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        <title>Cardiovascular Ultrasound - Latest Articles</title>
        <link>http://www.cardiovascularultrasound.com</link>
        <description>The latest research articles published by Cardiovascular Ultrasound</description>
        <dc:date>2009-07-03T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.cardiovascularultrasound.com/content/7/1/32" />
                                <rdf:li rdf:resource="http://www.cardiovascularultrasound.com/content/7/1/31" />
                                <rdf:li rdf:resource="http://www.cardiovascularultrasound.com/content/7/1/30" />
                                <rdf:li rdf:resource="http://www.cardiovascularultrasound.com/content/7/1/29" />
                                <rdf:li rdf:resource="http://www.cardiovascularultrasound.com/content/7/1/28" />
                                <rdf:li rdf:resource="http://www.cardiovascularultrasound.com/content/7/1/27" />
                                <rdf:li rdf:resource="http://www.cardiovascularultrasound.com/content/7/1/26" />
                                <rdf:li rdf:resource="http://www.cardiovascularultrasound.com/content/7/1/25" />
                                <rdf:li rdf:resource="http://www.cardiovascularultrasound.com/content/7/1/24" />
                                <rdf:li rdf:resource="http://www.cardiovascularultrasound.com/content/7/1/23" />
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        <item rdf:about="http://www.cardiovascularultrasound.com/content/7/1/32">
        <title>Cerebrovascular mental stress reactivity is impaired in hypertension</title>
        <description>Background:
Brachial artery reactivity in response to shear stress is altered in subjects with hypertension. Since endothelial dysfunction is generalized, we hypothesized that carotid artery (CA) reactivity would also be altered in hypertension. Purpose: To compare (CA endothelium-dependent vasodilation in response to mental stress in normal and hypertensive subjects. Methods: We evaluated CA reactivity to mental stress in 10 young healthy human volunteers (aged 23+/-4 years), 20 older healthy volunteers (aged 49+/-11 years) and in 28 patients with essential hypertension (aged 51+/-13 years). In 10 healthy volunteers and 12 hypertensive subjects, middle cerebral artery (MCA) PW transcranial Doppler was performed before and 3 minutes after mental stress. Results: Mental stress by Stroop color word conflict, math or anger recall tests caused CA vasodilation in young healthy subjects (0.61+/-0.06 to 0.65+/-0.07 cm, p&lt;0.05) and in older healthy subjects (0.63+/-0.06 to 0.66+/-0.07 cm, p&lt;0.05), whereas no CA vasodilation occurred in hypertensive subjects (0.69+/-0.06 to 0.68+/-0.07 cm; p, NS). CA blood flow in response to mental stress increased in young healthy subjects (419+/-134 to 541+/-209 ml, p&lt;0.01 vs. baseline) and in older healthy subjects (351+/-114 to 454+/-136 ml, p&lt;0.01 vs. baseline) whereas no change in blood flow (444+/-143 vs. 458+/-195 ml; p, 0.59) occurred in hypertensive subjects. There was no difference in the CA response to nitroglycerin in healthy and hypertensive subjects. Mental stress caused a significant increase in baseline to peak MCA systolic (84+/-22 to 95+/-22 cm/s, p&lt;0.05), diastolic (42+/-12 to 49+/-14 cm/s, p&lt;0.05) as well as mean (30+/-13 to 39+/-13 cm/s, p&lt;0.05) PW Doppler velocities  in normal subjects, whereas no change in systolic (70+/-18 to 73+/-22 cm/s, p&lt;0.05), diastolic (34+/-14 to 37+/-14 cm/s, p=ns) or mean velocities (25+/-9 to 26+/-9 cm/s, p=ns) occurred in hypertensive subjects, despite a similar increase in heart rate and blood pressure in response to mental stress in both groups. Conclusion: Mental stress produces CA vasodilation and is accompanied by an increase in CA and MCA blood flow in healthy subjects. This mental stress induced CA vasodilation and flow reserve is attenuated in subjects with hypertension and may reflect cerebral vascular endothelial dysfunction. Assessment of mental stress induced CA reactivity by ultrasound is a novel method for assessing the impact of hypertension on cerebrovascular endothelial function and blood flow reserve.</description>
        <link>http://www.cardiovascularultrasound.com/content/7/1/32</link>
                <dc:creator>Tasneem Naqvi</dc:creator>
                <dc:creator>Hahn Hyuhn</dc:creator>
                <dc:source>Cardiovascular Ultrasound 2009, 7:32</dc:source>
        <dc:date>2009-07-03T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7120-7-32</dc:identifier>
        <prism:publicationName>Cardiovascular Ultrasound</prism:publicationName>
        <prism:issn>1476-7120</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>32</prism:startingPage>
