
    <dc:creator>FH Ghorbel</dc:creator>
    <dc:creator>DL Ware</dc:creator>
    <dc:creator>A Bidani</dc:creator>
    <dc:source>Am J Physiol Heart Circ Physiol, Vol. 281, No. 6. (December 2001)</dc:source>
    <dc:date>2007-12-14T20:21:07-00:00</dc:date>
    <prism:publicationYear>2001</prism:publicationYear>
    <prism:publicationName>Am J Physiol Heart Circ Physiol</prism:publicationName>
    <prism:issn>0363-6135</prism:issn>
    <prism:volume>281</prism:volume>
    <prism:number>6</prism:number>
    <prism:category>baroreflex</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>physiological_model</prism:category>
    <prism:category>valsalva</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2120323">
    <title>Simulation of hemodynamic responses to the valsalva maneuver: an integrative computational model of the cardiovascular system and the autonomic nervous system.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2120323</link>
    <description>&lt;i&gt;J Physiol Sci, Vol. 56, No. 1. (February 2006), pp. 45-65.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The Valsalva maneuver is a frequently used physiological test in evaluating the cardiovascular autonomic functions in human. Although a large pool of experimental data has provided substantial insights into different aspects of the mechanisms underlying the cardiovascular regulations during the Valsalva maneuver, so far a complete comprehension of these mechanisms and the interactions among them is unavailable. In the present study, a computational model of the cardiovascular system (CVS) and its interaction with the autonomic nervous system (ANS) was developed for the purpose of quantifying the individual roles of the CVS and the ANS in the hemodynamic regulations during the Valsalva maneuver. A detailed computational compartmental parameter model of the global CVS, a system of mathematical equations representing the autonomic nervous reflex regulatory functions, and an empirical cerebral autoregulation (CA) model formed the main body of the present model. Based on simulations of the Valsalva maneuvers at several typical postures, it was demonstrated that hemodynamic responses to the maneuver were not only determined by the ANS-mediated cardiovascular regulations, but also significantly affected by the postural-change-induced hemodynamic alterations preceding the maneuver. Moreover, the large-magnitude overshoot in cerebral perfusion immediately after the Valsalva maneuver was found to result from a combined effect of the circulatory autonomic functions, the CA, and the cerebral venous blood pressure.</description>
    <dc:title>Simulation of hemodynamic responses to the valsalva maneuver: an integrative computational model of the cardiovascular system and the autonomic nervous system.</dc:title>

    <dc:creator>F Liang</dc:creator>
    <dc:creator>H Liu</dc:creator>
    <dc:source>J Physiol Sci, Vol. 56, No. 1. (February 2006), pp. 45-65.</dc:source>
    <dc:date>2007-12-14T20:15:52-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>J Physiol Sci</prism:publicationName>
    <prism:issn>1880-6546</prism:issn>
    <prism:volume>56</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>45</prism:startingPage>
    <prism:endingPage>65</prism:endingPage>
    <prism:category>autonomic_ns</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>physiological_model</prism:category>
    <prism:category>simulation</prism:category>
    <prism:category>valsalva</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2120304">
    <title>Simulation of cardiovascular system diseases by including the autonomic nervous system into a minimal model.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2120304</link>
    <description>&lt;i&gt;Comput Methods Programs Biomed, Vol. 86, No. 2. (May 2007), pp. 153-160.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Diagnosing cardiovascular system (CVS) diseases from clinically measured data is difficult, due to the complexity of the hemodynamic and autonomic nervous system (ANS) interactions. Physiological models could describe these interactions to enable simulation of a variety of diseases, and could be combined with parameter estimation algorithms to help clinicians diagnose CVS dysfunctions. This paper presents modifications to an existing CVS model to include a minimal physiological model of ANS activation. A minimal model is used so as to minimise the number of parameters required to specify ANS activation, enabling the effects of each parameter on hemodynamics to be easily understood. The combined CVS and ANS model is verified by simulating a variety of CVS diseases, and comparing simulation results with common physiological understanding of ANS function and the characteristic hemodynamics seen in these diseases. The model of ANS activation is required to simulate hemodynamic effects such as increased cardiac output in septic shock, elevated pulmonary artery pressure in left ventricular infarction, and elevated filling pressures in pericardial tamponade. This is the first known example of a minimal CVS model that includes a generic model of ANS activation and is shown to simulate diseases from throughout the CVS.</description>
    <dc:title>Simulation of cardiovascular system diseases by including the autonomic nervous system into a minimal model.</dc:title>

    <dc:creator>BW Smith</dc:creator>
    <dc:creator>S Andreassen</dc:creator>
    <dc:creator>GM Shaw</dc:creator>
    <dc:creator>PL Jensen</dc:creator>
    <dc:creator>SE Rees</dc:creator>
    <dc:creator>JG Chase</dc:creator>
    <dc:identifier>doi:10.1016/j.cmpb.2007.02.001</dc:identifier>
    <dc:source>Comput Methods Programs Biomed, Vol. 86, No. 2. (May 2007), pp. 153-160.</dc:source>
    <dc:date>2007-12-14T20:10:36-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Comput Methods Programs Biomed</prism:publicationName>
    <prism:issn>0169-2607</prism:issn>
    <prism:volume>86</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>153</prism:startingPage>
    <prism:endingPage>160</prism:endingPage>
    <prism:category>autonomic_ns</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>physiological_model</prism:category>
    <prism:category>simulation</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2195425">
    <title>Slow oscillations in blood pressure via a nonlinear feedback model.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2195425</link>
    <description>&lt;i&gt;Am J Physiol Regul Integr Comp Physiol, Vol. 280, No. 4. (April 2001)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Blood pressure is well established to contain a potential oscillation between 0.1 and 0.4 Hz, which is proposed to reflect resonant feedback in the baroreflex loop. A linear feedback model, comprising delay and lag terms for the vasculature, and a linear proportional derivative controller have been proposed to account for the 0.4-Hz oscillation in blood pressure in rats. However, although this model can produce oscillations at the required frequency, some strict relationships between the controller and vasculature parameters must be true for the oscillations to be stable. We developed a nonlinear model, containing an amplitude-limiting nonlinearity that allows for similar oscillations under a very mild set of assumptions. Models constructed from arterial pressure and sympathetic nerve activity recordings obtained from conscious rabbits under resting conditions suggest that the nonlinearity in the feedback loop is not contained within the vasculature, but rather is confined to the central nervous system. The advantage of the model is that it provides for sustained stable oscillations under a wide variety of situations even where gain at various points along the feedback loop may be altered, a situation that is not possible with a linear feedback model. Our model shows how variations in some of the nonlinearity characteristics can account for growth or decay in the oscillations and situations where the oscillations can disappear altogether. Such variations are shown to accord well with observed experimental data. Additionally, using a nonlinear feedback model, it is straightforward to show that the variation in frequency of the oscillations in blood pressure in rats (0.4 Hz), rabbits (0.3 Hz), and humans (0.1 Hz) is primarily due to scaling effects of conduction times between species. (Citado por 32)</description>
    <dc:title>Slow oscillations in blood pressure via a nonlinear feedback model.</dc:title>

