Article Text
Statistics from Altmetric.com
- IDC, idiopathic dilated cardiomyopathy
- GAPDH, glyceraldehyde-3-dehydrogenase
- LVEDD, left ventricular end diastolic diameter
- LVEF, left ventricular ejection fraction
- LVESD, left ventricular end systolic diameter
- PCR, polymerase chain reaction
- VEGF, vascular endothelial growth factor
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.
SUBJECTS AND METHODS
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 …