Path From Clinical Research to Implementation: Endovascular Treatment of Ischemic Stroke in the Netherlands.

Before 2015, endovascular treatment (EVT) for acute ischemic stroke was considered a promising treatment option. Based on limited evidence, it was performed in several dedicated stroke centers worldwide on selected patients. Since 2015, EVT for patients with intracranial large vessel occlusion has quickly been implemented as standard treatment in many countries worldwide, supported by the revised international guidelines based on solid evidence from multiple clinical trials. We describe the development in use of EVT in the Netherlands before, during, and after the pivotal EVT trials. We used data from all patients who were treated with EVT in the Netherlands from January 2002 until December 2018. We undertook a time-series analysis to examine trends in the use of EVT using Poisson regression analysis. Incidence rate ratios per year with 95% CIs were obtained to demonstrate the impact and implementation after the publication of the EVT trial results. We made regional observation plots, adjusted for stroke incidence, to assess the availability and use of the treatment in the country. In the buildup to the MR CLEAN (Multicenter Clinical Trial of Endovascular Treatment of Acute Ischemic Stroke in the Netherlands), a slow increase of EVT patients was observed, with 0.2% of all ischemic stroke patients receiving EVT. Before the trial results were formally announced, a statistically significant increase in EVT-treated patients per year was observed (incidence rate ratio, 1.72 [95% CI, 1.46-2.04]), and after the trial publication, an immediate steep increase was seen, followed by a more gradual increase (incidence rate ratio, 2.14 [95% CI, 1.77-2.59]). In 2018, the percentage of ischemic stroke patients receiving EVT increased to 5.8%. A well-developed infrastructure, a pragmatic approach toward the use of EVT in clinical practice, in combination with a strict adherence by the regulatory authorities to national evidence-based guidelines has led to successful implementation of EVT in the Netherlands. Ongoing efforts are directed at further increasing the proportion of stroke patients with EVT in all regions of the country.

Uncoupling of Microvascular Blood Flow and Capillary Density in Vascular Cognitive Impairment.

Cerebral small vessel disease (cSVD) plays an important role in dementia and is a major cause for vascular cognitive impairment (VCI). Recent studies hypothesized that capillary dysfunction including reduction of capillary patency, rather than a flow-limiting pathology is crucial in cSVD. As cSVD is considered a systemic microvascular disease, we examined sublingual microvascular blood flow and capillary density in patients with VCI and controls. Fifteen patients with VCI due to cSVD and 15 controls underwent intravital microscopy of the sublingual microvessels. Microvascular blood flow and capillary density in high and low flow areas were determined for each participant. Flow-density coupling was examined by determining the ratio of density changes to flow changes, and the ratio of feed vessel red blood cell (RBC) velocity to capillary RBC velocity. These were compared between VCI and controls. In healthy controls, capillary density increased proportionally with feed vessel blood flow increase. In patients with VCI, no increase of capillary density was observed. Moreover, increase of feed vessel RBC velocity led to significant increase of capillary RBC velocity in VCI, whereas in controls, the capillary RBC increased only slightly. Flow-density coupling differed significantly between VCI and controls, also after correcting for age and hypertension. Our findings suggest uncoupling of microvascular blood flow and capillary density in patients with VCI. This uncoupling may impair oxygen and nutrients exchange when blood flow increases in response to increased metabolic demand, ultimately leading to tissue damage.

The relevance of sexual responsiveness to sexual function in male stroke patients.

INTRODUCTION: Stroke may have negative consequences for the patients' quality of life, including sexual function. Whereas physical impairment will influence sexual positions and movement during sex, depression and medication may reduce sexual desire. So far, data on sexual dysfunction after stroke are scant. Although some support for physical as well as psychological explanations has been shown, further research to find the remedies for those patients with sexual problems after stroke is needed. The focus of the present study is on the identification of relevant psychological factors. AIM: The aim of this study was to study the impact of anxiety, depression, and sexual responsiveness on sexual function in male stroke patients. METHODS: Nineteen male stroke patients completed a number of self-report measures to assess psychological and sexual factors. MAIN OUTCOME MEASURES: Sexual function based on the International Index of Erectile Function, anxiety and depression based on the Symptom Checklist-90, and sexual responsiveness based on the Sexual Inhibition/Sexual Excitation Scale, including propensities for sexual excitation and sexual inhibition as a result of both performance failure and performance consequences, were assessed. RESULTS: Sexual excitation was positively related to sexual desire, whereas inhibition because of the threat of performance failure was negatively related to orgasmic function and sexual desire (P < 0.01). Patients with high levels of inhibition because of threat of performance failure were more likely to report low scores on overall sexual function than those with low levels. CONCLUSIONS: Although the statistical power is rather low, the results show the relevance of sexual responsiveness to sexual function in male stroke patients. The present study can be considered as a first step toward building a theoretical framework of relevant psychological and physical factors, which is needed to develop adequate interventions for those patients with sexual problems after stroke.

Cerebral hyperperfusion syndrome.

Cerebral hyperperfusion syndrome (CHS) after carotid endarterectomy is characterised by ipsilateral headache, hypertension, seizures, and focal neurological deficits. If not treated properly it can result in severe brain oedema, intracerebral or subarachnoid haemorrhage, and death. Knowledge of CHS among physicians is limited. Most studies report incidences of CHS of 0-3% after carotid endarterectomy. CHS is most common in patients with increases of more than 100% in perfusion compared with baseline after carotid endarterectomy and is rare in patients with increases in perfusion less than 100% compared with baseline. The most important risk factors in CHS are diminished cerebrovascular reserve, postoperative hypertension, and hyperperfusion lasting more than several hours after carotid endarterectomy. Impaired autoregulation as a result of endothelial dysfunction mediated by generation of free oxygen radicals is implicated in the pathogenesis of CHS. Treatment strategies are directed towards regulation of blood pressure and limitation of rises in cerebral perfusion. Complete recovery happens in mild cases, but disability and death can occur in more severe cases. More information about CHS and early institution of adequate treatment are of paramount importance in order to prevent these potentially severe complications.