<?xml version="1.0" encoding="UTF-8"?>
<?xml-stylesheet href="/rss.css" type="text/css"?>
<rdf:RDF xmlns="http://purl.org/rss/1.0/"
    xmlns:cc="http://web.resource.org/cc/"
    xmlns:dc="http://purl.org/dc/elements/1.1/"
    xmlns:extra="http://www.w3.org/1999/xhtml"
    xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/"
    xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#">
    <channel rdf:about="http://www.jcmr-online.com/feeds/mostaccessed/journal?quantity=&amp;format=rss&amp;version=">
        <title>Journal of Cardiovascular Magnetic Resonance - Most accessed articles</title>
        <link>http://jcmr-online.com</link>
        <description>The most accessed research articles published by Journal of Cardiovascular Magnetic Resonance</description>
        <dc:date>2012-05-06T00:00:00Z</dc:date>
        <items>
            <rdf:Seq>
                                <rdf:li rdf:resource="http://jcmr-online.com/content/14/1/28" />
                                <rdf:li rdf:resource="http://www.jcmr-online.com/content/14/1/24" />
                                <rdf:li rdf:resource="http://jcmr-online.com/content/14/1/27" />
                                <rdf:li rdf:resource="http://jcmr-online.com/content/14/1/26" />
                                <rdf:li rdf:resource="http://jcmr-online.com/content/14/1/23" />
                                <rdf:li rdf:resource="http://jcmr-online.com/content/14/1/25" />
                                <rdf:li rdf:resource="http://www.jcmr-online.com/content/14/1/17" />
                                <rdf:li rdf:resource="http://www.jcmr-online.com/content/10/1/35" />
                                <rdf:li rdf:resource="http://www.jcmr-online.com/content/14/1/22" />
                                <rdf:li rdf:resource="http://www.jcmr-online.com/content/12/1/71" />
                            </rdf:Seq>
        </items>
                 <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </channel>
        <item rdf:about="http://jcmr-online.com/content/14/1/28">
        <title>Cardiovascular magnetic resonance in systemic hypertension
</title>
        <description>Systemic hypertension is a highly prevalent potentially modifiable cardiovascular risk factor.Imaging plays an important role in the diagnosis of underlying causes for hypertension, inassessing cardiovascular complications of hypertension, and in understanding thepathophysiology of the disease process. Cardiovascular magnetic resonance (CMR) providesaccurate and reproducible measures of ventricular volumes, mass, function andhaemodynamics as well as uniquely allowing tissue characterization of diffuse and focalfibrosis. In addition, CMR is well suited for exclusion of common secondary causes forhypertension. We review the current and emerging clinical and research applications of CMRin hypertension.</description>
        <link>http://jcmr-online.com/content/14/1/28</link>
                <dc:creator>Alicia Maceira Gonzalez</dc:creator>
                <dc:creator>Raad Mohiaddin</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2012, null:28</dc:source>
        <dc:date>2012-05-06T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-14-28</dc:identifier>
                                <prism:require>/content/figures/1532-429X-14-28-toc.gif</prism:require>
                <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>28</prism:startingPage>
        <prism:publicationDate>2012-05-06T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.jcmr-online.com/content/14/1/24">
        <title>Cardiovascular magnetic resonance characterization of peri-infarct zone remodeling following myocardial infarction</title>
        <description>Background:
Clinical studies implementing late gadolinium-enhanced (LGE) cardiovascular magnetic resonance (CMR) studies suggest that the peri-infarct zone (PIZ) contains a mixture of viable and non-viable myocytes, and is associated with greater susceptibility to ventricular tachycardia induction and adverse cardiac outcomes. However, CMR data assessing the temporal formation and functional remodeling characteristics of this complex region are limited. We intended to characterize early temporal changes in scar morphology and regional function in the PIZ.Methods and resultsCMR studies were performed at six time points up to 90 days after induction of myocardial infarction (MI) in eight minipigs with reperfused, anterior-septal infarcts. Custom signal density threshold algorithms, based on the remote myocardium, were applied to define the infarct core and PIZ region for each time point. After the initial post-MI edema subsided, the PIZ decreased by 54% from day 10 to day 90 (p = 0.04). The size of infarct scar expanded by 14% and thinned by 56% from day 3 to 12 weeks (p = 0.004 and p &lt; 0.001, respectively). LVEDV increased from 34.7. &#177; 2.2 ml to 47.8 &#177; 3.0 ml (day3 and week12, respectively; p &lt; 0.001). At 30 days post-MI, regional circumferential strain was increased between the infarct scar and the PIZ (-2.1 &#177; 0.6 and -6.8 &#177; 0.9, respectively;* p &lt; 0.05).
