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    <title>Korte, C.L. de</title>
    <link>http://repub.eur.nl/res/aut/1589/</link>
    <description>List of Publications</description>
    <language>en</language>
    <image>
      <url>http://repub.eur.nl/static-eur/img/logo.png</url>
      <title>RePub, Erasmus University Rotterdam</title>
      <link>http://repub.eur.nl</link>
    </image>
    <item>
      <title>Ebstein's anomaly: Factors associated with death in childhood and adolescence: A multi-centre, long-term study (Article)</title>
      <link>http://repub.eur.nl/res/pub/35705/</link>
      <pubDate>2007-11-01T00:00:00Z</pubDate>
      <description>Aims: The objective of this study is to establish factors associated with death after diagnosis of Ebstein's anomaly (EA) during childhood and adolescence. Methods and results: This study is a retrospective chart review. All paediatric patients were diagnosed with EA and followed in tertiary-care university hospitals between 1980 and 2005. Factors associated with death were obtained using the Cox regression and log-rank tests. Of the 93 patients with EA, 18 (19%) died and 75 (81%) survived. The median age at EA diagnosis and follow-up was 0 (range 0-162) and 86 months (range 0-216), respectively. After 35 months of diagnosis, the Kaplan-Meier survival probability remains stable at 80%. Young age at presentation (≤12 months), hepatomegaly, the need for medication (diuretics and Prostin) and mechanical ventilation at presentation, pulmonary valve defects (defined as moderate-to-severe pulmonary stenosis and pulmonary atresia), patent arterial duct, and ventricular septal defect were significantly associated with death. Conclusion: The overall survival of patients with EA during childhood and adolescence has dramatically improved when compared with earlier reports. </description>
    </item> <item>
      <title>Incidence of High-Strain Patterns in Human Coronary Arteries: Assessment With Three-Dimensional Intravascular Palpography and Correlation With Clinical Presentation (Article)</title>
      <link>http://repub.eur.nl/res/pub/13390/</link>
      <pubDate>2004-06-08T00:00:00Z</pubDate>
      <description>BACKGROUND: Rupture of thin-cap fibroatheromatous plaques is a major cause of acute myocardial infarction (AMI). Such plaques can be identified in vitro by 3D intravascular palpography with high sensitivity and specificity. We used this technique in patients undergoing percutaneous intervention to assess the incidence of mechanically deformable regions. We further explored the relation of such regions to clinical presentation and to C-reactive protein levels. METHOD AND RESULTS: Three-dimensional palpograms were derived from continuous intravascular ultrasound pullbacks. Patients (n=55) were classified by clinical presentation as having stable angina, unstable angina, or AMI. In every patient, 1 coronary artery was scanned (culprit vessel in stable and unstable angina, nonculprit vessel in AMI), and the number of deformable plaques assessed. Stable angina patients had significantly fewer deformable plaques per vessel (0.6+/-0.6) than did unstable angina patients (P=0.0019) (1.6+/-0.7) or AMI patients (P&lt;0.0001) (2.0+/-0.7). Levels of C-reactive protein were positively correlated with the number of mechanically deformable plaques (R2=0.65, P&lt;0.0001). CONCLUSIONS: Three-dimensional intravascular palpography detects strain patterns in human coronary arteries that represent the level of deformation in plaques. The number of highly deformable plaques is correlated with both clinical presentation and levels of C-reactive protein. Further studies will assess the potential role of the technique to identify patients at risk of future clinical events</description>
    </item> <item>
      <title>Characterizing vulnerable plaque features with intravascular elastography. (Article)</title>
      <link>http://repub.eur.nl/res/pub/13253/</link>
      <pubDate>2003-11-25T00:00:00Z</pubDate>
      <description>BACKGROUND: In vivo detection of vulnerable plaques is presently limited by a lack of diagnostic tools. Intravascular ultrasound elastography is a new technique based on intravascular ultrasound and has the potential to differentiate between different plaques phenotypes. However, the predictive value of intravascular elastography to detect vulnerable plaques had not been studied. METHODS AND RESULTS: Postmortem coronary arteries were investigated with intravascular elastography and subsequently processed for histology. In histology, a vulnerable plaque was defined as a plaque consisting of a thin cap (&lt;250 microm) with moderate to heavy macrophage infiltration and at least 40% of atheroma. In elastography, a vulnerable plaque was defined as a plaque with a high strain region at the surface with adjacent low strain regions. In 24 diseased coronary arteries, we studied 54 cross sections. In histology, 26 vulnerable plaques and 28 nonvulnerable plaques were found. Receiver operator characteristic analysis revealed a maximum predictive power for a strain value threshold of 1.26%. The area under the receiver operator characteristic curve was 0.85. The sensitivity was 88%, and the specificity was 89% to detect vulnerable plaques. Linear regression showed high correlation between the strain in caps and the amount of macrophages (P&lt;0.006) and an inverse relation between the amount of smooth muscle cells and strain (P&lt;0.0001). Plaques, which are declared vulnerable in elastography, have a thinner cap than nonvulnerable plaques (P&lt;0.0001). CONCLUSIONS: Intravascular elastography has a high sensitivity and specificity to detect vulnerable plaques in vitro.</description>
