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        <title>Journal of Cardiovascular Magnetic Resonance - Latest Articles</title>
        <link>http://jcmr-online.com</link>
        <description>The latest research articles published by Journal of Cardiovascular Magnetic Resonance</description>
        <dc:date>2010-03-22T00:00:00Z</dc:date>
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        <item rdf:about="http://jcmr-online.com/content/12/1/16">
        <title>Truncus arteriosus with aortic arch interruption: cardiovascular magnetic resonance findings in the unrepaired adult
</title>
        <description>Truncus arteriosus (TA) is a rare congenital condition defined as a single arterial vessel arising from the heart that gives origin to the systemic, pulmonary and coronary circulations. We discuss the unique case of a 28 year-old female patient with unrepaired TA and interruption of the aortic arch who underwent cardiovascular magnetic resonance (CMR).</description>
        <link>http://jcmr-online.com/content/12/1/16</link>
                <dc:creator>David Verhaert</dc:creator>
                <dc:creator>Janine Arruda</dc:creator>
                <dc:creator>Paaladinesh Thavendinarathan</dc:creator>
                <dc:creator>Stephen Cook</dc:creator>
                <dc:creator>Subha Raman</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2010, 12:16</dc:source>
        <dc:date>2010-03-22T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-12-16</dc:identifier>
        <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>16</prism:startingPage>
        <prism:publicationDate>2010-03-22T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://jcmr-online.com/content/12/1/15">
        <title>Review of Journal of Cardiovascular Magnetic Resonance 2009</title>
        <description>There were 56 articles published in the Journal of Cardiovascular Magnetic Resonance in 2009. The editors were impressed with the high quality of the submissions, of which our acceptance rate was about 40%. In accordance with open-access publishing, the articles go on-line as they are accepted with no collating of the articles into sections or special thematic issues. We have therefore chosen to briefly summarise the papers in this article for quick reference for our readers in broad areas of interest, which we feel will be useful to practitioners of cardiovascular magnetic resonance (CMR). In some cases where it is considered useful, the articles are also put into the wider context with a short narrative and recent CMR references. It has been a privilege to serve as the Editor of the JCMR this past year. I hope that you find the open-access system increases wider reading and citation of your papers, and that you will continue to send your quality manuscripts to JCMR for publication.</description>
        <link>http://jcmr-online.com/content/12/1/15</link>
                <dc:creator>D Pennell</dc:creator>
                <dc:creator>D Firmin</dc:creator>
                <dc:creator>P Kilner</dc:creator>
                <dc:creator>W Manning</dc:creator>
                <dc:creator>R Mohiaddin</dc:creator>
                <dc:creator>S Neubauer</dc:creator>
                <dc:creator>S Prasad</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2010, 12:15</dc:source>
        <dc:date>2010-03-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-12-15</dc:identifier>
        <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>15</prism:startingPage>
        <prism:publicationDate>2010-03-19T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://jcmr-online.com/content/12/1/14">
        <title>Left ventricular T2 distribution in Duchenne Muscular Dystrophy</title>
        <description>Background:
Although previous studies have helped define the natural history of Duchenne Muscular Dystrophy (DMD)-associated cardiomyopathy, the myocardial pathobiology associated with functional impairment in DMD is not yet known.The objective of this study was to assess the distribution of transverse relaxation time (T2) in the left ventricle (LV) of DMD patients, and to determine the association of myocardial T2 heterogeneity to the severity of cardiac dysfunction. DMD patients (n=26) and normal control subjects (n=13) were studied by Cardiovascular Magnetic Resonance (CMR). DMD subject data was stratified based on subject age and LV Ejection Fraction (EF) into the following groups: A (&lt;12 years old, n=12); B ([greater than or equal to]12 years old, EF &gt;55%, n=8) and C ([greater than or equal to]12 years old, EF [less than or equal to] 55%, n=6). Controls were also stratified by age into Groups N1 (&lt;12 years, n=6) and N2 (&gt;12 years, n=5). LV mid-slice circumferential myocardial strain (epsiloncc) was calculated using tagged CMR imaging. T2 maps of the LV were generated for all subjects using a black blood dual spin echo method at two echo times. The Full Width at Half Maximum (FWHM) was calculated from a histogram of LV T2 distribution constructed for each subject.