    <dc:creator>JV Ringwood</dc:creator>
    <dc:creator>SC Malpas</dc:creator>
    <dc:source>Am J Physiol Regul Integr Comp Physiol, Vol. 280, No. 4. (April 2001)</dc:source>
    <dc:date>2008-01-04T18:23:53-00:00</dc:date>
    <prism:publicationYear>2001</prism:publicationYear>
    <prism:publicationName>Am J Physiol Regul Integr Comp Physiol</prism:publicationName>
    <prism:issn>0363-6119</prism:issn>
    <prism:volume>280</prism:volume>
    <prism:number>4</prism:number>
    <prism:category>baroreflex</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>cardiov_oscillations</prism:category>
    <prism:category>feedback</prism:category>
    <prism:category>nonlinear_dynamics</prism:category>
    <prism:category>physiological_model</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2177670">
    <title>Nonlinear dynamics in the cardiovascular and cardiorespiratory coordination: fundamentals, experimental-mathematical approaches, and results.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2177670</link>
    <description>&lt;i&gt;Engineering in Medicine and Biology Society, 1998. Proceedings of the 20th Annual International Conference of the IEEE, Vol. 3 (1998), pp. 1565-1568.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The dynamic nonlinear coordination of the common cardiovascular and cardiorespiratory autonomic system is introduced from the physiological and from the systems-theoretical point of view. Fundamental relations to chaos theory and synergetics as well as corresponding experimental-mathematical approaches are presented. The investigations, which were performed on humans and piglets, were focused on nonlinear coordinations. They encovered particular nonlinear couplings and intermittent phase synchronizations depending on the physiological behavioral state. It can be concluded that different aspects of nonlinear coordination exist which should be investigated by means of different appropriate methods. This opens particular windows into the complex functioning of the nervous system and its pathophysiological disorders</description>
    <dc:title>Nonlinear dynamics in the cardiovascular and cardiorespiratory coordination: fundamentals, experimental-mathematical approaches, and results.</dc:title>

    <dc:creator>D Hoyer</dc:creator>
    <dc:source>Engineering in Medicine and Biology Society, 1998. Proceedings of the 20th Annual International Conference of the IEEE, Vol. 3 (1998), pp. 1565-1568.</dc:source>
    <dc:date>2007-12-28T16:25:12-00:00</dc:date>
    <prism:publicationYear>1998</prism:publicationYear>
    <prism:publicationName>Engineering in Medicine and Biology Society, 1998. Proceedings of the 20th Annual International Conference of the IEEE</prism:publicationName>
    <prism:volume>3</prism:volume>
    <prism:startingPage>1565</prism:startingPage>
    <prism:endingPage>1568</prism:endingPage>
    <prism:category>cardiovascular</prism:category>
    <prism:category>nonlinear_dynamics</prism:category>
    <prism:category>physiological_model</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/306045">
    <title>System identification: a multi-signal approach for probing neural cardiovascular regulation.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/306045</link>
    <description>&lt;i&gt;Physiol Meas, Vol. 26, No. 3. (June 2005)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Short-term, beat-to-beat cardiovascular variability reflects the dynamic interplay between ongoing perturbations to the circulation and the compensatory response of neurally mediated regulatory mechanisms. This physiologic information may be deciphered from the subtle, beat-to-beat variations by using digital signal processing techniques. While single signal analysis techniques (e.g., power spectral analysis) may be employed to quantify the variability itself, the multi-signal approach of system identification permits the dynamic characterization of the neural regulatory mechanisms responsible for coupling the variability between signals. In this review, we provide an overview of applications of system identification to beat-to-beat variability for the quantitative characterization of cardiovascular regulatory mechanisms. After briefly summarizing the history of the field and basic principles, we take a didactic approach to describe the practice of system identification in the context of probing neural cardiovascular regulation. We then review studies in the literature over the past two decades that have applied system identification for characterizing the dynamical properties of the sinoatrial node, respiratory sinus arrhythmia, and the baroreflex control of sympathetic nerve activity, heart rate and total peripheral resistance. Based on this literature review, we conclude by advocating specific methods of practice and that future research should focus on nonlinear and time-varying behaviors, validation of identification methods, and less understood neural regulatory mechanisms. Ultimately, we hope that this review stimulates such future investigations by both new and experienced system identification researchers. (Citado por 2)</description>
    <dc:title>System identification: a multi-signal approach for probing neural cardiovascular regulation.</dc:title>

    <dc:creator>X Xiao</dc:creator>
    <dc:creator>TJ Mullen</dc:creator>
    <dc:creator>R Mukkamala</dc:creator>
    <dc:source>Physiol Meas, Vol. 26, No. 3. (June 2005)</dc:source>
    <dc:date>2005-08-29T11:53:46-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Physiol Meas</prism:publicationName>
    <prism:issn>0967-3334</prism:issn>
    <prism:volume>26</prism:volume>
    <prism:number>3</prism:number>
    <prism:category>cardiovascular</prism:category>
    <prism:category>identification</prism:category>
    <prism:category>physiological_model</prism:category>
    <prism:category>review_article</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2538928">
    <title>Insulin action in the vasculature: physiology and pathophysiology.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2538928</link>
    <description>&lt;i&gt;J Vasc Res, Vol. 38, No. 5. (t 2001), pp. 415-422.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Studies to date have provided convincing evidence that insulin has an important role in the normal functioning of the vasculature from the perspective of the regulated delivery of nutrients to a tissue bed. This is mediated by an effect on the endothelium analogous to other endothelial responses, and insulin resistance is reflected in, and in part due to, impaired vasodilatory actions of insulin. Because insulin normally stimulates the net production of nitric oxide, which is beneficial in both the short term for vasomotion and antithrombosis, and the long term for inhibition of smooth muscle cell growth and migration, vascular insulin resistance also has important implications for vascular pathophysiology. Further, recent evidence suggests that the hyperinsulinemia accompanying insulin resistance may aggravate this situation by augmenting the endothelial production and release of endothelin-1. The investigation of insulin resistance in the vasculature provides not only a unique and physiologically relevant window onto vascular pathology, but also an opportunity for therapeutic targeting in individuals affected by the clinical states of insulin resistance. The present review highlights the importance of insulin sensitivity in the maintenance of endothelial function and explores the relationships between vascular insulin resistance and whole body glucose disposal. In addition, the recent evidence linking insulin to endothelin-1 production is discussed. Improving insulin sensitivity with insulin sensitizers such as rosiglitazone may represent an important advance in our ability to improve vascular dysfunction in diabetes. (Citado por 81)</description>
    <dc:title>Insulin action in the vasculature: physiology and pathophysiology.</dc:title>

    <dc:creator>K Mather</dc:creator>
    <dc:creator>TJ Anderson</dc:creator>
    <dc:creator>S Verma</dc:creator>
    <dc:source>J Vasc Res, Vol. 38, No. 5. (t 2001), pp. 415-422.</dc:source>
    <dc:date>2008-03-16T12:59:23-00:00</dc:date>
    <prism:publicationYear>2001</prism:publicationYear>
    <prism:publicationName>J Vasc Res</prism:publicationName>
    <prism:issn>1018-1172</prism:issn>
    <prism:volume>38</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>415</prism:startingPage>
    <prism:endingPage>422</prism:endingPage>
    <prism:category>blood_pressure</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>hyperinsulinaemia</prism:category>
    <prism:category>insulin_resistance</prism:category>
    <prism:category>review_article</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/1091594">
    <title>A forward model-based validation of cardiovascular system identification.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/1091594</link>
    <description>&lt;i&gt;Am J Physiol Heart Circ Physiol, Vol. 281, No. 6. (December 2001)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;We present a theoretical evaluation of a cardiovascular system identification method that we previously developed for the analysis of beat-to-beat fluctuations in noninvasively measured heart rate, arterial blood pressure, and instantaneous lung volume. The method provides a dynamical characterization of the important autonomic and mechanical mechanisms responsible for coupling the fluctuations (inverse modeling). To carry out the evaluation, we developed a computational model of the cardiovascular system capable of generating realistic beat-to-beat variability (forward modeling). We applied the method to data generated from the forward model and compared the resulting estimated dynamics with the actual dynamics of the forward model, which were either precisely known or easily determined. We found that the estimated dynamics corresponded to the actual dynamics and that this correspondence was robust to forward model uncertainty. We also demonstrated the sensitivity of the method in detecting small changes in parameters characterizing autonomic function in the forward model. These results provide confidence in the performance of the cardiovascular system identification method when applied to experimental data. (Citado por 21)</description>
    <dc:title>A forward model-based validation of cardiovascular system identification.</dc:title>

