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Background Intracranial aneurysms may be associated with an underlying arteriopathy, leading to arterial wall fragility. Arterial tortuosity is a major characteristic of some connective tissue disease. Aim To determine whether intracranial aneurysm is associated with an underlying arteriopathy. Methods Using a case-control design, from May 2012 to May 2013, we selected intracranial aneurysm cases and controls from consecutive patients who had conventional cerebral angiography in our center. Cases were patients with newly diagnosed intracranial aneurysm. Controls were patients who had diagnostic cerebral angiography and free of aneurysm. The prevalence of tortuosity, retrospectively assessed according to standard definitions, was compared between cases and controls and, association between tortuosity and some aneurysm characteristics was examined, in cases only. Results About 659 arteries from 233 patients (112 cases and 121 controls) were examined. Tortuosity was found in 57 (51%) cases and 31 (26%) controls (adjusted OR = 2.71; 95%CI, 1.53–4.80). The same trend was found when looking at each tortuosity subtype (simple tortuosity, coil, kink) or at carotid or vertebral territory separately. In contrast, no association between tortuosity and rupture status, aneurysm number or neck size was found. Conclusions Cervical artery tortuosity is significantly associated with intracranial aneurysm, although not related to main aneurysm characteristics. Our results support the presence of an underlying diffuse arteriopathy in intracranial aneurysm patients.

Background Aortic stiffness is an independent predictor of coronary events. Aims We assessed the predictive value of aortic stiffness for ⩾50% asymptomatic coronary artery disease in a stroke/transient ischemic attack population. Methods We enrolled 300 consecutive patients aged 45–75 years with nondisabling, noncardioembolic ischemic stroke or transient ischemic attack, and no prior history of coronary artery disease. Coronary artery disease was assessed with 64-section computed tomography coronary angiography and all patients had a detailed cervicocephalic arterial work-up. Aortic stiffness was determined from carotid-femoral pulse wave velocity with 9·6 m/s as cutoff value. The predictive value of aortic stiffness was assessed by logistic regression and reclassification tables method after adjustment for the Framingham Risk Score and the presence of cervicocephalic stenosis, which were previously shown to be independent predictor of ⩾50% asymptomatic coronary artery disease. Results Among the 274 included patients who had computed tomography coronary angiography, 26% (95% CI, 21%–32%) had an increased stiffness (pulse wave velocity > 9·6 m/s) and 18% (14%–23%) had ⩾50% asymptomatic coronary artery disease. Increased aortic stiffness was associated with the presence of ⩾50% asymptomatic coronary artery disease, both in univariate (odds ratio = 3·4 [1·8–6·4]) and multivariate analyses (odds ratio = 2·3 [1·2–4·7]) after adjustment for Framingham Risk Score and presence of cervicocephalic stenosis. After carotid-femoral pulse wave velocity was added to the standard model including Framingham Risk Score and the presence of cervicocephalic stenosis, net reclassification improvement was 12·6% ( P < 0·005), integrated discrimination index was 2·51% ( P = 0·025), and model fit was improved (likelihood ratio = 4·99, P = 0·025). Conclusions In stroke/transient ischemic attack patients, aortic pulse wave velocity improves the prediction of ⩾50% asymptomatic coronary artery disease beyond classical risk factors.

Background Acute stressors, such as stressful life events, might trigger ischemic stroke. Aims Our objective was to investigate the association between life events exposure and ischemic stroke onset. Methods Consecutive patients were interviewed about life events exposure (e.g. bereavement) using the Interview for Recent Life Events. Using a case-crossover approach, life events exposure within one month of stroke onset (hazard period) was compared with exposure during five control periods of one month preceding the hazard period. Similarly, life events exposure within one week of stroke onset was compared with exposure during three control periods of one week. Odds ratios and 95% confidence intervals were calculated using conditional logistic regression. Results Two hundred forty-seven patients were interviewed within a median time of five days (interquartile range 3–7). Life events belonging to bereavement, health, and other categories accounted for half of life events. Over the six-month period, 187 patients were exposed to ≥1 life events. Patients were exposed to ≥1 life events more often during the first month preceding stroke onset than during the five control periods (odds ratio = 2·96; 95% confidence interval, 2·19–4·00). Over the four-week period, 97 patients were exposed to ≥1 life events. Patients were exposed to ≥1 life events more often during the first week preceding stroke onset than during the three control periods (odds ratio = 2·10; 1·40–3·17). Conclusions Recent life events exposure is associated with an increased risk of ischemic stroke.

About 15 million strokes occur each year worldwide. As the number one cause of morbidity and acquired disability, stroke is a major drain on public health-care funding, due to long hospital stays followed by ongoing support in the community or nursing-home care. Although during the last 10 years we have witnessed a remarkable progress in the understanding of the pathophysiology of ischemic stroke, reperfusion induced by recombinant tissue-type plasminogen activator (tPA—Actilyse) remains the only approved acute treatment by the health authorities. The objective of the present review is to provide an overview of our present knowledge about the impact of tPA on the neurovascular unit during acute ischemic stroke.

Fibromuscular dysplasia is an uncommon, segmental, nonatherosclerotic arterial disease of unknown aetiology. The disease primarily affects women and involves intermediate-sized arteries in many areas of the body, including cervical and intracranial arteries. Although often asymptomatic, fibromuscular dysplasia can also be associated with spontaneous dissection, severe stenosis that compromises the distal circulation, or intracranial aneurysm, and is therefore responsible for cerebral ischaemia or subarachnoid haemorrhage. Fibro-muscular dysplasia affects middle and distal portions of the internal carotid and vertebral arteries, and occasionally, intracranial arteries. Several pathological and angiographic patterns exist. The most frequent pathological type is medial fibromuscular dysplasia, which is associated with the ‘string of beads' angiographic pattern. Unifocal lesions are less common and can be associated with several pathological subtypes. The pathophysiology of the disease is widely unknown. Fibromuscular dysplasia may in fact result from various causes and reflect a non-specific response to different insults. The poor knowledge of the natural history and the lack of randomised trials that compared the different treatment options do not allow any satisfactory judgement to be made regarding the need for or the efficacy of any treatment.

Background The risk of coronary artery disease (CAD) is traditionally considered high in patients who had an ischemic stroke or a transient ischemic attack (TIA). However, few studies have specifically assessed the absolute risk of coronary events in those patients and predictors of such events are not well known. Summary of review The overall risks of myocardial infarction and nonstroke vascular death are each around 2% per year. However, those risks are only about 1% per year in patients without CAD (i.e. the only ones who are likely to benefit from specific additional strategies). The prevalence of asymptomatic CAD ranges from 15% to 60%. Although potentially higher, the risk of CAD in patients with stroke/TIA related to atherosclerosis also seems to vary widely depending on the extent of the disease. Given the relatively low CAD risk, a simple systematic reinforcement of medical treatment in all patients may be not relevant. Up to now, there have been only limited ways to stratify the CAD risk in stroke/TIA patients. High-risk patients may be identified using the traditional cardiac scoring systems, but their validity has never been specifically assessed in stroke populations. The relative influence of traditional risk factors may be altered after a first vascular event. Stroke patients could also be screened for asymptomatic CAD. However, there is no simple and valid screening test for asymptomatic CAD that could be applied to all patients. Finally, there is still uncertainty about the potential benefits of treating asymptomatic CAD. Therefore, should the identification of patients with asymptomatic CAD requiring revascularization become feasible, the relevance of this strategy would remain to be evaluated by a randomized clinical trial. Conclusion The absolute risk of CAD in stroke/TIA patients is moderately high. More research is needed to identify high risk patients who could benefit from specific strategies.