        <prism:publicationDate>2009-07-03T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.cardiovascularultrasound.com/content/7/1/31">
        <title>The subaortic tendon as a mimic of hypertrophic cardiomyopathy</title>
        <description>Originally described by Brock and Teare, today hypertrophic cardiomyopathy is clinically defined as left (or right) ventricular hypertrophy without a known cardiac or systemic cause, such as systemic hypertension, Fabry`s disease or aortic stenosis.Also appreciated today is the enormous genotypic and phenotypic heterogeneity of this disease with more than 300 mutations over more than 24 genes, encoding various sarcomeric, mitochondrial and calcium-handling proteins, all as genetic causes for hypertrophic cardiomyopathy.Phenotypically, the disease can vary from negligible to extreme hypertrophy, affecting either the left and/or right ventricle in an apical, midventricular or subaortic location.Left ventricular false tendons are thin, fibrous or fibromuscular structures that traverse the left ventricular cavity. Recently, a case report was presented where it was shown that such a false tendon, originating from a subaortic location, was responsible for striking ST-segment elevation on the surface electrocardiogram.In this case report, a case is presented where such a subaortic tendon led to the classic echocardiographic appearance of hypertrophic cardiomyopathy, thus in the assessment of hypertrophic cardiomyopathy, this entity needs to be excluded in order to prevent a false positive diagnosis of hypertrophic cardiomyopathy.</description>
        <link>http://www.cardiovascularultrasound.com/content/7/1/31</link>
                <dc:creator>James Ker</dc:creator>
                <dc:source>Cardiovascular Ultrasound 2009, 7:31</dc:source>
        <dc:date>2009-07-03T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7120-7-31</dc:identifier>
        <prism:publicationName>Cardiovascular Ultrasound</prism:publicationName>
        <prism:issn>1476-7120</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>31</prism:startingPage>
        <prism:publicationDate>2009-07-03T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.cardiovascularultrasound.com/content/7/1/30">
        <title>Ozone and cardiovascular injury</title>
        <description>Air pollution is increasingly recognized as an important and modifiable determinant of cardiovascular diseases in urban communities. The potential detrimental effects are both acute and chronic having a strong impact on morbidity and mortality. The acute exposure to pollutants has been linked to adverse cardiovascular events such as myocardial infarction, heart failure and life-threatening arrhythmias. The long-terms effects are related to the lifetime risk of death from cardiac causes. The WHO estimates that air pollution is responsible for 3 million premature deaths each year. The evidence supporting these data is very strong nonetheless, epidemiologic and observational data have the main limitation of imprecise measurements. Moreover, the lack of clinical experimental models makes it difficult to demonstrate the individual risk. The other limitation is related to the lack of a clear mechanism explaining the effects of pollution on cardiovascular mortality. In the present review we will explore the epidemiological, clinical and experimental evidence of the effects of ozone on cardiovascular diseases.</description>
        <link>http://www.cardiovascularultrasound.com/content/7/1/30</link>
                <dc:creator>Vera Srebot</dc:creator>
                <dc:creator>Emilio Gianicolo</dc:creator>
                <dc:creator>Giuseppe Rainaldi</dc:creator>
                <dc:creator>Maria Giovanna Trivella</dc:creator>
                <dc:creator>Rosa Sicari</dc:creator>
                <dc:source>Cardiovascular Ultrasound 2009, 7:30</dc:source>
        <dc:date>2009-06-24T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7120-7-30</dc:identifier>
        <prism:publicationName>Cardiovascular Ultrasound</prism:publicationName>
        <prism:issn>1476-7120</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>30</prism:startingPage>
        <prism:publicationDate>2009-06-24T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.cardiovascularultrasound.com/content/7/1/29">
        <title>Are measurements of systolic myocardial velocities and displacement with colour and spectral Tissue Doppler compatible?</title>
        <description>Background:
Tissue Doppler (TD) in pulsed mode (spectral TD) and colour TD are the two modalities today available in tissue velocity echocardiography (TVE). Previous studies have shown poor agreement between these two methods when measuring myocardial velocities and displacement. In this study, the concordance between the myocardial velocity and displacement measurements using colour TD and different spectral TD procedures was evaluated.