    <dc:creator>R Mukkamala</dc:creator>
    <dc:creator>RJ Cohen</dc:creator>
    <dc:source>Am J Physiol Heart Circ Physiol, Vol. 281, No. 6. (December 2001)</dc:source>
    <dc:date>2007-02-07T04:59:24-00:00</dc:date>
    <prism:publicationYear>2001</prism:publicationYear>
    <prism:publicationName>Am J Physiol Heart Circ Physiol</prism:publicationName>
    <prism:issn>0363-6135</prism:issn>
    <prism:volume>281</prism:volume>
    <prism:number>6</prism:number>
    <prism:category>cardiovascular</prism:category>
    <prism:category>identification</prism:category>
    <prism:category>physiological_model</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/370344">
    <title>Hemodynamic fluctuations and baroreflex sensitivity in humans: a beat-to-beat model.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/370344</link>
    <description>&lt;i&gt;Am J Physiol, Vol. 253, No. 3 Pt 2. (September 1987)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;A beat-to-beat model of the cardiovascular system is developed to study the spontaneous short-term variability in arterial blood pressure (BP) and heart rate (HR) data from humans at rest. The model consists of a set of difference equations representing the following mechanisms: 1) control of HR and peripheral resistance by the baroreflex, 2) Windkessel properties of the systemic arterial tree, 3) contractile properties of the myocardium (Starling's law and restitution), and 4) mechanical effects of respiration on BP. The model is tested by comparing power spectra and cross spectra of simulated data from the model with spectra of actual data from resting subjects. To make spectra from simulated data and from actual data tally, it must be assumed that respiratory sinus arrhythmia at rest is caused by the conversion of respiratory BP variability into HR variability by the fast, vagally mediated baroreflex. The so-called 10-s rhythm in HR and BP appears as a resonance phenomenon due to the delay in the sympathetic control loop of the baroreflex. The simulated response of the model to an imposed increase of BP is shown to correspond with the BP and HR response in patients after administration of a BP-increasing drug, such as phenylephrine. It is concluded that the model correctly describes a number of important features of the cardiovascular system. Mathematical properties of the difference-equation model are discussed. (Citado por 367)</description>
    <dc:title>Hemodynamic fluctuations and baroreflex sensitivity in humans: a beat-to-beat model.</dc:title>

    <dc:creator>RW de Boer</dc:creator>
    <dc:creator>JM Karemaker</dc:creator>
    <dc:creator>J Strackee</dc:creator>
    <dc:source>Am J Physiol, Vol. 253, No. 3 Pt 2. (September 1987)</dc:source>
    <dc:date>2005-10-29T15:57:51-00:00</dc:date>
    <prism:publicationYear>1987</prism:publicationYear>
    <prism:publicationName>Am J Physiol</prism:publicationName>
    <prism:issn>0002-9513</prism:issn>
    <prism:volume>253</prism:volume>
    <prism:number>3 Pt 2</prism:number>
    <prism:category>baroreflex</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>physiological_model</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2141373">
    <title>Heart rate variability: a review.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2141373</link>
    <description>&lt;i&gt;Med Biol Eng Comput, Vol. 44, No. 12. (December 2006), pp. 1031-1051.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Heart rate variability (HRV) is a reliable reflection of the many physiological factors modulating the normal rhythm of the heart. In fact, they provide a powerful means of observing the interplay between the sympathetic and parasympathetic nervous systems. It shows that the structure generating the signal is not only simply linear, but also involves nonlinear contributions. Heart rate (HR) is a nonstationary signal; its variation may contain indicators of current disease, or warnings about impending cardiac diseases. The indicators may be present at all times or may occur at random-during certain intervals of the day. It is strenuous and time consuming to study and pinpoint abnormalities in voluminous data collected over several hours. Hence, HR variation analysis (instantaneous HR against time axis) has become a popular noninvasive tool for assessing the activities of the autonomic nervous system. Computer based analytical tools for in-depth study of data over daylong intervals can be very useful in diagnostics. Therefore, the HRV signal parameters, extracted and analyzed using computers, are highly useful in diagnostics. In this paper, we have discussed the various applications of HRV and different linear, frequency domain, wavelet domain, nonlinear techniques used for the analysis of the HRV.</description>
    <dc:title>Heart rate variability: a review.</dc:title>

    <dc:creator>U Rajendra Acharya</dc:creator>
    <dc:creator>K Paul Joseph</dc:creator>
    <dc:creator>N Kannathal</dc:creator>
    <dc:creator>CM Lim</dc:creator>
    <dc:creator>JS Suri</dc:creator>
    <dc:identifier>doi:10.1007/s11517-006-0119-0</dc:identifier>
    <dc:source>Med Biol Eng Comput, Vol. 44, No. 12. (December 2006), pp. 1031-1051.</dc:source>
    <dc:date>2007-12-18T15:57:19-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Med Biol Eng Comput</prism:publicationName>
    <prism:issn>0140-0118</prism:issn>
    <prism:volume>44</prism:volume>
    <prism:number>12</prism:number>
    <prism:startingPage>1031</prism:startingPage>
    <prism:endingPage>1051</prism:endingPage>
    <prism:category>autonomic_ns</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>hrv</prism:category>
    <prism:category>nonlinear_dynamics</prism:category>
    <prism:category>review_article</prism:category>
    <prism:category>rr_interval</prism:category>
    <prism:category>spectral_analysis</prism:category>
    <prism:category>vfc</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2152634">
    <title>Poincaré plot interpretation using a physiological model of HRV based on a network of oscillators.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2152634</link>
    <description>&lt;i&gt;Am J Physiol Heart Circ Physiol, Vol. 283, No. 5. (November 2002)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;In this paper, we develop a physiological oscillator model of which the output mimics the shape of the R-R interval Poincaré plot. To validate the model, simulations of various nervous conditions are compared with heart rate variability (HRV) data obtained from subjects under each prescribed condition. For a variety of sympathovagal balances, our model generates Poincaré plots that undergo alterations strongly resembling those of actual R-R intervals. By exploiting the oscillator basis of our model, we detail the way that low- and high-frequency modulation of the sinus node translates into R-R interval Poincaré plot shape by way of simulations and analytic results. With the use of our model, we establish that the length and width of a Poincaré plot are a weighted combination of low- and high-frequency power. This provides a theoretical link between frequency-domain spectral analysis techniques and time-domain Poincaré plot analysis. We ascertain the degree to which these principles apply to real R-R intervals by testing the mathematical relationships on a set of data and establish that the principles are clearly evident in actual HRV records.</description>
    <dc:title>Poincaré plot interpretation using a physiological model of HRV based on a network of oscillators.</dc:title>