Results:
In DMD subject groups, FWHM of the T2 histogram rose progressively with age and decreasing EF (Group A FWHM= 25.3+/-3.8 ms; Group B FWHM= 30.9+/-5.3 ms; Group C FWHM= 33.0+/-6.4ms). Further, FWHM was significantly higher in those with reduced circumferential strain (|epsiloncc|[less than or equal to]12%) (Group B, and C) than those with |epsiloncc|&gt;12% (Group A). Group A FWHM was not different from the two normal groups (N1 FWHM = 25.3+/-3.5 ms; N2 FWHM= 24.0+/-7.3ms).
Conclusion:
Reduced EF and epsiloncc correlates well with increased T2 heterogeneity quantified by FWHM, indicating that subclinical functional impairments could be associated with pre-existing abnormalities in tissue structure in young DMD patients.</description>
        <link>http://jcmr-online.com/content/12/1/14</link>
                <dc:creator>Janaka Wansapura</dc:creator>
                <dc:creator>Kan Hor</dc:creator>
                <dc:creator>Wojciech Mazur</dc:creator>
                <dc:creator>Robert Fleck</dc:creator>
                <dc:creator>Sean Hagenbuch</dc:creator>
                <dc:creator>D Woodrow Benson</dc:creator>
                <dc:creator>William Gottliebson</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2010, 12:14</dc:source>
        <dc:date>2010-03-18T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-12-14</dc:identifier>
        <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>14</prism:startingPage>
        <prism:publicationDate>2010-03-18T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.jcmr-online.com/content/12/1/13">
        <title>How do hypertrophic cardiomyopathy mutations affect myocardial function in carriers with normal wall thickness? Assessment with cardiovascular magnetic resonance</title>
        <description>Background:
Clinical data on myocardial function in HCM mutation carriers (carriers) is sparse but suggests that subtle functional abnormalities can be measured with tissue Doppler imaging before the development of overt hypertrophy. We aimed to confirm the presence of functional abnormalities using cardiovascular magnetic resonance (CMR), and to investigate if sensitive functional assessment could be employed to identify carriers.
Results:
28 carriers and 28 controls were studied. Global left atrial (LA) and left ventricular (LV) dimensions, segmental peak systolic circumferential strain (SCS) and peak diastolic circumferential strain rate (DCSR), as well as the presence of late Gadolinium enhancement (LGE) were determined with CMR. Septal and lateral myocardial velocities were measured with echocardiographic tissue Doppler imaging. lv mass and volumes were comparable between groups. Maximal septal to lateral wall thickness ratio (SL ratio) was larger in carriers than in controls (1.3 &#177; 0.2 versus 1.1 &#177; 0.1, p &lt; 0.001). Also, LA volumes were larger in carriers compared to controls (p &lt; 0.05). Both peak SCS (p &lt; 0.05) and peak DCSR (p &lt; 0.01) were lower in carriers compared to controls, particularly in the basal lateral wall. Focal LGE was present in 2 carriers and not in controls. The combination of a SL ratio &gt;1.2 and a peak DCSR &lt;105%.s-1 was present in 45% of carriers and in none of the controls, yielding a positive predictive value of 100%. Two carriers and 18 controls had a SL ratio &lt; 1.2 and peak DCSR &gt;105%.s-1, yielding a negative predictive value of 90%. With multivariate analysis, HCM mutation carriership was an independent determinant of reduced peak SCS and peak DCSR.