    </item> <item>
      <title>From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part II. (Article)</title>
      <link>http://repub.eur.nl/res/pub/13247/</link>
      <pubDate>2003-10-14T00:00:00Z</pubDate>
      <description>Atherosclerotic cardiovascular disease results in &gt;19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document will focus on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients.</description>
    </item> <item>
      <title>From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I. (Article)</title>
      <link>http://repub.eur.nl/res/pub/13244/</link>
      <pubDate>2003-10-07T00:00:00Z</pubDate>
      <description>Atherosclerotic cardiovascular disease results in &gt;19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document focuses on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients.</description>
    </item> <item>
      <title>Intravascular palpography for high-risk vulnerable plaque assessment. (Article)</title>
      <link>http://repub.eur.nl/res/pub/4714/</link>
      <pubDate>2003-01-01T00:00:00Z</pubDate>
      <description></description>
    </item> <item>
      <title>Inflammation and atherosclerosis: mechanisms underlying vulnerable plaque. (Article)</title>
      <link>http://repub.eur.nl/res/pub/4732/</link>
      <pubDate>2003-01-01T00:00:00Z</pubDate>
      <description>Introduction
Atherosclerosis belongs to the chronic diseases with
the highest mortality in the Western world. While the
disease has traditionally been explained by risk factors
like high cholesterol and hypertension, evidence is now
accumulating for a role of the immune system in the
progression of atherosclerosis. This article will explore
the role of innate and adaptive immunity in atherosclerosis
only. It does not aim at describing all facets of the
immune system. In order to facilitate the reading of the
article the pathophysiology of the immune system in
atherosclerosis is preceded by the relevant physiology.</description>
    </item> <item>
      <title>Identification of Atherosclerotic Plaque Components With Intravascular Ultrasound Elastography In Vivo: A Yucatan Pig Study (Article)</title>
      <link>http://repub.eur.nl/res/pub/9885/</link>
      <pubDate>2002-04-09T00:00:00Z</pubDate>
      <description>BACKGROUND: Intravascular ultrasound elastography assesses the local strain of the atherosclerotic vessel wall. In the present study, the potential to identify different plaque components in vivo was investigated. METHODS AND RESULTS: Atherosclerotic external iliac and femoral arteries (n=24) of 6 Yucatan pigs were investigated. Before termination, elastographic data were acquired with a 20-MHz Visions catheter. Two frames acquired at end-diastole with a pressure differential of approximately 4 mm Hg were acquired to obtain the elastograms. Before dissection, x-ray was used to identify the arterial segments that had been investigated by ultrasound. Specimens were stained for collagen, fat, and macrophages. Plaques were classified as absent, early fibrous lesion, early fatty lesion, or advanced fibrous plaque. The average strains in the plaque-free arterial wall (0.21%) and the early (0.24%) and advanced fibrous plaques (0.22%) were similar. Higher average strain values were observed in fatty lesions (0.46%) compared with fibrous plaques (P=0.007). After correction for confounding by lipid content, no additional differences in average strain were found between plaques with and without macrophages (P=0.966). Receiver operating characteristic analysis revealed a sensitivity and a specificity of 100% and 80%, respectively, to identify fatty plaques. The presence of a high-strain spot (strain &gt;1%) has 92% sensitivity and 92% specificity to identify macrophages. CONCLUSIONS: To the best of our knowledge, this is the first time that intravascular ultrasound elastography has been validated in vivo. Fatty plaques have an increased mean strain value. High-strain spots are associated with the presence of macrophages.</description>
    </item> <item>
      <title>Morphological and mechanical information of coronary arteries obtained with intravascular elastography; feasibility study in vivo. (Article)</title>
      <link>http://repub.eur.nl/res/pub/13019/</link>
      <pubDate>2002-03-01T00:00:00Z</pubDate>