    <dc:creator>M Brennan</dc:creator>
    <dc:creator>M Palaniswami</dc:creator>
    <dc:creator>P Kamen</dc:creator>
    <dc:identifier>doi:10.1152/ajpheart.00405.2000</dc:identifier>
    <dc:source>Am J Physiol Heart Circ Physiol, Vol. 283, No. 5. (November 2002)</dc:source>
    <dc:date>2007-12-20T18:18:04-00:00</dc:date>
    <prism:publicationYear>2002</prism:publicationYear>
    <prism:publicationName>Am J Physiol Heart Circ Physiol</prism:publicationName>
    <prism:issn>0363-6135</prism:issn>
    <prism:volume>283</prism:volume>
    <prism:number>5</prism:number>
    <prism:category>autonomic_ns</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>hrv</prism:category>
    <prism:category>ipfm_model</prism:category>
    <prism:category>nonlinear_dynamics</prism:category>
    <prism:category>physiological_model</prism:category>
    <prism:category>vfc</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2124291">
    <title>Evidence for central organization of cardiovascular rhythms.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2124291</link>
    <description>&lt;i&gt;Ann N Y Acad Sci, Vol. 940 (June 2001), pp. 299-306.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Spectral analysis of heart rate and arterial pressure variabilities is a powerful noninvasive tool that is increasingly used to infer alterations of cardiovascular autonomic regulation in a variety of physiological and pathophysiological conditions such as hypertension, myocardial infarction, and congestive heart failure. A most important methodological issue to properly interpret the results obtained by the spectral analysis of cardiovascular variability signals is represented by the attribution of neurophysiological correlates to these spectral components. In this regard, recent application of spectral techniques to the evaluation of the oscillatory properties of sympathetic efferent activity in animals as well as in humans offers a new approach to a better understanding of the relationship between cardiovascular oscillations and autonomic regulation. The data so far collected seem to suggest the presence of a centrally organized neural code, characterized by excitatory and inhibitory neural mechanisms subserving the genesis and the regulation of cardiovascular oscillations concerning the major variables of autonomic regulation.</description>
    <dc:title>Evidence for central organization of cardiovascular rhythms.</dc:title>

    <dc:creator>N Montano</dc:creator>
    <dc:creator>A Porta</dc:creator>
    <dc:creator>A Malliani</dc:creator>
    <dc:source>Ann N Y Acad Sci, Vol. 940 (June 2001), pp. 299-306.</dc:source>
    <dc:date>2007-12-15T16:50:09-00:00</dc:date>
    <prism:publicationYear>2001</prism:publicationYear>
    <prism:publicationName>Ann N Y Acad Sci</prism:publicationName>
    <prism:issn>0077-8923</prism:issn>
    <prism:volume>940</prism:volume>
    <prism:startingPage>299</prism:startingPage>
    <prism:endingPage>306</prism:endingPage>
    <prism:category>autonomic_ns</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>hrv</prism:category>
    <prism:category>spectral_analysis</prism:category>
    <prism:category>vfc</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2142478">
    <title>Cardiovascular variability signals: towards the identification of a closed-loop model of the neural control mechanisms</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2142478</link>
    <description>&lt;i&gt;IEEE Transactions on Biomedical Engineering, Vol. 35, No. 12. (1988), pp. 1033-1046.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The authors consider parametric methods for processing cardiovascular signals and try to provide a global, although indirect evaluation of some neural regulatory activities. In particular, the variability signals of the heart rate (under the form of interval tachogram) and arterial blood pressure (systogram) together with respiratory movement signal (respirogram) are considered as inputs to a closed-loop model which describes a few aspects of the physiological interactions among the signals themselves. The identifiability of the transfer function of the model is demonstrated from the joint process black-box description of the signals. A direct identification procedure is proposed dividing the system into two dynamic adjustment models. A few suggestions are deduced on how and where the respirogram enters the model and on the genesis of the 10-s rhythm, parameters relevant to the Starling effect, Windkessel model, and the gain of baroreceptor mechanisms. The approach presented is intended also to provide a general frame for closed-loop identification in different pathophysiological conditions. (Citado por 111)</description>
    <dc:title>Cardiovascular variability signals: towards the identification of a closed-loop model of the neural control mechanisms</dc:title>

    <dc:creator>G Baselli</dc:creator>
    <dc:creator>S Cerutti</dc:creator>
    <dc:creator>S Civardi</dc:creator>
    <dc:creator>A Malliani</dc:creator>
    <dc:creator>M Pagani</dc:creator>
    <dc:source>IEEE Transactions on Biomedical Engineering, Vol. 35, No. 12. (1988), pp. 1033-1046.</dc:source>
    <dc:date>2007-12-18T20:37:50-00:00</dc:date>
    <prism:publicationYear>1988</prism:publicationYear>
    <prism:publicationName>IEEE Transactions on Biomedical Engineering</prism:publicationName>
    <prism:volume>35</prism:volume>
    <prism:number>12</prism:number>
    <prism:startingPage>1033</prism:startingPage>
    <prism:endingPage>1046</prism:endingPage>
    <prism:category>cardiovascular</prism:category>
    <prism:category>feedback</prism:category>
    <prism:category>physiological_model</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2181869">
    <title>Spectrum analysis of cardiovascular time series.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2181869</link>
    <description>&lt;i&gt;Am J Physiol, Vol. 273, No. 4 Pt 2. (October 1997)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The demand for noninvasive assessment of cardiovascular control parameters has promoted the use of spectrum analysis. These techniques have been applied on a broad basis; however, because of the abstract mathematical approach, spectrum analysis in physiology is still not fully accepted by some circles in the scientific community. Thus it is the goal of the following review to focus on the rationale for applying spectrum analysis in different fields of circulation research, which range from determining arterial baroreceptor reflex sensitivity to the early detection of heart allograft rejection. Within this scope, major findings regarding the physiological and pathophysiological regulation of the cardiovascular system are discussed. In addition, inherent limitations of these methods are made clear. Toward the end of this survey, a perspective is provided for the general readership.</description>
    <dc:title>Spectrum analysis of cardiovascular time series.</dc:title>

    <dc:creator>PB Persson</dc:creator>
    <dc:source>Am J Physiol, Vol. 273, No. 4 Pt 2. (October 1997)</dc:source>
    <dc:date>2007-12-30T16:37:47-00:00</dc:date>
    <prism:publicationYear>1997</prism:publicationYear>
    <prism:publicationName>Am J Physiol</prism:publicationName>
    <prism:issn>0002-9513</prism:issn>
    <prism:volume>273</prism:volume>
    <prism:number>4 Pt 2</prism:number>
    <prism:category>cardiovascular</prism:category>
    <prism:category>review_article</prism:category>
    <prism:category>spectral_analysis</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2563984">
    <title>Assessment: Clinical autonomic testing report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2563984</link>
    <description>&lt;i&gt;Neurology, Vol. 46, No. 3. (March 1996), pp. 873-880.&lt;/i&gt;</description>
    <dc:title>Assessment: Clinical autonomic testing report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology.</dc:title>

    <dc:source>Neurology, Vol. 46, No. 3. (March 1996), pp. 873-880.</dc:source>
    <dc:date>2008-03-19T19:08:13-00:00</dc:date>
    <prism:publicationYear>1996</prism:publicationYear>
    <prism:publicationName>Neurology</prism:publicationName>
    <prism:issn>0028-3878</prism:issn>
    <prism:volume>46</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>873</prism:startingPage>
    <prism:endingPage>880</prism:endingPage>
    <prism:category>autonomic_ns</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>hrv</prism:category>
    <prism:category>ssr</prism:category>
    <prism:category>sudomotor_function</prism:category>
    <prism:category>valsalva</prism:category>
    <prism:category>vfc</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2285790">
    <title>Adaptation to mechanical load determines shape and properties of heart and circulation: the CircAdapt model.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2285790</link>
    <description>&lt;i&gt;Am J Physiol Heart Circ Physiol, Vol. 288, No. 4. (April 2005)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;With circulatory pathology, patient-specific simulation of hemodynamics is required to minimize invasiveness for diagnosis, treatment planning, and followup. We investigated the advantages of a smart combination of often already known hemodynamic principles. The CircAdapt model was designed to simulate beat-to-beat dynamics of the four-chamber heart with systemic and pulmonary circulation while incorporating a realistic relation between pressure-volume load and tissue mechanics and adaptation of tissues to mechanical load. Adaptation was modeled by rules, where a locally sensed signal results in a local action of the tissue. The applied rules were as follows: For blood vessel walls, 1) flow shear stress dilates the wall and 2) tensile stress thickens the wall; for myocardial tissue, 3) strain dilates the wall material, 4) larger maximum sarcomere length increases contractility, and 5) contractility increases wall mass. The circulation was composed of active and passive compliances and inertias. A realistic circulation developed by self-structuring through adaptation provided mean levels of systemic pressure and flow. Ability to simulate a wide variety of patient-specific circumstances was demonstrated by application of the same adaptation rules to the conditions of fetal circulation followed by a switch to the newborn circulation around birth. It was concluded that a few adaptation rules, directed to normalize mechanical load of the tissue, were sufficient to develop and maintain a realistic circulation automatically. Adaptation rules appear to be the key to reduce dramatically the number of input parameters for simulating circulation dynamics. The model may be used to simulate circulation pathology and to predict effects of treatment.</description>
    <dc:title>Adaptation to mechanical load determines shape and properties of heart and circulation: the CircAdapt model.</dc:title>