Methods:
Left ventricular (LV) longitudinal systolic myocardial velocities and displacement during ejection period were quantified at the basal septal and lateral wall in 24 healthy individuals (4 women and 20 men, 34+/-12 years) using spectral TD, colour TD and M-mode recordings. Mean, maximal and minimal spectral TD systolic velocities and the corresponding displacement values were obtained by measurements at the outer and inner borders of the spectral velocity signal. The results were then compared with those obtained with the two other modalities used.
Results:
Systolic myocardial velocities derived from mean spectral TD frequencies were highly concordant with corresponding colour TD measurements (mean difference 0.10+/-0.54 cm/sec, septal wall). Similarly, the agreement between spectral and colour TD (mean difference 0.22+/-0.74 mm, septal wall) as well as M-mode was good when mean spectral velocities were temporally integrated and the results did not differ statistically. Conversely, displacement values from the inner or outer border of the spectral signal differed significantly from values obtained with colour TD and M-mode (p&lt;0.001, in both cases).
Conclusion:
LV systolic myocardial measurements based on mean spectral TD frequencies are highly concordant with those provided by colour TD and M-mode. Hence, in order to maintain compatibility of the results, the use of this particular spectral TD procedure should be advocated in clinical praxis.</description>
        <link>http://www.cardiovascularultrasound.com/content/7/1/29</link>
                <dc:creator>Aristomenis Manouras</dc:creator>
                <dc:creator>Arben Shala</dc:creator>
                <dc:creator>Evangelia Nyktari</dc:creator>
                <dc:creator>Kambiz Shahgaldi</dc:creator>
                <dc:creator>Reidar Winter</dc:creator>
                <dc:creator>Panos Vardas</dc:creator>
                <dc:creator>Lars Ake Brodin</dc:creator>
                <dc:creator>Jacek Nowak</dc:creator>
                <dc:source>Cardiovascular Ultrasound 2009, 7:29</dc:source>
        <dc:date>2009-06-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7120-7-29</dc:identifier>
        <prism:publicationName>Cardiovascular Ultrasound</prism:publicationName>
        <prism:issn>1476-7120</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>29</prism:startingPage>
        <prism:publicationDate>2009-06-23T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.cardiovascularultrasound.com/content/7/1/28">
        <title>Quantitative detection of myocardial ischaemia by stress echocardiography; A comparison with SPECT.</title>
        <description>AimsReal-time perfusion (RTP) adenosine stress echocardiography (ASE) can be used to visually evaluate myocardial ischaemia. The RTP power modulation technique angio-mode (AM), provides images for off-line perfusion quantification using Qontrast(R) software, generating values of peak signal intensity (A), myocardial blood flow velocity (beta) and myocardial blood flow (Axbeta). By comparing rest and stress values, their respective reserve values (A-r, beta-r, Axbeta-r) are generated. We evaluated myocardial ischaemia by RTP-ASE Qontrast(R) quantification, compared to visual perfusion evaluation with 99mTc-tetrofosmin single-photon emission computed tomography (SPECT).Methods and ResultsPatients admitted to SPECT underwent RTP-ASE (SONOS 5500) using AM during Sonovue(R) infusion, before and throughout adenosine stress, also used for SPECT. Visual myocardial perfusion and wall motion analysis, and Qontrast(R) quantification, were blindly compared to one another and to SPECT, at different time points off-line.We analyzed 201 coronary territories (left anterior descendent [LAD], left circumflex [LCx] and right coronary [RCA] artery territories) in 67 patients. SPECT showed ischaemia in 18 patients and 19 territories. Receiver operator characteristics and kappa values showed significant agreement with SPECT only for beta-r and Axbeta-r in all segments: area under the curve 0.678 and 0.665; P&lt;0.001 and &lt;0.01, respectively. The closest agreements were seen in the LAD territory: kappa 0.442 for both beta-r and Axbeta-r; P&lt;0.01. Visual evaluation of ischaemia showed good agreement with SPECT: accuracy 93%; kappa 0.67; P&lt;0.001; without non-interpretable territories.
