Abstract
The endothelium plays a crucial role in maintaining cardiovascular homeostasis. Shear stress generated by flowing blood regulates the release of substances that provide adequate tissue perfusion. The extent of damage to endothelial cells depends on locally disturbed shear stress caused by the deteriorated flow. Patients with heart failure have reduced cardiac output, which results in reduced blood flow and negative shear stress. Reduced shear stress also affects microcirculation and reduces tissue perfusion. Consequently, the production of free oxygen radicals is increased and bioavailability of nitric oxide is additionally decreased. Therefore, endothelial dysfunction is involved in the progression of heart failure and cardiovascular events. Left ventricular assist devices (LVAD) are used for the treatment of patients with advanced heart failure. Older pulsatile flow LVADs were mostly substituted by continuous-flow LVADs (cf-LVADs). Despite the advantages of the cf-LVADs, the loss of pulsatility leads to different complications on the micro- and macrovascular levels. One of the pathogenetic mechanisms of cardiovascular complications with cf-LVADs may be endothelial dysfunction, which after the implantation of the device does not improve and may even deteriorate. In contrast, the pulsatile pattern of LVADs on blood flow could preserve endothelial function.
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