    <dc:creator>T Arts</dc:creator>
    <dc:creator>T Delhaas</dc:creator>
    <dc:creator>P Bovendeerd</dc:creator>
    <dc:creator>X Verbeek</dc:creator>
    <dc:creator>FW Prinzen</dc:creator>
    <dc:identifier>doi:10.1152/ajpheart.00444.2004</dc:identifier>
    <dc:source>Am J Physiol Heart Circ Physiol, Vol. 288, No. 4. (April 2005)</dc:source>
    <dc:date>2008-01-24T19:45:07-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Am J Physiol Heart Circ Physiol</prism:publicationName>
    <prism:issn>0363-6135</prism:issn>
    <prism:volume>288</prism:volume>
    <prism:number>4</prism:number>
    <prism:category>cardiovascular</prism:category>
    <prism:category>physiological_model</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2541073">
    <title>Differential control of sympathetic outflow.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2541073</link>
    <description>&lt;i&gt;Am J Physiol Regul Integr Comp Physiol, Vol. 281, No. 3. (September 2001)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;With advances in experimental techniques, the early views of the sympathetic nervous system as a monolithic effector activated globally in situations requiring a rapid and aggressive response to life-threatening danger have been eclipsed by an organizational model featuring an extensive array of functionally specific output channels that can be simultaneously activated or inhibited in combinations that result in the patterns of autonomic activity supporting behavior and mediating homeostatic reflexes. With this perspective, the defense response is but one of the many activational states of the central autonomic network. This review summarizes evidence for the existence of tissue-specific sympathetic output pathways, which are likely to include distinct populations of premotor neurons whose target specificity could be assessed using the functional fingerprints developed from characterizations of postganglionic efferents to known targets. The differential responses in sympathetic outflows to stimulation of reflex inputs suggest that the circuits regulating the activity of sympathetic premotor neurons must have parallel access to groups of premotor neurons controlling different functions but that these connections vary in their ability to influence different sympathetic outputs. Understanding the structural and physiological substrates antecedent to premotor neurons that mediate the differential control of sympathetic outflows, including those to noncardiovascular targets, represents a challenge to our current technical and analytic approaches.</description>
    <dc:title>Differential control of sympathetic outflow.</dc:title>

    <dc:creator>SF Morrison</dc:creator>
    <dc:source>Am J Physiol Regul Integr Comp Physiol, Vol. 281, No. 3. (September 2001)</dc:source>
    <dc:date>2008-03-16T18:00:09-00:00</dc:date>
    <prism:publicationYear>2001</prism:publicationYear>
    <prism:publicationName>Am J Physiol Regul Integr Comp Physiol</prism:publicationName>
    <prism:issn>0363-6119</prism:issn>
    <prism:volume>281</prism:volume>
    <prism:number>3</prism:number>
    <prism:category>autonomic_ns</prism:category>
    <prism:category>baroreflex</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>electrodermal</prism:category>
    <prism:category>norepinephrine</prism:category>
    <prism:category>review_article</prism:category>
    <prism:category>sudomotor_function</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/524134">
    <title>Cardiovascular neural regulation explored in the frequency domain.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/524134</link>
    <description>&lt;i&gt;Circulation, Vol. 84, No. 2. (August 1991), pp. 482-492.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;A consistent link appears to exist between predominance of vagal or sympathetic activity and predominance of HF or LF oscillations, respectively: RR variability contains both of these rhythms, and their relative powers appear to subserve a reciprocal relation like that commonly found in sympathovagal balance. In this respect, it is our opinion that rhythms and neural components always interact, just like flexor and extensor tones or excitatory and inhibitory cardiovascular reflexes, and that it is misleading to separately consider vagal and sympathetic modulations of heart rate. In humans and experimental animals, functional states likely to be accompanied by an increased sympathetic activity are characterized by a shift of the LF-HF balance in favor of the LF component; the opposite occurs during presumed increases in vagal activity. In addition, LF oscillation evaluated from SAP variability appears to be a convenient marker of the sympathetic modulation of vasomotor activity. Although based on indirect markers, the exploration in the frequency domain of cardiovascular neural regulation might disclose a unitary vision hard to reach through the assemblage of more specific but fragmented pieces of information. (Citado por 1260)</description>
    <dc:title>Cardiovascular neural regulation explored in the frequency domain.</dc:title>

    <dc:creator>A Malliani</dc:creator>
    <dc:creator>M Pagani</dc:creator>
    <dc:creator>F Lombardi</dc:creator>
    <dc:creator>S Cerutti</dc:creator>
    <dc:source>Circulation, Vol. 84, No. 2. (August 1991), pp. 482-492.</dc:source>
    <dc:date>2006-02-28T11:41:06-00:00</dc:date>
    <prism:publicationYear>1991</prism:publicationYear>
    <prism:publicationName>Circulation</prism:publicationName>
    <prism:issn>0009-7322</prism:issn>
    <prism:volume>84</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>482</prism:startingPage>
    <prism:endingPage>492</prism:endingPage>
    <prism:category>autonomic_ns</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>hrv</prism:category>
    <prism:category>review_article</prism:category>
    <prism:category>spectral_analysis</prism:category>
    <prism:category>sympathovagal_balance</prism:category>
    <prism:category>vfc</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2541027">
    <title>Sympathetic neural control of integrated cardiovascular function: insights from measurement of human sympathetic nerve activity.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2541027</link>
    <description>&lt;i&gt;Muscle Nerve, Vol. 36, No. 5. (November 2007), pp. 595-614.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Sympathetic neural control of cardiovascular function is essential for normal regulation of blood pressure and tissue perfusion. In the present review we discuss sympathetic neural mechanisms in human cardiovascular physiology and pathophysiology, with a focus on evidence from direct recordings of sympathetic nerve activity using microneurography. Measurements of sympathetic nerve activity to skeletal muscle have provided extensive information regarding reflex control of blood pressure and blood flow in conditions ranging from rest to postural changes, exercise, and mental stress in populations ranging from healthy controls to patients with hypertension and heart failure. Measurements of skin sympathetic nerve activity have also provided important insights into neural control, but are often more difficult to interpret since the activity contains several types of nerve impulses with different functions. Although most studies have focused on group mean differences, we provide evidence that individual variability in sympathetic nerve activity is important to the ultimate understanding of these integrated physiological mechanisms.</description>
    <dc:title>Sympathetic neural control of integrated cardiovascular function: insights from measurement of human sympathetic nerve activity.</dc:title>