Conclusions:
HCM mutation carriership is an independent determinant of reduced peak SCS and peak DCSR when LV wall thickness is within normal limits, and is associated with increased LA volumes and SL ratio. Using SL ratio and peak DCSR has a high accuracy to identify carriers. However, since carriers also display structural abnormalities and focal LGE, we advocate to also evaluate morphology and presence of LGE when screening for carriers.</description>
        <link>http://www.jcmr-online.com/content/12/1/13</link>
                <dc:creator>Tjeerd Germans</dc:creator>
                <dc:creator>Iris Russel</dc:creator>
                <dc:creator>Marco Gotte</dc:creator>
                <dc:creator>Marieke Spreeuwenberg</dc:creator>
                <dc:creator>Pieter Doevendans</dc:creator>
                <dc:creator>Yigal Pinto</dc:creator>
                <dc:creator>Rob van der Geest</dc:creator>
                <dc:creator>Jolanda van der Velden</dc:creator>
                <dc:creator>Arthur Wilde</dc:creator>
                <dc:creator>Albert van Rossum</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2010, 12:13</dc:source>
        <dc:date>2010-03-15T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-12-13</dc:identifier>
        <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>13</prism:startingPage>
        <prism:publicationDate>2010-03-15T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://jcmr-online.com/content/12/1/12">
        <title>Thoracic aortopathy in Turner syndrome and the influence of bicuspid aortic valves and blood pressure: a CMR study</title>
        <description>Background:
To investigate aortic dimensions in women with Turner syndrome (TS) in relation to aortic valve morphology, blood pressure, karyotype, and clinical characteristics.Methods and results:A cross sectional study of 102 women with TS (mean age 37.7; 18-62 years) examined by cardiovascular magnetic resonance (CMR- successful in 95), echocardiography, and 24-hour ambulatory blood pressure. Aortic diameters were measured by CMR at 8 positions along the thoracic aorta. Twenty-four healthy females were recruited as controls. In TS, aortic dilatation was present at one or more positions in 22 (23%). Aortic diameter in women with TS and bicuspid aortic valve was significantly larger than in TS with tricuspid valves in both the ascending (32.4+/-6.7 vs. 26.0+/-4.4mm; p&lt;0.001) and descending (21.4+/-3.5 vs. 18.8+/-2.4mm; p&lt;0.001) aorta. Aortic diameter correlated to age (R=0.2 - 0.5; p&lt;0.01), blood pressure (R= 0.4; p&lt;0.05), a history of coarctation (R= 0.3; p=0.01) and bicuspid aortic valve (R=0.2-0.5; p&lt;0.05). Body surface area only correlated with descending aortic diameter (R=0.23; p=0.024).
Conclusions:
Aortic dilatation was present in 23% of adult TS women, where aortic valve morphology, age and blood pressure were major determinants of the aortic diameter.</description>
        <link>http://jcmr-online.com/content/12/1/12</link>
                <dc:creator>Britta Hjerrild</dc:creator>
                <dc:creator>Kristian Mortensen</dc:creator>
                <dc:creator>Keld Sorensen</dc:creator>
                <dc:creator>Erik Pedersen</dc:creator>
                <dc:creator>Niels Andersen</dc:creator>
                <dc:creator>Erik Lundorf</dc:creator>
                <dc:creator>Klavs Hansen</dc:creator>
                <dc:creator>Arne Horlyck</dc:creator>
                <dc:creator>Alfred Hager</dc:creator>
                <dc:creator>Jens Christian</dc:creator>
                <dc:creator>Claus Gravholt</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2010, 12:12</dc:source>
        <dc:date>2010-03-11T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-12-12</dc:identifier>
        <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>12</prism:startingPage>
        <prism:publicationDate>2010-03-11T00:00:00Z</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/12/1/11">
        <title>Baseline correction of phase-contrast images in congenital  cardiovascular magnetic resonance</title>
        <description>Background:
One potential source of error in phase contrast (PC) congenital CMR flow measurements is caused by phase offsets due to local non-compensated eddy currents. Phantom correction of these phase offset errors has been shown to result in more accurate measurements of blood flow in adults with structurally normal hearts.  We report the effect of phantom correction on PC flow measurements at a clinical congenital CMR program.