Conclusions:
The PIZ is dynamic and decreases in mass following reperfused MI. Tensile forces in the PIZ undergo changes following MI. Remodeling characteristics of the PIZ may provide mechanistic insights into the development of life-threatening arrhythmias and sudden cardiac death post-MI.</description>
        <link>http://www.jcmr-online.com/content/14/1/24</link>
                <dc:creator>Karl Schuleri</dc:creator>
                <dc:creator>Marco Centola</dc:creator>
                <dc:creator>Kristine Evers</dc:creator>
                <dc:creator>Adam Zviman</dc:creator>
                <dc:creator>Robert Evers</dc:creator>
                <dc:creator>Joao Lima</dc:creator>
                <dc:creator>Albert Lardo</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2012, null:24</dc:source>
        <dc:date>2012-04-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-14-24</dc:identifier>
                                <prism:require>/content/figures/1532-429X-14-24-toc.gif</prism:require>
                <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>24</prism:startingPage>
        <prism:publicationDate>2012-04-17T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://jcmr-online.com/content/14/1/27">
        <title>T1 mapping of the myocardium: Intra-individual assessment of the effect of field strength, cardiac cycle and variation by myocardial region</title>
        <description>Purpose: Myocardial T1 relaxation time (T1 time) and extracellular volume fraction (ECV) are altered in the presence of myocardial fibrosis. The purpose of this study was to evaluate acquisition factors that may result in variation of measured T1 time and ECV including magnetic field strength, cardiac phase and myocardial region.
Methods:
31 study subjects were enrolled and underwent one cardiovascular MR exam at 1.5T and two exams at 3T, each on separate days. A Modified Look-Locker Inversion Recovery (MOLLI) sequence was acquired before and 5, 10, 12, 20, 25 and 30 min after administration of 0.15mmol/kg gadopentetate dimeglumine (Gd-DTPA; Magnevist) at 1.5T (exam 1). For exam 2, MOLLI sequences were acquired at 3T both during diastole and systole, before and after administration of Gd-DTPA (0.15mmol/kg Magnevist). Exam 3 was identical to exam 2 except gadobenate dimeglumine was administered (Gd-BOPTA; 0.1mmol/kg Multihance). T1 times were measured in myocardium and blood. ECV was calculated by (DeltaR1myocardium /DeltaR1blood)*(1-hematocrit).
Results:
Before gadolinium, T1 times of myocardium and blood were significantly greater at 3T versus 1.5T (28% and 31% greater, respectively, p&lt;0.001); after gadolinium, 3T values remained greater than those at 1.5T (14% and 12% greater for myocardium and blood at 3T with Gd-DTPA, respectively, p&lt;0.0001 and 18% and 15% greater at 3T with Gd-BOPTA, respectively, p&lt;0.0001). However, ECV did not vary significantly with field strength when using the same contrast agent at equimolar dose (p=0.2). Myocardial T1 time was 1% shorter at systole compared to diastole pre-contrast and 2% shorter at diastole compared to systole post-contrast (p&lt;0.01). ECV values were greater during diastole compared to systole on average by 0.01 (p&lt;0.01 to p&lt;0.0001). ECV was significantly higher for the septum compared to the non-septal myocardium for all three exams (p&lt;0.0001-0.01) with mean absolute differences of 0.01, 0.004, and 0.07, respectively, for exams 1, 2 and 3.