    <dc:creator>BG Wallin</dc:creator>
    <dc:creator>N Charkoudian</dc:creator>
    <dc:identifier>doi:10.1002/mus.20831</dc:identifier>
    <dc:source>Muscle Nerve, Vol. 36, No. 5. (November 2007), pp. 595-614.</dc:source>
    <dc:date>2008-03-16T17:37:53-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Muscle Nerve</prism:publicationName>
    <prism:issn>0148-639X</prism:issn>
    <prism:volume>36</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>595</prism:startingPage>
    <prism:endingPage>614</prism:endingPage>
    <prism:category>autonomic_ns</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>microneurography</prism:category>
    <prism:category>review_article</prism:category>
    <prism:category>ssna</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2712686">
    <title>Glycemic index and disease.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2712686</link>
    <description>&lt;i&gt;The American journal of clinical nutrition, Vol. 76, No. 1. (July 2002)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;It has been suggested that foods with a high glycemic index are detrimental to health and that healthy people should be told to avoid these foods. This paper takes the position that not enough valid scientific data are available to launch a public health campaign to disseminate such a recommendation. This paper explores the glycemic index and its validity and discusses the effect of postprandial glucose and insulin responses on food intake, obesity, type 1 diabetes, and cardiovascular disease. Presented herein are the reasons why it is premature to recommend that the general population avoid foods with a high glycemic index.</description>
    <dc:title>Glycemic index and disease.</dc:title>

    <dc:creator>FX Pi-Sunyer</dc:creator>
    <dc:source>The American journal of clinical nutrition, Vol. 76, No. 1. (July 2002)</dc:source>
    <dc:date>2008-04-24T10:43:35-00:00</dc:date>
    <prism:publicationYear>2002</prism:publicationYear>
    <prism:publicationName>The American journal of clinical nutrition</prism:publicationName>
    <prism:issn>0002-9165</prism:issn>
    <prism:volume>76</prism:volume>
    <prism:number>1</prism:number>
    <prism:category>cardiovascular</prism:category>
    <prism:category>diabetes</prism:category>
    <prism:category>glycemic_index</prism:category>
    <prism:category>higea</prism:category>
    <prism:category>metabolism</prism:category>
    <prism:category>review_article</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2204386">
    <title>Interaction between carotid baroregulation and the pulsating heart: a mathematical model.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2204386</link>
    <description>&lt;i&gt;Am J Physiol, Vol. 275, No. 5 Pt 2. (November 1998)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;A mathematical model of short-term arterial pressure control by the carotid baroreceptors in pulsatile conditions is presented. The model includes an elastance variable description of the left and right heart, the systemic (splanchnic and extrasplanchnic) and pulmonary circulations, the afferent carotid baroreceptor pathway, the sympathetic and vagal efferent activities, and the action of several effector mechanisms. The latter mechanisms work, in response to sympathetic and vagal action, by modifying systemic peripheral resistances, systemic venous unstressed volumes, heart period, and end-systolic elastances. The model is used to simulate the interaction among the carotid baroreflex, the pulsating heart, and the effector responses in different experiments. In all cases, there has been satisfactory agreement between model and experimental results. Experimental data on heart rate control can be explained fairly well by assuming that the sympathetic-parasympathetic systems interact linearly on the heart period. The carotid baroreflex can significantly modulate the cardiac function curve. However, this effect is masked in vivo by changes in arterial and atrial pressures. During heart pacing, cardiac output increases with frequency at moderate levels of heart rate and then fails to increase further because of a reduction in stroke volume. Shifting from nonpulsatile to pulsatile perfusion of the carotid sinuses decreases the overall baroreflex gain and significantly modifies operation of the carotid baroreflex. Finally, a sensitivity analysis suggests that venous unstressed volume control plays the major role in the early hemodynamic response to acute hemorrhage, whereas systemic resistance and heart rate controls are a little less important.</description>
    <dc:title>Interaction between carotid baroregulation and the pulsating heart: a mathematical model.</dc:title>

    <dc:creator>M Ursino</dc:creator>
    <dc:source>Am J Physiol, Vol. 275, No. 5 Pt 2. (November 1998)</dc:source>
    <dc:date>2008-01-07T16:45:03-00:00</dc:date>
    <prism:publicationYear>1998</prism:publicationYear>
    <prism:publicationName>Am J Physiol</prism:publicationName>
    <prism:issn>0002-9513</prism:issn>
    <prism:volume>275</prism:volume>
    <prism:number>5 Pt 2</prism:number>
    <prism:category>autonomic_ns</prism:category>
    <prism:category>baroreflex</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>physiological_model</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2184667">
    <title>From inverse problems in mathematical physiology to quantitative differential diagnoses.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2184667</link>
    <description>&lt;i&gt;PLoS Comput Biol, Vol. 3, No. 11. (November 2007)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The improved capacity to acquire quantitative data in a clinical setting has generally failed to improve outcomes in acutely ill patients, suggesting a need for advances in computer-supported data interpretation and decision making. In particular, the application of mathematical models of experimentally elucidated physiological mechanisms could augment the interpretation of quantitative, patient-specific information and help to better target therapy. Yet, such models are typically complex and nonlinear, a reality that often precludes the identification of unique parameters and states of the model that best represent available data. Hypothesizing that this non-uniqueness can convey useful information, we implemented a simplified simulation of a common differential diagnostic process (hypotension in an acute care setting), using a combination of a mathematical model of the cardiovascular system, a stochastic measurement model, and Bayesian inference techniques to quantify parameter and state uncertainty. The output of this procedure is a probability density function on the space of model parameters and initial conditions for a particular patient, based on prior population information together with patient-specific clinical observations. We show that multimodal posterior probability density functions arise naturally, even when unimodal and uninformative priors are used. The peaks of these densities correspond to clinically relevant differential diagnoses and can, in the simplified simulation setting, be constrained to a single diagnosis by assimilating additional observations from dynamical interventions (e.g., fluid challenge). We conclude that the ill-posedness of the inverse problem in quantitative physiology is not merely a technical obstacle, but rather reflects clinical reality and, when addressed adequately in the solution process, provides a novel link between mathematically described physiological knowledge and the clinical concept of differential diagnoses. We outline possible steps toward translating this computational approach to the bedside, to supplement today's evidence-based medicine with a quantitatively founded model-based medicine that integrates mechanistic knowledge with patient-specific information.</description>
    <dc:title>From inverse problems in mathematical physiology to quantitative differential diagnoses.</dc:title>

    <dc:creator>S Zenker</dc:creator>
    <dc:creator>J Rubin</dc:creator>
    <dc:creator>G Clermont</dc:creator>
    <dc:identifier>doi:10.1371/journal.pcbi.0030204</dc:identifier>
    <dc:source>PLoS Comput Biol, Vol. 3, No. 11. (November 2007)</dc:source>
    <dc:date>2008-01-01T09:21:58-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>PLoS Comput Biol</prism:publicationName>
    <prism:issn>1553-7358</prism:issn>
    <prism:volume>3</prism:volume>
    <prism:number>11</prism:number>
    <prism:category>cardiovascular</prism:category>
    <prism:category>physiological_model</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2177707">
    <title>Modulation of cardiovascular control mechanisms and their interaction.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2177707</link>
    <description>&lt;i&gt;Physiol Rev, Vol. 76, No. 1. (January 1996), pp. 193-244.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;It is generally held that the role of a specific control element can only be understood within its physiological environment. The reviewed studies make it clear that there is a potent interplay between locally produced substances such as adenosine, nitric oxide, prostaglandins, and various others all interacting with the central level of control. This can occur at central sites (e.g., nitric oxide in the brain) or in the periphery (e.g., neural influence on autoregulation). The interactions are more or less pronounced during specific physiological challenges. Furthermore, several of these interactions are altered under pathological circumstances, and in some cases, the interactions seem to maintain or even augment the severity of disease. When more than three parameters participate in an interaction, the resulting regulation may become extremely complex. If these parameters are nonlinearly coupled with each other, the only way to shed light onto the nature of control network is by treating it as a black box. With the use of spectral analysis or nonlinear methods, it is possible to disentangle the fundamental nature of the system in terms of the complexity and stability. Therefore, modern developments in cardiovascular physiology utilizing these techniques, some of which are derived from the &#34;chaos theory,&#34; are reviewed. (Citado por 99)</description>
    <dc:title>Modulation of cardiovascular control mechanisms and their interaction.</dc:title>

