Kjel Andersen
University of Düsseldorf
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Featured researches published by Kjel Andersen.
Clinical Imaging | 2010
Kjel Andersen; Marcus Hennersdorf; Mathias Cohnen; Dirk Blondin; U. Mödder; L. W. Poll
Purpose: In arterial hypertension left ventricular hypertrophy comprises myocyte hypertrophy, interstitial fibrosis and structural alterations of the coronary microcirculation. MRI enables the detection of myocardial fibrosis, infarction and scar tissue by delayed enhancement (DE) after contrast media application. Aim of this study was to investigate patients with arterial hypertension but without known coronary disease or previous myocardial infarction to detect areas of DE. Methods and material: Twenty patients with arterial hypertension with clinical symptoms of myocardial ischemia, but without history of myocardial infarction and normal coronary arteries during coronary angiography were investigated on a 1.0 T superconducting magnet (Gyroscan T10-NT, Intera Release 8.0, Philips). Fast gradient-echo cine sequences and T2-weighted STIR-sequences were acquired. Fifteen minutes after injection of Gadobenate dimeglumine inversion recovery gradient-echo sequences were performed for detection of myocardial DE. Presence or absence of DE on MRI was correlated with clinical data and the results of echocardiography and electrocardiography, respectively. Results: Nine of 20 patients showed DE in the interventricular septum and the anteroseptal left ventricular wall. In 6 patients, DE was localized intramurally and in 3 patients subendocardially. There was a significant correlation between myocardial DE and ST-segment depressions during exercise and between DE and left-ventricular enddiastolic pressure. Patients with intermittent atrial fibrillation showed a myocardial DE more often than patients without atrial fibrillation. Conclusion: In our series, 45% of patients with arterial hypertension showed DE on cardiac MRI. In this clinical setting, delayed enhancement may be due to coronary microangiopathy. The more intramurally localization of DE, however, rather indicates myocardial interstitial fibrosis.
European Journal of Radiology | 2009
Kjel Andersen; Marcus Hennersdorf; Mathias Cohnen; Dirk Blondin; U. Mödder; L. W. Poll
PURPOSE In arterial hypertension left ventricular hypertrophy comprises myocyte hypertrophy, interstitial fibrosis and structural alterations of the coronary microcirculation. MRI enables the detection of myocardial fibrosis, infarction and scar tissue by delayed enhancement (DE) after contrast media application. Aim of this study was to investigate patients with arterial hypertension but without known coronary disease or previous myocardial infarction to detect areas of DE. METHODS AND MATERIAL Twenty patients with arterial hypertension with clinical symptoms of myocardial ischemia, but without history of myocardial infarction and normal coronary arteries during coronary angiography were investigated on a 1.0 T superconducting magnet (Gyroscan T10-NT, Intera Release 8.0, Philips). Fast gradient-echo cine sequences and T2-weighted STIR-sequences were acquired. Fifteen minutes after injection of Gadobenate dimeglumine inversion recovery gradient-echo sequences were performed for detection of myocardial DE. Presence or absence of DE on MRI was correlated with clinical data and the results of echocardiography and electrocardiography, respectively. RESULTS Nine of 20 patients showed DE in the interventricular septum and the anteroseptal left ventricular wall. In 6 patients, DE was localized intramurally and in 3 patients subendocardially. There was a significant correlation between myocardial DE and ST-segment depressions during exercise and between DE and left-ventricular enddiastolic pressure. Patients with intermittent atrial fibrillation showed a myocardial DE more often than patients without atrial fibrillation. CONCLUSION In our series, 45% of patients with arterial hypertension showed DE on cardiac MRI. In this clinical setting, delayed enhancement may be due to coronary microangiopathy. The more intramurally localization of DE, however, rather indicates myocardial interstitial fibrosis.
European Heart Journal | 2006
Tienush Rassaf; L. W. Poll; Paris Brouzos; Thomas Lauer; Matthias Totzeck; Petra Kleinbongard; Putrika Gharini; Kjel Andersen; Rainer Schulz; Gerd Heusch; U. Mödder; Malte Kelm
European Journal of Radiology | 2006
Kjel Andersen; Christoph Vogt; Dirk Blondin; Andreas Beck; Wolfram Heinen; Volker Aurich; Dieter Häussinger; U. Mödder; Mathias Cohnen
Clinical Imaging | 2006
Kjel Andersen; C. Vogt; Dirk Blondin; A. Beck; W. Heinen; V. Aurich; D. Häussinger; U. Mödder; M. Conen
European Journal of Radiology | 2009
Dirk Blondin; A. Koester; Kjel Andersen; K.D. Kurz; U. Moedder; Mathias Cohnen
Archive | 2007
Ulrich Moedder; Mathias Cohnen; Kjel Andersen
European Journal of Radiology Extra | 2006
Kjel Andersen; Mathias Cohnen; Verena Klar; L. W. Poll
Archive | 2011
Kjel Andersen; Mathias Cohnen; Ulrich Moedder
Archive | 2009
Ulrich Moedder; Mathias Cohnen; Kjel Andersen; Volkher Engelbrecht; Benjamin Fritz