Results:
Flow was measured in the ascending aorta, main pulmonary artery, and right and left pulmonary arteries as clinically indicated, and additional values such as Qp/Qs were derived from these measurements.  Phantom correction in our study population of 149 patients resulted in clinically significant changes in 13% to 48% of these phase-contrast measurements in patients with known or suspected heart disease. Overall, 640 measurements or calculated values were analyzed, and clinically significant changes were found in 31%.  Larger vessels were associated with greater phase offset errors, with 22% of the changes in PC flow measurements attributed to the size of the vessel measured. In patients with structurally normal hearts, the pulmonary-to-systemic flow ratio after phantom correction was closer to 1.0 than before phantom correction. There was no significant difference in the effect of phantom correction for patients with tetralogy of Fallot as compared to the group as a whole.
Conclusions:
Phantom correction often resulted in clinically significant changes in PC blood flow measurements in patients with known or suspected congenital heart disease. In laboratories performing clinical CMR with suspected phase offset errors of significance, the routine use of phantom correction for PC flow measurements should be considered.</description>
        <link>http://jcmr-online.com/content/12/1/11</link>
                <dc:creator>Brian Holland</dc:creator>
                <dc:creator>Beth Printz</dc:creator>
                <dc:creator>Wyman Lai</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2010, 12:11</dc:source>
        <dc:date>2010-03-05T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-12-11</dc:identifier>
        <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>11</prism:startingPage>
        <prism:publicationDate>2010-03-05T00:00:00Z</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/12/1/10">
        <title>Variations in atherosclerosis and remodeling patterns in aorta and carotids</title>
        <description>Background:
Atherosclerosis is a progressive disease that causes vascular remodeling that can be positive or negative. The evolution of arterial wall thickening and changes in lumen size under current &quot;standard of care&quot; in different arterial beds is unclear. The purpose of this study was to examine arterial remodeling and progression/regression of atherosclerosis in aorta and carotid arteries of individuals at risk for atherosclerosis normalized over a 1-year period.
Methods:
In this study, 28 patients underwent at least 2 black-blood in vivo cardiovascular magnetic resonance (CMR) scans of aorta and carotids over a one-year period (Mean 17.8+/-7.5 months). Clinical risk profiles for atherosclerosis and medications were documented and patients were followed by their referring physicians under current &quot;standard of care&quot; guidelines. Carotid and aortic wall and lumen areas were matched across the time-points from cross-sectional images.
Results:
The wall area increased by 8.67%, 10.64%, and 13.24% per year (carotid artery, thoracic aorta and abdominal aorta respectively, p&lt;0.001). The lumen area of the abdominal aorta increased by 4.97% per year (p=0.002), but the carotid artery and thoracic aorta lumen areas did not change significantly. The use of statin therapy did not change the rate of increase of wall area of carotid artery, thoracic and abdominal aorta, but decreased the rate of change of lumen area of carotid artery (-3.08+/-11.34 vs. 0.19+/-12.91 p&lt;0.05).