    <dc:creator>PB Persson</dc:creator>
    <dc:source>Physiol Rev, Vol. 76, No. 1. (January 1996), pp. 193-244.</dc:source>
    <dc:date>2007-12-28T16:43:23-00:00</dc:date>
    <prism:publicationYear>1996</prism:publicationYear>
    <prism:publicationName>Physiol Rev</prism:publicationName>
    <prism:issn>0031-9333</prism:issn>
    <prism:volume>76</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>193</prism:startingPage>
    <prism:endingPage>244</prism:endingPage>
    <prism:category>cardiovascular</prism:category>
    <prism:category>cardiov_oscillations</prism:category>
    <prism:category>nonlinear_dynamics</prism:category>
    <prism:category>review_article</prism:category>
    <prism:category>spectral_analysis</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2204810">
    <title>System identification of closed-loop cardiovascular control mechanisms: diabetic autonomic neuropathy.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2204810</link>
    <description>&lt;i&gt;Am J Physiol, Vol. 276, No. 3 Pt 2. (March 1999)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;We applied cardiovascular system identification (CSI) to characterize closed-loop cardiovascular regulation in patients with diabetic autonomic neuropathy (DAN). The CSI method quantitatively analyzes beat-to-beat fluctuations in noninvasively measured heart rate, arterial blood pressure (ABP), and instantaneous lung volume (ILV) to characterize four physiological coupling mechanisms, two of which are autonomically mediated (the heart rate baroreflex and the coupling of respiration, measured in terms of ILV, to heart rate) and two of which are mechanically mediated (the coupling of ventricular contraction to the generation of the ABP wavelet and the coupling of respiration to ABP). We studied 37 control and 60 diabetic subjects who were classified as having minimal, moderate, or severe DAN on the basis of standard autonomic tests. The autonomically mediated couplings progressively decreased with increasing severity of DAN, whereas the mechanically mediated couplings were essentially unchanged. CSI identified differences between the minimal DAN and control groups, which were indistinguishable based on the standard autonomic tests. CSI may provide a powerful tool for assessing DAN.</description>
    <dc:title>System identification of closed-loop cardiovascular control mechanisms: diabetic autonomic neuropathy.</dc:title>

    <dc:creator>R Mukkamala</dc:creator>
    <dc:creator>JM Mathias</dc:creator>
    <dc:creator>TJ Mullen</dc:creator>
    <dc:creator>RJ Cohen</dc:creator>
    <dc:creator>R Freeman</dc:creator>
    <dc:source>Am J Physiol, Vol. 276, No. 3 Pt 2. (March 1999)</dc:source>
    <dc:date>2008-01-07T20:11:07-00:00</dc:date>
    <prism:publicationYear>1999</prism:publicationYear>
    <prism:publicationName>Am J Physiol</prism:publicationName>
    <prism:issn>0002-9513</prism:issn>
    <prism:volume>276</prism:volume>
    <prism:number>3 Pt 2</prism:number>
    <prism:category>cardiovascular</prism:category>
    <prism:category>dan</prism:category>
    <prism:category>feedback</prism:category>
    <prism:category>identification</prism:category>
    <prism:category>physiological_model</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2161653">
    <title>Point:Counterpoint: Cardiovascular variability is/is not an index of autonomic control of circulation</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2161653</link>
    <description>&lt;i&gt;J Appl Physiol, Vol. 101, No. 2. (1 August 2006), pp. 676-682.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;PURPOSE AND SCOPE OF THE POINT:COUNTERPOINT DEBATES: This series of debates was initiated for the Journal of Applied Physiology because we believe an important means of searching for truth is through debate where contradictory viewpoints are put forward. This dialectic process whereby a thesis is advanced, then opposed by an antithesis, with a synthesis subsequently arrived at, is a powerful and often entertaining method for gaining knowledge and for understanding the source of a controversy. Before reading these Point:Counterpoint manuscripts or preparing a brief commentary on their content (see below for instructions), the reader should understand that authors on each side of the debate are expected to advance a polarized viewpoint and to select the most convincing data to support their position. This approach differs markedly from the review article where the reader expects the author to present balanced coverage of the topic. Each of the authors has been strictly limited in the lengths of both the manuscript (1,200 words) and the rebuttal (400). The number of references to publications is also limited to 30, and citation of unpublished findings is prohibited. 10.1152/japplphysiol.00446.2006</description>
    <dc:title>Point:Counterpoint: Cardiovascular variability is/is not an index of autonomic control of circulation</dc:title>

    <dc:creator>Gianfranco Parati</dc:creator>
    <dc:creator>Giuseppe Mancia</dc:creator>
    <dc:creator>Marco Rienzo</dc:creator>
    <dc:creator>Paolo Castiglioni</dc:creator>
    <dc:creator>Andrew Taylor</dc:creator>
    <dc:creator>Peter Studinger</dc:creator>
    <dc:identifier>doi:10.1152/japplphysiol.00446.2006</dc:identifier>
    <dc:source>J Appl Physiol, Vol. 101, No. 2. (1 August 2006), pp. 676-682.</dc:source>
    <dc:date>2007-12-23T13:55:54-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>J Appl Physiol</prism:publicationName>
    <prism:volume>101</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>676</prism:startingPage>
    <prism:endingPage>682</prism:endingPage>
    <prism:category>autonomic_ns</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>hrv</prism:category>
    <prism:category>spectral_analysis</prism:category>
    <prism:category>vfc</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/1024708">
    <title>A realistic coupled nonlinear artificial ECG, BP, and respiratory signal generator for assessing noise performance of biomedical signal processing algorithms</title>
    <link>http://www.citeulike.org/user/Prodiana/article/1024708</link>
    <description>&lt;i&gt;Fluctuations and Noise in Biological, Biophysical, and Biomedical Systems II, Vol. 5467, No. 1. (2004), pp. 290-301.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Extensions to a previously published nonlinear model for generating realistic artificial electrocardiograms to include blood pressure and respiratory signals are presented. The model accurately reproduces many of the important clinical qualities of these signals such as QT dispersion, realistic beat to beat variability in timing and morphology and pulse transit time. The advantage of this artificial model is that the signal is completely known (and therefore its clinical descriptors can be specified exactly) and contains no noise. Artifact and noise can therefore be added in a quantifiable and controlled manner in order to test relevant biomedical signal processing algorithms. Application examples using Independent Component Analysis to remove artifacts are presented. (Citado por 9)</description>
    <dc:title>A realistic coupled nonlinear artificial ECG, BP, and respiratory signal generator for assessing noise performance of biomedical signal processing algorithms</dc:title>