Conclusion:
In this agreement study with SPECT, RTP-ASE Qontrast(R) quantification of myocardial ischaemia was less accurate and less feasible than visual evaluation and needs further development to be clinically useful.</description>
        <link>http://www.cardiovascularultrasound.com/content/7/1/28</link>
                <dc:creator>Petri Gudmundsson</dc:creator>
                <dc:creator>Kambiz Shahgaldi</dc:creator>
                <dc:creator>Reidar Winter</dc:creator>
                <dc:creator>Magnus Dencker</dc:creator>
                <dc:creator>Mariusz Kitlinski</dc:creator>
                <dc:creator>Ola Thorsson</dc:creator>
                <dc:creator>Ronnie Willenheimer</dc:creator>
                <dc:creator>Lennart Ljunggren</dc:creator>
                <dc:source>Cardiovascular Ultrasound 2009, 7:28</dc:source>
        <dc:date>2009-06-18T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7120-7-28</dc:identifier>
        <prism:publicationName>Cardiovascular Ultrasound</prism:publicationName>
        <prism:issn>1476-7120</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>28</prism:startingPage>
        <prism:publicationDate>2009-06-18T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.cardiovascularultrasound.com/content/7/1/27">
        <title>Comparison of contrast enhanced three dimensional echocardiography with MIBI gated SPECT for the evaluation of left ventricular function</title>
        <description>Background:
In clinical practice and in clinical trials, echocardiography and scintigraphy are used the most for the evaluation of global left ejection fraction (LVEF) and left ventricular (LV) volumes. Actually, poor quality imaging and geometrical assumptions are the main limitations of LVEF measured by echocardiography. Contrast agents and 3D echocardiography are new methods that may alleviate these potential limitations.
Methods:
Therefore we sought to examine the accuracy of contrast 3D echocardiography for the evaluation of LV volumes and LVEF relative to MIBI gated SPECT as an independent reference. In 43 patients addressed for chest pain, contrast 3D echocardiography (RT3DE) and MIBI gated SPECT were prospectively performed on the same day. The accuracy and the variability of LV volumes and LVEF measurements were evaluated.
Results:
Due to good endocardial delineation, LV volumes and LVEF measurements by contrast RT3DE were feasible in 99% of the patients. The mean LV end-diastolic volume (LVEDV) of the group by scintigraphy was 143 &#177; 65 mL and was underestimated by triplane contrast RT3DE (128 &#177; 60 mL; p &lt; 0.001) and less by full-volume contrast RT3DE (132 &#177; 62 mL; p &lt; 0.001). Limits of agreement with scintigraphy were similar for triplane andfull-volume, modalities with the best results for full-volume. Results were similar for calculation of LV end-systolic volume (LVESV). The mean LVEF was 44 &#177; 16% with scintigraphy and was not significantly different with both triplane contrast RT3DE (45 &#177; 15%) and full-volume contrast RT3DE (45 &#177; 15%). There was an excellent correlation between two different observers for LVEDV, LVESV and LVEF measurements and inter observer agreement was also good for both contrast RT3DE techniques.
Conclusion:
Contrast RT3DE allows an accurate assessment of LVEF compared to the LVEF measured by SPECT, and shows low variability between observers. Although RT3DE triplane provides accurate evaluation of left ventricular function, RT3DE full-volume is superior to triplane modality in patients with suspected coronary artery disease.</description>
        <link>http://www.cardiovascularultrasound.com/content/7/1/27</link>
                <dc:creator>Bernard Cosyns</dc:creator>
                <dc:creator>David Haberman</dc:creator>
                <dc:creator>Steven Droogmans</dc:creator>
                <dc:creator>Sandrine Warzee</dc:creator>
                <dc:creator>Philippe Mahieu</dc:creator>
                <dc:creator>Eric Laurent</dc:creator>
                <dc:creator>Marie Moonen</dc:creator>
                <dc:creator>Sophie Hernot</dc:creator>
                <dc:creator>Patrizio Lancellotti</dc:creator>
                <dc:source>Cardiovascular Ultrasound 2009, 7:27</dc:source>
        <dc:date>2009-06-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7120-7-27</dc:identifier>
        <prism:publicationName>Cardiovascular Ultrasound</prism:publicationName>
        <prism:issn>1476-7120</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>27</prism:startingPage>
        <prism:publicationDate>2009-06-16T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.cardiovascularultrasound.com/content/7/1/26">
        <title>Hypertrophic cardiomyopathy with midventricular obstruction and apical aneurysm formation in a single family: case report</title>
        <description>Background:
Hypertrophic cardiomyopathy (HCM) is an extremely heterogeneous disease. An under recognized and very often missed subgroup within this broad spectrum concerns patients with left ventricular (LV) apical aneurysms in the absence of coronary artery disease.Case presentationWe describe a case of HCM with midventricular obstruction and apical aneurysm formation  in 3 patients coming from  a single family. This HCM pattern was detected by 2D-echocardiography and confirmed by cardiac magnetic resonance imaging.A cardioverter defibrillator was implanted in one of the patients because of non-sustained ventricular tachycardia detected in 24-h Holter monitoring and an abrupt drop in systolic blood pressure during maximal exercise test. The defibrillator activated 8 months after implantation by suppression of a ventricular tachycardia providing anti-tachycardia pacing. The patient died due to refractory heart failure 2 years after initial evaluation. The rest of the patients are stable after a 2.5-y follow-up period.