Conclusions:
Results of this study of multiple vascular beds indicated that different vascular locations exhibited varying progression of atherosclerosis and remodeling as monitored by CMR.</description>
        <link>http://jcmr-online.com/content/12/1/10</link>
                <dc:creator>Katsumi Hayashi</dc:creator>
                <dc:creator>Venkatesh Mani</dc:creator>
                <dc:creator>Ajay Nemade</dc:creator>
                <dc:creator>Silvia Aguiar</dc:creator>
                <dc:creator>John Postley</dc:creator>
                <dc:creator>Valentin Fuster</dc:creator>
                <dc:creator>Zahi Fayad</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2010, 12:10</dc:source>
        <dc:date>2010-03-05T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-12-10</dc:identifier>
        <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>10</prism:startingPage>
        <prism:publicationDate>2010-03-05T00:00:00Z</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/12/1/9">
        <title>Semi-automatic quantification of 4D left ventricular blood flow</title>
        <description>Background:
The beating heart is the generator of blood flow through the cardiovascular system. Within the heart&apos;s own chambers, normal complex blood flow patterns can be disturbed by diseases. Methods for the quantification of intra-cardiac blood flow, with its 4D (3D+time) nature, are lacking. We sought to develop and validate a novel semi-automatic analysis approach that integrates flow and morphological data.MethodIn six healthy subjects and three patients with dilated cardiomyopathy, three-directional, three-dimensional cine phase-contrast cardiovascular magnetic resonance (CMR) velocity data and balanced steady-state free-precession long- and short-axis images were acquired. The LV endocardium was segmented from the short-axis images at the times of isovolumetric contraction (IVC) and isovolumetric relaxation (IVR). At the time of IVC, pathlines were emitted from the IVC LV blood volume and traced forwards and backwards in time until IVR, thus including the entire cardiac cycle. The IVR volume was used to determine if and where the pathlines left the LV. This information was used to automatically separate the pathlines into four different components of flow: Direct Flow, Retained Inflow, Delayed Ejection Flow and Residual Volume. Blood volumes were calculated for every component by multiplying the number of pathlines with the blood volume represented by each pathline. The accuracy and inter- and intra-observer reproducibility of the approach were evaluated by analyzing volumes of LV inflow and outflow, the four flow components, and the end-diastolic volume.
Results:
The volume and distribution of the LV flow components were determined in all subjects. The calculated LV outflow volumes [ml] (67 &#177; 13) appeared to fall in between those obtained by through-plane phase-contrast CMR (77 &#177; 16) and Doppler ultrasound (58 &#177; 10), respectively. Calculated volumes of LV inflow (68 &#177; 11) and outflow (67 &#177; 13) were well matched (NS). Low inter- and intra-observer variability for the assessment of the volumes of the flow components was obtained.
Conclusions:
This semi-automatic analysis approach for the quantification of 4D blood flow resulted in accurate LV inflow and outflow volumes and a high reproducibility for the assessment of LV flow components.</description>
        <link>http://www.jcmr-online.com/content/12/1/9</link>
                <dc:creator>Jonatan Eriksson</dc:creator>
                <dc:creator>Carl Johan Carlhall</dc:creator>
                <dc:creator>Petter Dyverfeldt</dc:creator>
                <dc:creator>Jan Engvall</dc:creator>
                <dc:creator>Ann Bolger</dc:creator>
                <dc:creator>Tino Ebbers</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2010, 12:9</dc:source>
        <dc:date>2010-02-12T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-12-9</dc:identifier>
        <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>9</prism:startingPage>
        <prism:publicationDate>2010-02-12T00:00:00Z</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/12/1/8">
        <title>Relation between cardiac dimensions and peak oxygen uptake</title>
        <description>Background:
Long term endurance training is known to increase peak oxygen uptake (

) and induce morphological changes of the heart such as increased left ventricular mass (LVM). However, the relationship between 

 and the total heart volume (THV), considering both the left and right ventricular dimensions in both males and females, is not completely described. Therefore, the aim of this study was to test the hypothesis that THV is an independent predictor of 

 and to determine if the left and right ventricles enlarge in the same order of magnitude in males and females with a presumed wide range of THV.Methods and ResultsThe study population consisted of 131 subjects of whom 71 were athletes (30 female) and 60 healthy controls (20 female). All subjects underwent cardiovascular MR and maximal incremental exercise test. Total heart volume, LVM and left- and right ventricular end-diastolic volumes (LVEDV, RVEDV) were calculated from short-axis images. 