Conclusion:
ECV is similar at field strengths of 1.5T and 3T. Due to minor variations in T1 time and ECV during the cardiac cycle and in different myocardial regions, T1 measurements should be obtained at the same cardiac phase and myocardial region in order to obtain consistent results.</description>
        <link>http://jcmr-online.com/content/14/1/27</link>
                <dc:creator>Nadine Kawel</dc:creator>
                <dc:creator>Marcelo Nacif</dc:creator>
                <dc:creator>Anna Zavodni</dc:creator>
                <dc:creator>Jacquin Jones</dc:creator>
                <dc:creator>Songtao Liu</dc:creator>
                <dc:creator>Christopher Sibley</dc:creator>
                <dc:creator>David Bluemke</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2012, null:27</dc:source>
        <dc:date>2012-05-01T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-14-27</dc:identifier>
                                <prism:require>/content/figures/1532-429X-14-27-toc.gif</prism:require>
                <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>27</prism:startingPage>
        <prism:publicationDate>2012-05-01T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://jcmr-online.com/content/14/1/26">
        <title>T1 mapping of the myocardium: intra-individual assessment of post-contrast T1 time evolution and extracellular volume fraction at 3T for Gd-DTPA and Gd-BOPTA</title>
        <description>Background:
Myocardial T1 relaxation time (T1 time) and extracellular volume fraction (ECV) are altered in patients with diffuse myocardial fibrosis. The purpose of this study was to perform an intra-individual assessment of normal T1 time and ECV for two different contrast agents.
Methods:
A modified Look-Locker Inversion Recovery (MOLLI) sequence was acquired at 3 T in 24 healthy subjects (8 men; 28 +/- 6 years) at mid-ventricular short axis pre-contrast and every 5 min between 5-45 min after injection of a bolus of 0.15 mmol/kg gadopentetate dimeglumine (Gd-DTPA; Magnevist(R)) (exam 1) and 0.1 mmol/kg gadobenate dimeglumine (Gd-BOPTA; Multihance(R)) (exam 2) during two separate scanning sessions. T1 times were measured in myocardium and blood on generated T1 maps. ECVs were calculated as  .
Results:
Mean pre-contrast T1 relaxation times for myocardium and blood were similar for both the first and second CMR exam (p &gt; 0.5). Overall mean post-contrast myocardial T1 time was 15 +/- 2 ms (2.5 +/- 0.7%) shorter for Gd-DTPA at 0.15 mmol/kg compared to Gd-BOPTA at 0.1 mmol/kg (p &lt; 0.01) while there was no significant difference for T1 time of blood pool (p &gt; 0.05). Between 5 and 45 minutes after contrast injection, mean ECV values increased linearly with time for both contrast agents from 0.27 +/- 0.03 to 0.30 +/- 0.03 (p &lt; 0.0001). Mean ECV values were slightly higher (by 0.01, p &lt; 0.05) for Gd-DTPA compared to Gd-BOPTA. Inter-individual variation of ECV was higher (CV 8.7% [exam 1, Gd-DTPA] and 9.4% [exam 2, Gd-BOPTA], respectively) compared to variation of pre-contrast myocardial T1 relaxation time (CV 4.5% [exam 1] and 3.0% [exam 2], respectively). ECV with Gd-DTPA was highly correlated to ECV by Gd-BOPTA (r = 0.803; p &lt; 0.0001).
Conclusions:
In comparison to pre-contrast myocardial T1 relaxation time, variation in ECV values of normal subjects is larger. However, absolute differences in ECV between Gd-DTPA and Gd-BOPTA were small and rank correlation was high. There is a small and linear increase in ECV over time, therefore ideally images should be acquired at the same delay after contrast injection.</description>
        <link>http://jcmr-online.com/content/14/1/26</link>
                <dc:creator>Nadine Kawel</dc:creator>
                <dc:creator>Marcelo Nacif</dc:creator>
                <dc:creator>Anna Zavodni</dc:creator>
                <dc:creator>Jacquin Jones</dc:creator>
                <dc:creator>Songtao Liu</dc:creator>
                <dc:creator>Christopher Sibley</dc:creator>
                <dc:creator>David Bluemke</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2012, null:26</dc:source>
        <dc:date>2012-04-28T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-14-26</dc:identifier>
                                <prism:require>/content/figures/1532-429X-14-26-toc.gif</prism:require>
                <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>26</prism:startingPage>
        <prism:publicationDate>2012-04-28T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://jcmr-online.com/content/14/1/23">