Conclusion:
The detection of apical aneurysm by echocardiography in HCM patients may be complicated. Ventricular tachycardia arising from the scarred aneurysm wall may often occur, predisposing to sudden death.</description>
        <link>http://www.cardiovascularultrasound.com/content/7/1/26</link>
                <dc:creator>Georgios Efthimiadis</dc:creator>
                <dc:creator>Christodoulos Pliakos</dc:creator>
                <dc:creator>Efstathios Pagourelias</dc:creator>
                <dc:creator>Despoina Parcharidou</dc:creator>
                <dc:creator>Georgios Spanos</dc:creator>
                <dc:creator>Stylianos Paraskevaidis</dc:creator>
                <dc:creator>Ioannis Styliadis</dc:creator>
                <dc:creator>Georgios Parcharidis</dc:creator>
                <dc:source>Cardiovascular Ultrasound 2009, 7:26</dc:source>
        <dc:date>2009-06-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7120-7-26</dc:identifier>
        <prism:publicationName>Cardiovascular Ultrasound</prism:publicationName>
        <prism:issn>1476-7120</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>26</prism:startingPage>
        <prism:publicationDate>2009-06-16T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.cardiovascularultrasound.com/content/7/1/25">
        <title>The relation between endothelial dependent flow mediated dilation of the brachial artery and coronary collateral development - a cross sectional study</title>
        <description>Background:
Endothelial dysfunction is thought to be a potential mechanism for the decreased presence of coronary collaterals. The aim of the study was to investigate the association between systemic endothelial function and the extent of coronary collaterals.
Methods:
We investigated the association between endothelial function assessed via flow mediated dilation (FMD) of the brachial artery following reactive hyperemia and the extent of coronary collaterals graded from 0 to 3 according to Rentrop classification in a cohort of 171 consecutive patients who had high grade coronary stenosis or occlusion on their angiograms.
Results:
Mean age was 61 years and 75% were males. Of the 171 patients 88 (51%) had well developed collaterals (grades of 2 or 3) whereas 83 (49%) had impaired collateral development (grades of 0 or 1). Patients with poor collaterals were significantly more likely to have diabetes (p = 0.001), but less likely to have used statins (p = 0.083). FMD measurements were not significantly different among good and poor collateral groups (11.5 &#177; 5.6 vs. 10.4 &#177; 6.2% respectively, p = 0.214). Nitroglycerin mediated dilation was also similar (13.4 &#177; 5.9 vs. 12.8 &#177; 6.5%, p = 0.521).
Conclusion:
No significant association was found between the extent of angiographically visible coronary collaterals and systemic endothelial function assessed by FMD of the brachial artery.</description>
        <link>http://www.cardiovascularultrasound.com/content/7/1/25</link>
                <dc:creator>Aydan Ongun Ozdemir</dc:creator>
                <dc:creator>Sadi Gulec</dc:creator>
                <dc:creator>Nihal Uslu</dc:creator>
                <dc:creator>Cansin Tulunay Kaya</dc:creator>
                <dc:creator>Cagdas Ozdol</dc:creator>
                <dc:creator>Sibel Turhan</dc:creator>
                <dc:creator>Yusuf Atmaca</dc:creator>
                <dc:creator>Timucin Altin</dc:creator>
                <dc:creator>Cetin Erol</dc:creator>
                <dc:source>Cardiovascular Ultrasound 2009, 7:25</dc:source>
        <dc:date>2009-06-15T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7120-7-25</dc:identifier>
        <prism:publicationName>Cardiovascular Ultrasound</prism:publicationName>
        <prism:issn>1476-7120</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>25</prism:startingPage>
        <prism:publicationDate>2009-06-15T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.cardiovascularultrasound.com/content/7/1/24">
        <title>Prognostic value of exercise echocardiography in diabetic patients</title>
        <description>Background:
Coronary artery disease (CAD) is the leading cause of death in diabetic patients. Although exercise echocardiography (EE) is established as a useful method for diagnosis and stratification of risk for CAD in the general population, there are few studies on its value as a prognostic tool in diabetic patients. The purpose of this investigation was to evaluate the value of EE in predicting cardiac events in diabetics.