    <dc:creator>Gari Clifford</dc:creator>
    <dc:creator>Patrick Mcsharry</dc:creator>
    <dc:identifier>doi:10.1117/12.544525</dc:identifier>
    <dc:source>Fluctuations and Noise in Biological, Biophysical, and Biomedical Systems II, Vol. 5467, No. 1. (2004), pp. 290-301.</dc:source>
    <dc:date>2007-01-04T11:01:51-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>Fluctuations and Noise in Biological, Biophysical, and Biomedical Systems II</prism:publicationName>
    <prism:volume>5467</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>290</prism:startingPage>
    <prism:endingPage>301</prism:endingPage>
    <prism:publisher>SPIE</prism:publisher>
    <prism:category>cardiovascular</prism:category>
    <prism:category>model</prism:category>
    <prism:category>physiological_model</prism:category>
    <prism:category>simulation</prism:category>
    <prism:category>synthetic_ecg</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2587026">
    <title>Cardiovascular autonomic nervous system tests: determination of normative values and effect of confounding variables.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2587026</link>
    <description>&lt;i&gt;J Auton Nerv Syst, Vol. 62, No. 1-2. (12 January 1997), pp. 40-44.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;OBJECTIVE: To determine normative values for heart rate variation to deep breathing (VAR) and Valsalva ratio (VAL) as well as the effect of various confounding variables on these measures using data from a large group of normal subjects collected from multiple centers. RESEARCH DESIGN AND METHODS: VAR and VAL were measured on 611 normal subjects, age range 9-79, from 63 centers and was analyzed at a single Autonomic Nervous System Reading Center. Using simple and stepwise logistic regression the effect of age, gender, height, weight, mean arterial blood pressure (MAP) and body mass index (BMI), on VAR and VAL was evaluated. RESULTS: The 95% normative values range (values at 2.5 to 97.5 percentile) for VAR (n = 580) was 12.8-103.5 (mean 49.7) and for VAL (n = 425) was 1.31-2.97 (mean 1.97). No gender effect was found for either VAR or VAL (p &#62; 0.05). VAR correlated inversely with both age and MAP, while VAL correlated inversely with both age and BMI. Since age is the principal confounding variable for both VAR and VAL, normative values are also presented stratified by age. CONCLUSION: Normative values for VAR and VAL based on a large population sample are presented. However, the values presented may not be valid in patients with morbid obesity or malignant hypertension. These data are applicable for either individual patients or for use in multicenter research trials.</description>
    <dc:title>Cardiovascular autonomic nervous system tests: determination of normative values and effect of confounding variables.</dc:title>

    <dc:creator>DA Gelber</dc:creator>
    <dc:creator>M Pfeifer</dc:creator>
    <dc:creator>B Dawson</dc:creator>
    <dc:creator>M Schumer</dc:creator>
    <dc:source>J Auton Nerv Syst, Vol. 62, No. 1-2. (12 January 1997), pp. 40-44.</dc:source>
    <dc:date>2008-03-25T17:46:07-00:00</dc:date>
    <prism:publicationYear>1997</prism:publicationYear>
    <prism:publicationName>J Auton Nerv Syst</prism:publicationName>
    <prism:issn>0165-1838</prism:issn>
    <prism:volume>62</prism:volume>
    <prism:number>1-2</prism:number>
    <prism:startingPage>40</prism:startingPage>
    <prism:endingPage>44</prism:endingPage>
    <prism:category>autonomic_ns</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>valsalva</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2161560">
    <title>Aging and the complexity of cardiovascular dynamics.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2161560</link>
    <description>&lt;i&gt;Biophys J, Vol. 59, No. 4. (April 1991), pp. 945-949.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Biomedical signals often vary in a complex and irregular manner. Analysis of variability in such signals generally does not address directly their complexity, and so may miss potentially useful information. We analyze the complexity of heart rate and beat-to-beat blood pressure using two methods motivated by nonlinear dynamics (chaos theory). A comparison of a group of healthy elderly subjects with healthy young adults indicates that the complexity of cardiovascular dynamics is reduced with aging. This suggests that complexity of variability may be a useful physiological marker. (Citado por 147)</description>
    <dc:title>Aging and the complexity of cardiovascular dynamics.</dc:title>

    <dc:creator>DT Kaplan</dc:creator>
    <dc:creator>MI Furman</dc:creator>
    <dc:creator>SM Pincus</dc:creator>
    <dc:creator>SM Ryan</dc:creator>
    <dc:creator>LA Lipsitz</dc:creator>
    <dc:creator>AL Goldberger</dc:creator>
    <dc:source>Biophys J, Vol. 59, No. 4. (April 1991), pp. 945-949.</dc:source>
    <dc:date>2007-12-23T13:01:01-00:00</dc:date>
    <prism:publicationYear>1991</prism:publicationYear>
    <prism:publicationName>Biophys J</prism:publicationName>
    <prism:issn>0006-3495</prism:issn>
    <prism:volume>59</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>945</prism:startingPage>
    <prism:endingPage>949</prism:endingPage>
    <prism:category>approximate_entropy</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>nonlinear_dynamics</prism:category>
    <prism:category>spectral_analysis</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/2206206">
    <title>System identification of closed-loop cardiovascular control: effects of posture and autonomic blockade.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/2206206</link>
    <description>&lt;i&gt;Am J Physiol, Vol. 272, No. 1 Pt 2. (January 1997)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;We applied system identification to the analysis of fluctuations in heart rate (HR), arterial blood pressure (ABP), and instantaneous lung volume (ILV) to characterize quantitatively the physiological mechanisms responsible for the couplings between these variables. We characterized two autonomically mediated coupling mechanisms [the heart rate baroreflex (HR baroreflex) and respiratory sinus arrhythmia (ILV-HR)] and two mechanically mediated coupling mechanisms [the blood pressure wavelet generated with each cardiac contraction (circulatory mechanics) and the direct mechanical effects of respiration on blood pressure (ILV--&#62;ABP)]. We evaluated the method in humans studied in the supine and standing postures under control conditions and under conditions of beta-sympathetic and parasympathetic pharmacological blockades. Combined beta-sympathetic and parasympathetic blockade abolished the autonomically mediated couplings while preserving the mechanically mediated coupling. Selective autonomic blockade and postural changes also altered the couplings in a manner consistent with known physiological mechanisms. System identification is an &#34;inverse-modeling&#34; technique that provides a means for creating a closed-loop model of cardiovascular regulation for an individual subject without altering the underlying physiological control mechanisms.</description>
    <dc:title>System identification of closed-loop cardiovascular control: effects of posture and autonomic blockade.</dc:title>

    <dc:creator>TJ Mullen</dc:creator>
    <dc:creator>ML Appel</dc:creator>
    <dc:creator>R Mukkamala</dc:creator>
    <dc:creator>JM Mathias</dc:creator>
    <dc:creator>RJ Cohen</dc:creator>
    <dc:source>Am J Physiol, Vol. 272, No. 1 Pt 2. (January 1997)</dc:source>
    <dc:date>2008-01-08T01:55:15-00:00</dc:date>
    <prism:publicationYear>1997</prism:publicationYear>
    <prism:publicationName>Am J Physiol</prism:publicationName>
    <prism:issn>0002-9513</prism:issn>
    <prism:volume>272</prism:volume>
    <prism:number>1 Pt 2</prism:number>
    <prism:category>cardiovascular</prism:category>
    <prism:category>identification</prism:category>
    <prism:category>physiological_model</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Prodiana/article/1029155">
    <title>A delay recruitment model of the cardiovascular control system.</title>
    <link>http://www.citeulike.org/user/Prodiana/article/1029155</link>
    <description>&lt;i&gt;J Math Biol, Vol. 51, No. 5. (November 2005), pp. 508-526.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;We develop a nonlinear delay-differential equation for the human cardiovascular control system, and use it to explore blood pressure and heart rate variability under short-term baroreflex control. The model incorporates an intrinsically stable heart rate in the absence of nervous control, and allows us to compare the baroreflex influence on heart rate and peripheral resistance. Analytical simplifications of the model allow a general investigation of the rôles played by gain and delay, and the effects of ageing.</description>
    <dc:title>A delay recruitment model of the cardiovascular control system.</dc:title>

    <dc:creator>AC Fowler</dc:creator>
    <dc:creator>MJ McGuinness</dc:creator>
    <dc:identifier>doi:10.1007/s00285-005-0339-1</dc:identifier>
    <dc:source>J Math Biol, Vol. 51, No. 5. (November 2005), pp. 508-526.</dc:source>
    <dc:date>2007-01-07T20:51:52-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>J Math Biol</prism:publicationName>
    <prism:issn>0303-6812</prism:issn>
    <prism:volume>51</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>508</prism:startingPage>
    <prism:endingPage>526</prism:endingPage>
    <prism:category>baroreflex</prism:category>
    <prism:category>cardiovascular</prism:category>
    <prism:category>hrv</prism:category>
    <prism:category>physiological_model</prism:category>
    <prism:category>vfc</prism:category>
</item>



</rdf:RDF>