        <title>Cardiovascular magnetic resonance evaluation of aortic stenosis severity using single plane measurement of effective orifice area</title>
        <description>Background:
Transthoracic echocardiography (TTE) is the standard method for the evaluation of the severity of aortic stenosis (AS). Valve effective orifice area (EOA) measured by the continuity equation is one of the most frequently used stenotic indices. However, TTE measurement of aortic valve EOA is not feasible or not reliable in a significant proportion of patients. Cardiovascular magnetic resonance (CMR) has emerged as a non-invasive alternative to evaluate EOA using velocity measurements. The objectives of this study were: 1) to validate a new CMR method using jet shear layer detection (JSLD) based on acoustical source term (AST) concept to estimate the valve EOA; 2) to introduce a simplified JSLD method not requiring vorticity field derivation.Methods and resultsWe performed an in vitro study where EOA was measured by CMR in 4 fixed stenoses (EOA = 0.48, 1.00, 1.38 and 2.11 cm2) under the same steady flow conditions (4-20 L/min). The in vivo study included eight (8) healthy subjects and 37 patients with mild to severe AS (0.72 cm2 &lt;= EOA &lt;= 1.71 cm2). All subjects underwent TTE and CMR examinations. EOA was determinated by TTE with the use of continuity equation method (TTECONT). For CMR estimation of EOA, we used 3 methods: 1) Continuity equation (CMRCONT); 2) Shear layer detection (CMRJSLD), which was computed from the velocity field of a single CMR velocity profile at the peak systolic phase; 3) Single plane velocity truncation (CMRSPVT), which is a simplified version of CMRJSLD method. There was a good agreement between the EOAs obtained in vitro by the different CMR methods and the EOA predicted from the potential flow theory. In the in vivo study, there was good correlation and concordance between the EOA measured by the TTECONT method versus those measured by each of the CMR methods: CMRCONT (r = 0.88), CMRJSLD (r = 0.93) and CMRSPVT (r = 0.93). The intra- and inter- observer variability of EOA measurements was 5 +/- 5% and 9 +/- 5% for TTECONT, 2 +/- 1% and 7 +/- 5% for CMRCONT, 7 +/- 5% and 8 +/- 7% for CMRJSLD, 1 +/- 2% and 3 +/- 2% for CMRSPVT. When repeating image acquisition, reproducibility of measurements was 10 +/- 8% and 12 +/- 5% for TTECONT, 9 +/- 9% and 8 +/- 8% for CMRCONT, 6 +/- 5% and 7 +/- 4% for CMRJSLD and 3 +/- 2% and 2 +/- 2% for CMRSPVT.
Conclusion:
There was an excellent agreement between the EOA estimated by the CMRJSLD or CMRSPVT methods and: 1) the theoretical EOA in vitro, and 2) the TTECONT EOA in vivo. The CMRSPVT method was superior to the TTE and other CMR methods in terms of measurement variability. The novel CMR-based methods proposed in this study may be helpful to corroborate stenosis severity in patients for whom Doppler-echocardiography exam is inconclusive.</description>
        <link>http://jcmr-online.com/content/14/1/23</link>
                <dc:creator>Julio Garcia</dc:creator>
                <dc:creator>Oscar Marrufo</dc:creator>
                <dc:creator>Alfredo Rodriguez</dc:creator>
                <dc:creator>Eric Larose</dc:creator>
                <dc:creator>Philippe Pibarot</dc:creator>
                <dc:creator>Lyes Kadem</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2012, null:23</dc:source>
        <dc:date>2012-04-06T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-14-23</dc:identifier>
                                <prism:require>/content/figures/1532-429X-14-23-toc.gif</prism:require>
                <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>23</prism:startingPage>
        <prism:publicationDate>2012-04-06T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://jcmr-online.com/content/14/1/25">
        <title>Systemic-to-pulmonary collateral flow in patients 
with palliated univentricular heart physiology: 
measurement using cardiovascular magnetic 
resonance 4D velocity acquisition</title>
        <description>Background:
Systemic-to-pulmonary collateral flow (SPCF) may constitute a risk factor for increasedmorbidity and mortality in patients with single-ventricle physiology (SV). However, clinicalresearch is limited by the complexity of multi-vessel two-dimensional (2D) cardiovascularmagnetic resonance (CMR) flow measurements. We sought to validate four-dimensional(4D) velocity acquisition sequence for concise quantification of SPCF and flow distributionin patients with SV.