 was significantly correlated to THV, LVM, LVEDV and RVEDV in both males and females. Multivariable analysis showed that THV was a strong, independent predictor of 

 (R2 = 0.74, p &lt; 0.001). As LVEDV increased, RVEDV increased in the same order of magnitude in both males and females (R2 = 0.87, p &lt; 0.001).
Conclusion:
Total heart volume is a strong, independent predictor of maximal work capacity for both males and females. Long term endurance training is associated with a physiologically enlarged heart with a balance between the left and right ventricular dimensions in both genders.</description>
        <link>http://www.jcmr-online.com/content/12/1/8</link>
                <dc:creator>Katarina Steding</dc:creator>
                <dc:creator>Henrik Engblom</dc:creator>
                <dc:creator>Torsten Buhre</dc:creator>
                <dc:creator>Marcus Carlsson</dc:creator>
                <dc:creator>Henrik Mosen</dc:creator>
                <dc:creator>Bjorn Wohlfart</dc:creator>
                <dc:creator>Hakan Arheden</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2010, 12:8</dc:source>
        <dc:date>2010-02-01T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-12-8</dc:identifier>
        <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>8</prism:startingPage>
        <prism:publicationDate>2010-02-01T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.jcmr-online.com/content/12/1/7">
        <title>Relation between regional and global systolic function in patients with ischemic cardiomyopathy after beta-Blocker therapy or revascularization</title>
        <description>Background:
To assess the relationship between improved regional and global myocardial function in patients with ischemic cardiomyopathy in response to &#946;-blocker therapy or revascularization.Materials and methodsCardiovascular Magnetic Resonance (CMR) was performed in 32 patients with ischemic cardiomyopathy before and 8 &#177; 2 months after therapy. Patients were assigned clinically to &#946;-blocker therapy (n = 20) or revascularization (n = 12). CMR at baseline was performed to assess regional and global LV function at rest and under low-dose dobutamine. Wall thickening was analyzed in dysfunctional, adjacent, and remote segments. Follow-up CMR included rest function evaluation.
Results:
Augmentation of wall thickening during dobutamine at baseline was similar in dysfunctional, adjacent and remote segments in both patient groups. Therefore, baseline characteristics were similar for both patient groups. In both patient groups resting LV ejection fraction and end-systolic volume improved significantly (p &lt; 0.05) at follow-up. Stepwise multivariate analysis revealed that improvement in global LV ejection fraction in the &#946;-blocker treated patients was significantly related to improved function of remote myocardium (p &lt; 0.05), whereas in the revascularized patients improved function in dysfunctional and adjacent segments was more pronounced (p &lt; 0.05).
Conclusion:
In patients with chronic ischemic LV dysfunction, &#946;-Blocker therapy or revascularization resulted in a similar improvement of global systolic LV function. However, after &#946;-blocker therapy, improved global systolic function was mainly related to improved contraction of remote myocardium, whereas after revascularization the dysfunctional and adjacent regions contributed predominantly to the improved global systolic function.</description>
        <link>http://www.jcmr-online.com/content/12/1/7</link>
                <dc:creator>T Kaandorp</dc:creator>
                <dc:creator>J Bax</dc:creator>
                <dc:creator>S Bleeker</dc:creator>
                <dc:creator>J Doornbos</dc:creator>
                <dc:creator>E Viergever</dc:creator>
                <dc:creator>D Poldermans</dc:creator>
                <dc:creator>E van der Wall</dc:creator>
                <dc:creator>A de Roos</dc:creator>
                <dc:creator>H Lamb</dc:creator>
                <dc:source>Journal of Cardiovascular Magnetic Resonance 2010, 12:7</dc:source>
        <dc:date>2010-01-27T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1532-429X-12-7</dc:identifier>
        <prism:publicationName>Journal of Cardiovascular Magnetic Resonance</prism:publicationName>
        <prism:issn>1532-429X</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>7</prism:startingPage>
        <prism:publicationDate>2010-01-27T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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