Background and Purpose-Progression of asymptomatic carotid artery stenosis (ACAS) in patients with >50% luminal narrowing is considered a potential risk factor for ischemic stroke; however, subclinical molecular biomarkers of ACAS progression are lacking. Recent studies suggest a regulatory function for several microRNAs (miRNAs) on the evolution of carotid plaque, but its role in ACAS progression is mostly unknown. The aim of our study was to investigate a wide miRNA panel in peripheral blood exosomes from patients with ACAS to associate circulating miRNA expression profiles with stenosis progression. Methods-The study included 60 patients with ACAS carrying >50% luminal narrowing. First, miRNA expression profiles of circulating exosomes were determined by Affymetrix microarrays from plasma samples of 16 patients from the cohort. Second, those miRNAs among the most differentially expressed in patients with ACAS progression were quantified by real-time polymerase chain reaction in a separate replication cohort of 39 subjects within the patient sample. Results-Our results showed that ACAS progression was associated with development of stroke. , and miR-24-3p presented significant higher expression in those patients with ACAS progression. Conclusions-In conclusion, our study supports that specific circulating miRNA expression profiles could provide a new tool that complements the monitoring of ACAS progression, improving therapeutic approaches to prevent ischemic stroke.
Background and purpose Relative signal intensity of acute ischemic stroke lesions in fluid-attenuated inversion recovery (FLAIR-rSI) magnetic resonance imaging is associated with time elapsed since stroke onset with higher intensities signifying longer time intervals. In the randomized controlled WAKE-UP trial, intravenous alteplase was effective in patients with unknown onset stroke selected by visual assessment of DWI-FLAIR mismatch, i.e., in those with no marked FLAIR hyperintensity in the region of the acute DWI lesion. In this post-hoc analysis, we investigated if quantitatively measured FLAIR-rSI modifies treatment effect of intravenous alteplase. Methods FLAIR-rSI of stroke lesions was measured relative to signal intensity in a mirrored region in the contralesional hemisphere. The relationship between FLAIR-rSI and treatment effect on functional outcome assessed by the modified Rankin Scale (mRS) after 90 days was analysed by binary logistic regression using different endpoints, i.e., favourable outcome defined as mRS 0-1, independent outcome defined as mRS 0-2, ordinal analysis of mRS scores (shift analysis). All models were adjusted for NIHSS at symptom onset and stroke lesion volume. Results FLAIR-rSI was successfully quantified in stroke lesions in 433 patients (86% of 503 patients included in WAKE-UP). Mean FLAIR-rSI was 1.06 (SD 0.09). Interaction of FLAIR-rSI and treatment effect was not significant for mRS 0-1 (p=0.169) and shift analysis (p=0.086), but 2 reached significance for mRS 0-2 (p=0.004). We observed a smooth continuing trend of decreasing treatment effects in relation to clinical endpoints with increasing FLAIR-rSI. Conclusion In patients in whom no marked parenchymal FLAIR hyperintensity was detected by visual judgement in the WAKE-UP trial, higher FLAIR-rSI of DWI lesions was associated with decreased treatment effects of intravenous thrombolysis. This parallels the known association of treatment effect and elapsing time of stroke onset.
Na-NPM-SAH patients without an identifiable bleeding source on initial angiography might have a more benign short- and long-term prognosis than aneurysmal SAH patients. Our study confirms an important diagnostic advantage of a second arteriography. Still, despite the major concern of an undetected aneurysm, the long-term rebleeding rate was low in this subgroup of patients.
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