Methods:
29 patients with SV physiology prospectively underwent CMR (1.5 T) (n = 14 bidirectionalcavopulmonary connection [BCPC], age 2.9 +/- 1.3 years; and n = 15 Fontan, 14.4 +/- 5.9 years)and 20 healthy volunteers (age, 28.7 +/- 13.1 years) served as controls. A single whole-heart4D velocity acquisition and five 2D flow acquisitions were performed in the aorta,superior/inferior caval veins, right/left pulmonary arteries to serve as gold-standard. The five2D velocity acquisition measurements were compared with 4D velocity acquisition forvalidation of individual vessel flow quantification and time efficiency. The SPCF wascalculated by evaluating the disparity between systemic (aortic minus caval vein flows) andpulmonary flows (arterial and venour return). The pulmonary right to left and the systemiclower to upper body flow distribution were also calculated.
Results:
The comparison between 4D velocity and 2D flow acquisitions showed good Bland-Altmanagreement for all individual vessels (mean bias, 0.05+/-0.24 l/min/m2), calculated SPCF(0.02+/-0.18 l/min/m2) and significantly shorter 4D velocity acquisition-time (12:34min/17:28 min,p &lt; 0.01). 4D velocity acquisition in patients versus controls revealed (1) goodagreement between systemic versus pulmonary estimator for SPFC; (2) significant SPCF inpatients (BCPC 0.79+/-0.45 l/min/m2; Fontan 0.62+/-0.82 l/min/m2) and not in controls (0.01 +0.16 l/min/m2), (3) inverse relation of right/left pulmonary artery perfusion and right/leftSPCF (Pearson = 0.47,p = 0.01) and (4) upper to lower body flow distribution trend relatedto the weight (r = 0.742, p &lt; 0.001) similar to the controls.
Conclusions:
4D velocity acquisition is reliable, operator-independent and more time-efficient than 2Dflow acquisition to quantify SPCF. There is considerable SPCF in BCPC and Fontan patients.SPCF was more pronounced towards the respective lung with less pulmonary arterial flowsuggesting more collateral flow where less anterograde branch pulmonary artery perfusion.</description>
        <link>http://jcmr-online.com/content/14/1/25</link>
                <dc:creator>Israel Valverde</dc:creator>
                <dc:creator>Sarah Nordmeyer</dc:creator>
                <dc:creator>Sergio Uribe</dc:creator>
                <dc:creator>Gerald Greil</dc:creator>
                <dc:creator>Felix Berger</dc:creator>
                <dc:creator>Titus Kuehne</dc:creator>
                <dc:creator>Philipp Beerbaum</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2012, null:25</dc:source>
        <dc:date>2012-04-27T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-14-25</dc:identifier>
                                <prism:require>/content/figures/1532-429X-14-25-toc.gif</prism:require>
                <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>25</prism:startingPage>
        <prism:publicationDate>2012-04-27T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.jcmr-online.com/content/14/1/17">
        <title>The diagnosis of hypertrophic cardiomyopathy by cardiovascular magnetic resonance</title>
        <description>Hypertrophic cardiomyopathy (HCM) is the most common genetic disease of the heart. HCM is characterized by a wide range of clinical expression, ranging from asymptomatic mutation carriers to sudden cardiac death as the first manifestation of the disease. Over 1000 mutations have been identified, classically in genes encoding sarcomeric proteins. Noninvasive imaging is central to the diagnosis of HCM and cardiovascular magnetic resonance (CMR) is increasingly used to characterize morphologic, functional and tissue abnormalities associated with HCM. The purpose of this review is to provide an overview of the clinical, pathological and imaging features relevant to understanding the diagnosis of HCM. The early and overt phenotypic expression of disease that may be identified by CMR is reviewed. Diastolic dysfunction may be an early marker of the disease, present in mutation carriers prior to the development of left ventricular hypertrophy (LVH). Late gadolinium enhancement by CMR is present in approximately 60% of HCM patients with LVH and may provide novel information regarding risk stratification in HCM. It is likely that integrating genetic advances with enhanced phenotypic characterization of HCM with novel CMR techniques will importantly improve our understanding of this complex disease.</description>
        <link>http://www.jcmr-online.com/content/14/1/17</link>