      <description>AIMS: Plaque composition is a major determinant of coronary related clinical syndromes. In vitro experiments on human coronary and femoral arteries have demonstrated that different plaque types were detectable with intravascular ultrasound elastography. The aim of this study was to investigate the feasibility of applying intravascular elastography during interventional catheterization procedures. METHODS AND RESULTS: Data were acquired in patients (n=12) during PTCA procedures with an EndoSonics InVision echoapparatus equipped with radiofrequency output. The systemic pressure was used to strain the tissue, and the strain was determined using cross-correlation analysis of sequential frames. A likelihood function was determined to obtain the frames with minimal motion of the catheter in the lumen, since motion of the catheter prevents reliable strain estimation. Minimal motion was observed near end-diastole. Reproducible strain estimates were obtained within one pressure cycle and over several pressure cycles. Validation of the results was limited to the information provided by the echogram. Strain in calcified material (0.20%+/-0.07) was lower (P&lt;0.001) than in non-calcified tissue (0.51%+/-0.20). CONCLUSION: In vivo intravascular elastography is feasible. Significantly higher strain values were found in non-calcified plaques than in calcified plaques.</description>
    </item> <item>
      <title>Advancing intravascular ultrasonic palpation toward clinical applications. (Article)</title>
      <link>http://repub.eur.nl/res/pub/4811/</link>
      <pubDate>2001-12-01T00:00:00Z</pubDate>
      <description>This paper describes the first reported attempt to develop a real-time intravascular ultrasonic palpation system. We also report on our first experience in the catherization laboratory with this new elastographic imaging technique. The prototype system was based on commercially available intravascular ultrasound (US) scanner that was equipped with a 20-MHz array catheter. Digital beam-formed radiofrequency (RF) echo data (i.e., 12 bits, 100 Hz) was captured at full frame rate from the scanner and transferred to personal computer (PC) memory using a fast data-acquisition system. Composite palpograms were created by applying a one-dimensional (1-D) echo tracking technique in combination with global motion compensation and multiframe averaging to several pairs of RF echo frames that were obtained in the diastolic phase of the cardiac cycle. The quality of palpograms was assessed by conducting experiments on vessel phantoms and on patients. The results demonstrated that robust and consistent palpograms could be generated in almost real-time using the proposed system. Good correlation was observed between low strain values and regions of calcification as identified from the intravascular US (IVUS) sonograms. Although the clinical results are clearly preliminary, it was concluded that the prototype system performed sufficiently well to warrant further and more in-depth clinical investigation.</description>
    </item> <item>
      <title>Characterization of plaque components with intravascular ultrasound elastography in human femoral and coronary arteries in vitro (Article)</title>
      <link>http://repub.eur.nl/res/pub/9434/</link>
      <pubDate>2000-01-01T00:00:00Z</pubDate>
      <description>BACKGROUND: The composition of plaque is a major determinant of
      coronary-related clinical syndromes. Intravascular ultrasound (IVUS)
      elastography has proven to be a technique capable of reflecting the
      mechanical properties of phantom material and the femoral arterial wall.
      The aim of this study was to investigate the capability of intravascular
      elastography to characterize different plaque components. METHODS AND
      RESULTS: Diseased human femoral (n=9) and coronary (n=4) arteries were
      studied in vitro. At each location (n=45), 2 IVUS images were acquired at
      different intraluminal pressures (80 and 100 mm Hg). With the use of
      cross-correlation analysis on the high-frequency (radiofrequency)
      ultrasound signal, the local strain in the tissue was determined. The
      strain was color-coded and plotted as an additional image to the IVUS
      echogram. The visualized segments were stained on the presence of
      collagen, smooth muscle cells, and macrophages. Matching of elastographic
      data and histology were performed with the use of the IVUS echogram. The
      cross sections were segmented in regions (n=125) that were based on the
      strain value on the elastogram. The dominant plaque types in these regions
      (fibrous, fibro-fatty, or fatty) were obtained from histology and
      correlated with the average strain and echo intensity. The strain for the
      3 plaque types as determined by histology differed significantly
      (P=0.0002). This difference was mainly evident between fibrous and fatty
      tissue (P=0.0004). The plaque types did not reveal echo-intensity
      differences in the IVUS echogram (P=0.882). CONCLUSIONS: Different strain
      values are found between fibrous, fibro-fatty, and fatty plaque
      components, indicating the potential of intravascular elastography to
      distinguish different plaque morphologies.</description>
    </item> <item>
      <title>Intravascular Ultrasound Elastography (Doctoral Thesis)</title>
      <link>http://repub.eur.nl/res/pub/19903/</link>
      <pubDate>1999-06-23T00:00:00Z</pubDate>
      <description></description>
    </item>
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