Methods:
193 diabetic patients, 97 males, 59.8 &#177; 9.3 yrs (mean &#177; SD) were submitted to EE between 2001 and 2006 and followed from 7 to 65 months with median of 29 months by phone calls and personal interviews with patients and their primary physician, and reviewing medical records and death certificates. The end points were cardiac events, defined as non-fatal myocardial infarction, late myocardial revascularization and cardiac death. Sudden death without another explanation was considered cardiac death. Survival free of end points was estimated by the Kaplan-Meier method.
Results:
Twenty-six cardiac events were registered in 24 individuals during the follow-up. The rates of cardiac events were 20.6 and 7% in patients with positive and negative EE, respectively (p &lt; 0.001). Predictors of cardiac events included sedentary lifestyle, with RR of 2.57 95%CI [1.09 to 6.02] (P = 0.03) and positive EE, with RR 3.63, 95%CI [1.44 to 9.16] (P = 0.01). Patients with positive EE presented higher rates of cardiac events at 12 months (6.8% vs. 2.2%), p = 0.004.
Conclusion:
EE is a useful method to predict cardiac events in diabetic patients with suspected or known CAD.</description>
        <link>http://www.cardiovascularultrasound.com/content/7/1/24</link>
                <dc:creator>Joselina Oliveira</dc:creator>
                <dc:creator>Jose Barreto-Filho</dc:creator>
                <dc:creator>Antonio Sousa</dc:creator>
                <dc:creator>Carla Oliveira</dc:creator>
                <dc:creator>Thaiana Santana</dc:creator>
                <dc:creator>Fernando Anjos-Andrade</dc:creator>
                <dc:creator>Erica Alves</dc:creator>
                <dc:creator>Adao Nascimento-Junior</dc:creator>
                <dc:creator>Thiago Goes</dc:creator>
                <dc:creator>Nathalie Santana</dc:creator>
                <dc:creator>Francis Vasconcelos</dc:creator>
                <dc:creator>Martha Barreto</dc:creator>
                <dc:creator>Argemiro D'Oliveira</dc:creator>
                <dc:creator>Roberto Salvatori</dc:creator>
                <dc:creator>Manuel Aguiar-Oliveira</dc:creator>
                <dc:source>Cardiovascular Ultrasound 2009, 7:24</dc:source>
        <dc:date>2009-05-29T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7120-7-24</dc:identifier>
        <prism:publicationName>Cardiovascular Ultrasound</prism:publicationName>
        <prism:issn>1476-7120</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>24</prism:startingPage>
        <prism:publicationDate>2009-05-29T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.cardiovascularultrasound.com/content/7/1/23">
        <title>Doppler ultrasonography and exercise testing in diagnosing a popliteal artery adventitial cyst</title>
        <description>We describe popliteal arterial adventitial cystic disease which causes intermittent claudication in a young athletic man, with atypical manifestation, without loss of foot pulses on knee flexion nor murmur in the popliteal fossa. The findings obtained from Magnetic Resonance Imaging were non-diagnostic. The diagnosis resulted from Echo-Doppler ultrasonography along with peak exercise testing. Ultrasonography also provided useful physiopathological informations suggesting that a popliteal artery adventitial cyst can become symptomatic if muscle exertion increases fluid pressure within the cyst, enough to cause hemodynamically significant endoluminal stenosis. Rapid diagnosis is essential to prevent progressive claudication threatening limb viability. To guarantee this professional sportsman a reliable and durable outcome, instead of less aggressive management, we resected the involved arterial segment and interposed an autologous saphenous-vein graft.</description>
        <link>http://www.cardiovascularultrasound.com/content/7/1/23</link>
                <dc:creator>Maurizio Taurino</dc:creator>
                <dc:creator>Luigi Rizzo</dc:creator>
                <dc:creator>Nazzareno Stella</dc:creator>
                <dc:creator>Massimo Mastroddi</dc:creator>
                <dc:creator>Fabio Conteduca</dc:creator>
                <dc:creator>Claudia Maggiore</dc:creator>
                <dc:creator>Vittorio Faraglia</dc:creator>
                <dc:source>Cardiovascular Ultrasound 2009, 7:23</dc:source>
        <dc:date>2009-05-27T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7120-7-23</dc:identifier>
        <prism:publicationName>Cardiovascular Ultrasound</prism:publicationName>
        <prism:issn>1476-7120</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>23</prism:startingPage>
        <prism:publicationDate>2009-05-27T00:00:00Z</prism:publicationDate>
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