                <dc:creator>Radwa Noureldin</dc:creator>
                <dc:creator>Songtao Liu</dc:creator>
                <dc:creator>Marcelo Nacif</dc:creator>
                <dc:creator>Daniel Judge</dc:creator>
                <dc:creator>Marc Halushka</dc:creator>
                <dc:creator>Theodore Abraham</dc:creator>
                <dc:creator>Carolyn Ho</dc:creator>
                <dc:creator>David Bluemke</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2012, null:17</dc:source>
        <dc:date>2012-02-20T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-14-17</dc:identifier>
                                <prism:require>/content/figures/1532-429X-14-17-toc.gif</prism:require>
                <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>17</prism:startingPage>
        <prism:publicationDate>2012-02-20T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.jcmr-online.com/content/10/1/35">
        <title>Standardized cardiovascular magnetic resonance imaging (CMR) protocols, society for cardiovascular magnetic resonance: board of trustees task force on standardized protocols</title>
        <description>Index1. General techniques1.1. Stress and safety equipment1.2. Left ventricular (LV) structure and function module1.3. Right ventricular (RV) structure and function module1.4. Gadolinium dosing module.1.5. First pass perfusion1.6. Late gadolinium enhancement (LGE)2. Disease specific protocols2.1. Ischemic heart disease2.1.1. Acute myocardial infarction (MI)2.1.2. Chronic ischemic heart disease and viability2.1.3. Dobutamine stress2.1.4. Adenosine stress perfusion2.2. Angiography:2.2.1. Peripheral magnetic resonance angiography (MRA)2.2.2. Thoracic MRA2.2.3. Anomalous coronary arteries2.2.4. Pulmonary vein evaluation2.3. Other2.3.1. Non-ischemic cardiomyopathy2.3.2. Arrhythmogenic right ventricular cardiomyopathy (ARVC)2.3.3. Congenital heart disease2.3.4. Valvular heart disease2.3.5. Pericardial disease2.3.6. Masses</description>
        <link>http://www.jcmr-online.com/content/10/1/35</link>
                <dc:creator>Christopher Kramer</dc:creator>
                <dc:creator>Jorg Barkhausen</dc:creator>
                <dc:creator>Scott Flamm</dc:creator>
                <dc:creator>Raymond Kim</dc:creator>
                <dc:creator>Eike Nagel</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2008, null:35</dc:source>
        <dc:date>2008-07-07T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-10-35</dc:identifier>
                                <prism:require>/content/figures/1532-429X-10-35-toc.gif</prism:require>
                <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>35</prism:startingPage>
        <prism:publicationDate>2008-07-07T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.jcmr-online.com/content/14/1/22">
        <title>Cardiovascular magnetic resonance of myocardial edema using a short inversion time inversion recovery (STIR) black-blood technique: Diagnostic accuracy of visual and semi-quantitative assessment</title>
        <description>Background:
The short inversion time inversion recovery (STIR) black-blood technique has been used to visualize myocardial edema, and thus to differentiate acute from chronic myocardial lesions. However, some cardiovascular magnetic resonance (CMR) groups have reported variable image quality, and hence the diagnostic value of STIR in routine clinical practice has been put into question. The aim of our study was to analyze image quality and diagnostic performance of STIR using a set of pulse sequence parameters dedicated to edema detection, and to discuss possible factors that influence image quality. We hypothesized that STIR imaging is an accurate and robust way of detecting myocardial edema in non-selected patients with acute myocardial infarction.
Methods:
Forty-six consecutive patients with acute myocardial infarction underwent CMR (day 4.5, +/- 1.6) including STIR for the assessment of myocardial edema and late gadolinium enhancement (LGE) for quantification of myocardial necrosis. Thirty of these patients underwent a follow-up CMR at approximately six months (195 +/- 39 days). Both STIR and LGE images were evaluated separately on a segmental basis for image quality as well as for presence and extent of myocardial hyper-intensity, with both visual and semi-quantitative (threshold-based) analysis. LGE was used as a reference standard for localization and extent of myocardial necrosis (acute) or scar (chronic).
