In patients with DeBakey left ventricular assist devices, a high load of clinically silent microemboli can be detected within the cerebral arteries despite a low incidence of embolic complications. It needs to be investigated whether such continuous, presumably gaseous microembolization causes cognitive or neuropsychologic deficits.

Molecular imaging with contrast-enhanced ultrasound uses targeted microbubbles that are retained in diseased tissue. The resonant properties of these microbubbles produce acoustic signals in an ultrasound field. The microbubbles are targeted to diseased tissue by using certain chemical constituents in the microbubble shell or by attaching disease-specific ligands such as antibodies to the microbubble. In this review, we discuss the applications of this technique to pathological states in the cerebrovascular system including atherosclerosis, tumor angiogenesis, ischemia, intravascular thrombus, and inflammation.

The reduction of MES under oxygen delivery confirms the gaseous nature in a substantial number of circulating microemboli produced by the DeBakey LVAD. However, SVL and frequency modulation of MES did not appear to provide valuable information regarding the structural nature of the underlying microembolic material.

Microembolic signals (MES) have shown to be associated with increased risk of ischemic stroke in patients with pulsatile left ventricular assist devices (LVADs) in contrast to continuous-flow DeBakey LVAD. The pathogenesis of microembolization in LVAD-patients is still not known. We investigated whether systemic markers of inflammation or pump dynamic correlate with cerebral microembolization in nine patients with DeBakey LVAD. We performed transcranial Doppler (TCD) for MES-detection and evaluated parameters of inflammation (i.e. Leukocytes, CRP, Fibrinogen) and pump dynamic (i.e. power, speed, flow). During a mean LVAD duration of 203.7 +/- 179 days, thromboembolic events occurred in five patients with an incidence of 0.38% (approximately 0.38 events/100 LVAD-days). We performed 290 TCD monitorings with a MES mean count of 50.4 +/- 346 signals/hour (0-5042) and prevalence of 42.8%. There was no association between individual microembolic activity and the markers of inflammation or pump dynamic. In patients with DeBakey LVAD, a high load of clinically silent cerebral microemboli can be detected. However, there is no correlation between markers of inflammation or pump dynamic and the individual amount of microembolization. We hypothesize that a gaseous nature of the majority of detected microemboli in the DeBakey LVAD may be the underlying reason for this discrepancy.

Ischemic stroke in the young (age: 18-45 years) constitutes a diagnostic and therapeutic challenge. A broad spectrum of potential causes of juvenile strokes exists. Above all, nonatherosclerotic arteriopathies with dissections as their main proponent, paradoxical embolism, and thrombophilias have to be considered. Transient brief episodes with neurological deficits are difficult to discriminate from migrainous aura, epileptic seizure, psychogenic disorder. Therefore, the diagnostic work-up of juvenile stroke patients usually exceeds the amount of compulsory tests recommended in official guidelines. Various therapeutic modalities are not based on randomized large-scale studies and have to be selected on an individual basis. Despite good compliance, the annual risk of stroke recurrence is 2-3% and 1% for myocardial infarction.