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Identification of a specific pattern of downregulation in expression of isoforms of vascular endothelial growth factor in dilated cardiomyopathy
  1. R A De Boer1,
  2. R H Henning2,
  3. R A Tio1,
  4. Y M Pinto1,
  5. R M H J Brouwer3,
  6. R J Ploeg4,
  7. M Böhm5,
  8. W H Van Gilst2,
  9. D J Van Veldhuisen1
  1. 1Thoraxcenter, Department of Cardiology, University Hospital Groningen, The Netherlands
  2. 2Department of Clinical Pharmacology, University of Groningen, The Netherlands
  3. 3Institute for Cardiothoracic Surgery, University Hospital Nijmegen, The Netherlands
  4. 4Department of Surgery, University Hospital, Groningen, The Netherlands
  5. 5Universitäts und Poliklinik für Innere Medizin III, Homburg/Saar, Germany
  1. Correspondence to:
    Rudolf A de Boer MD, Thoraxcenter, Department of Cardiology; University Hospital Groningen; PO Box 30.001, Groningen 9700 RB, The Netherlands;{at}

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Recent work suggests that myocardial hypoxia or ischaemia are also pathophysiologic factors in idiopathic dilated cardiomyopathy (IDC).1 Besides several other factors (increased wall stress, endothelial dysfunction, decreased coronary reserve), the observed decreased capillarisation in IDC, disproportionate to the rate of hypertrophy, may further contribute to this oxygen demand–supply mismatch. The reason for this seemingly decreased angiogenic capacity remains unclear, however a role for microvascular abnormalities in heart failure is now recognised.2

Hypoxia is the key factor in the induction of vascular endothelial growth factor (VEGF). Increased expression of VEGF causes angiogenesis, and expression level of VEGF could therefore mediate the capillarisation in IDC. Recently, data have been reported on this issue,3 and the authors found a downregulation of VEGF165 and VEGF189 isoforms. The VEGF121 however was not investigated, although it has been suggested that this isoform in particular has powerful angiogenic capacities. Additionally, it is unclear whether VEGF expression is related to the severity of the disease.


We analysed 28 patients with IDC. Patients had enlarged left ventricular end diastolic and systolic diameters (LVEDD 69 (2.1) mm, LVESD 61 (2.6) mm), and decreased left ventricular ejection fraction (LVEF) (0.27 (0.03)), and elevated wedge (15 (1.9) mm Hg) and left ventricular end diastolic pressures (14.1 (2.7) mm Hg). Echocardiography did not reveal cardiac disease in the 10 brain dead subjects, who served as controls. Endomyocardial biopsy taken from the right ventricle showed cardiomyocyte hypertrophy and interstitial …

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