Results:
Image quality of STIR images was rated as diagnostic in 99.5% of cases. At the acute stage, the sensitivity and specificity of STIR to detect infarcted segments on visual assessment was 95% and 78% respectively, and on semi-quantitative assessment was 99% and 83%, respectively. STIR differentiated acutely from chronically infarcted segments with a sensitivity of 95% by both methods and with a specificity of 99% by visual assessment and 97% by semi-quantitative assessment. The extent of hyper-intense areas on acute STIR images was 85% larger than those on LGE images, with a larger myocardial salvage index in reperfused than in non-reperfused infarcts (p = 0.035).
Conclusions:
STIR with appropriate pulse sequence settings is accurate in detecting acute myocardial infarction (MI) and distinguishing acute from chronic MI with both visual and semi-quantitative analysis. Due to its unique technical characteristics, STIR should be regarded as an edema-weighted rather than a purely T2-weighted technique.</description>
        <link>http://www.jcmr-online.com/content/14/1/22</link>
                <dc:creator>Darach O h-Ici</dc:creator>
                <dc:creator>John Ridgway</dc:creator>
                <dc:creator>Titus Kuehne</dc:creator>
                <dc:creator>Felix Berger</dc:creator>
                <dc:creator>Sven Plein</dc:creator>
                <dc:creator>Mohan Sivananthan</dc:creator>
                <dc:creator>Daniel Messroghli</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2012, null:22</dc:source>
        <dc:date>2012-03-28T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-14-22</dc:identifier>
                                <prism:require>/content/figures/1532-429X-14-22-toc.gif</prism:require>
                <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>22</prism:startingPage>
        <prism:publicationDate>2012-03-28T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.jcmr-online.com/content/12/1/71">
        <title>Cardiac magnetic resonance physics for clinicians: part I</title>
        <description>There are many excellent specialised texts and articles that describe the physical principles of cardiovascular magnetic resonance (CMR) techniques. There are also many texts written with the clinician in mind that provide an understandable, more general introduction to the basic physical principles of magnetic resonance (MR) techniques and applications. There are however very few texts or articles that attempt to provide a basic MR physics introduction that is tailored for clinicians using CMR in their daily practice. This is the first of two reviews that are intended to cover the essential aspects of CMR physics in a way that is understandable and relevant to this group. It begins by explaining the basic physical principles of MR, including a description of the main components of an MR imaging system and the three types of magnetic field that they generate. The origin and method of production of the MR signal in biological systems are explained, focusing in particular on the two tissue magnetisation relaxation properties (T1 and T2) that give rise to signal differences from tissues, showing how they can be exploited to generate image contrast for tissue characterisation. The method most commonly used to localise and encode MR signal echoes to form a cross sectional image is described, introducing the concept of k-space and showing how the MR signal data stored within it relates to properties within the reconstructed image. Before describing the CMR acquisition methods in detail, the basic spin echo and gradient pulse sequences are introduced, identifying the key parameters that influence image contrast, including appearances in the presence of flowing blood, resolution and image acquisition time. The main derivatives of these two pulse sequences used for cardiac imaging are then described in more detail. Two of the key requirements for CMR are the need for data acquisition first to be to be synchronised with the subject&apos;s ECG and to be fast enough for the subject to be able to hold their breath. Methods of ECG synchronisation using both triggering and retrospective gating approaches, and accelerated data acquisition using turbo or fast spin echo and gradient echo pulse sequences are therefore outlined in some detail. It is shown how double inversion black blood preparation combined with turbo or fast spin echo pulse sequences acquisition is used to achieve high quality anatomical imaging. For functional cardiac imaging using cine gradient echo pulse sequences two derivatives of the gradient echo pulse sequence; spoiled gradient echo and balanced steady state free precession (bSSFP) are compared. In each case key relevant imaging parameters and vendor-specific terms are defined and explained.</description>
        <link>http://www.jcmr-online.com/content/12/1/71</link>
                <dc:creator>John Ridgway</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2010, null:71</dc:source>
        <dc:date>2010-11-30T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-12-71</dc:identifier>
                                <prism:require>/content/figures/1532-429X-12-71-toc.gif</prism:require>
                <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>71</prism:startingPage>
        <prism:publicationDate>2010-11-30T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <cc:License rdf:about="http://creativecommons.org/licenses/by/2.0/">
        <cc:permits rdf:resource="http://creativecommons.org/ns#Reproduction" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#Distribution" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#DerivativeWorks" />
    </cc:License>
</rdf:RDF>

