Carotid intima-media thickness and cerebrovascular vasoreactivity in patients with intracranial aneurysms : A sonographic study of potential predictors for aneurysm rupture risk and delayed cerebral ischemia
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Background and aims Intracranial aneurysms can rupture and cause an aneurysmal subarachnoid hemorrhage (aSAH), a bleeding under the arachnoid meninges covering the brain. This is a devastating event, in which delayed cerebral ischemia (DCI) is a major cause of death and disability. In this thesis, we assess two possible ultrasonographic predictors for aneurysm rupture risk and DCI: carotid intima-media thickness (IMT) and cerebrovascular reactivity (CVR). Carotid IMT is the combined thickness of the inner two layers of the carotid artery wall. IMT provides information about the degree of atherosclerosis and is an established risk marker for myocardial infarction and ischemic stroke. Persons with atherosclerosis have an increased prevalence of intracranial aneurysms, and smoking and hypertension are shared risk factors for aneurysm rupture, myocardial infarction and ischemic stroke. We thus hypothesized that IMT also could be associated with risk of aneurysm rupture. Cerebral arterioles regulate vascular resistance and play an important role in maintaining constant cerebral blood flow during variations in cerebral perfusion pressure. CVR is defined as the change in cerebral blood flow, or blood flow velocity, in response to a vasoactive stimulus. Proximal arterial narrowing in vasospastic vessels causes a poststenotic pressure drop and compensatory arteriolar dilation. The suggested theory is that when vasospasm develops, pre-existing compensatory arteriolar dilation limits the capacity for further arteriolar dilation in a CVR test. Literature have indicated that impaired CVR may be a potential predictor for DCI after aSAH. Still, sample sizes have been limited and varying methodology and inconsistent and outdated definitions of DCI have been used. Material and methods Patients treated for unruptured and ruptured intracranial aneurysms at the Department of Neurosurgery, Haukeland University Hospital between February 2011 and May 2013 were included. Clinical, ultrasonographic and radiographic assessment were done after aneurysm treatment and at one-year follow up. Carotid ultrasound was performed with evaluation of IMT, and CVR was assessed by transcranial Doppler and acetazolamide test. Patients were followed prospectively for development of delayed cerebral ischemia (DCI), separated into clinical and radiographic findings. Results Carotid IMT was higher in patients treated for ruptured aneurysms than in patients with unruptured aneurysms. The probability of belonging to the aneurysm rupture group increased with higher IMT values. CVR was reduced on the ipsilateral side in all patients after aneurysm treatment, regardless of rupture status or DCI development. Patients with clinical deterioration due to DCI had lower CVR, and the difference was bigger on the contralateral side. Including CVR in a prediction model with established predictors increased the area under the receiving operator curve, indicating improved prediction of DCI. Conclusions There is an association between carotid IMT and aneurysm rupture status at the time of aneurysm treatment. Carotid IMT is a potential predictor of aneurysm rupture, and is a possible adjunct in the assessment of aneurysm rupture risk, and thus a helpful tool in patient counseling. Impaired CVR is a potential independent predictor of clinical deterioration due to DCI, and may assist in identifying patients at risk after aSAH. Our prediction model can be useful in clinical practice, but first needs to be validated. Ipsi- and contralateral CVR needs to be considered separately.
Has partsPaper I: Carotid intima-media thickness – a potential predictor for rupture risk of intracranial aneurysms. Lundervik M, Fromm A, Haaland ØA, Waje-Andreassen U, Svendsen F, Thomassen L, Helland CA. International Journal of Stroke. 2014 Oct;9(7):866-72. The article is not available in BORA due to publisher restrictions. The published version is available at: https://doi.org/10.1111/ijs.12159
Paper II: Cerebrovascular reactivity after treatment of unruptured intracranial aneurysms - A transcranial Doppler sonography and acetazolamide study. Bøthun ML, Haaland ØA, Logallo N, Svendsen F, Thomassen L, Helland CA. Journal of the Neurological Sciences, 2016 Apr 15;363:97-103. The article is available in the main thesis. The article is also available at: https://doi.org/10.1016/j.jns.2015.12.024
Paper III: Time-course of cerebrovascular reactivity in patients treated for unruptured intracranial aneurysms - A one-year transcranial Doppler and acetazolamide follow-up study. Bøthun ML, Haaland ØA, Logallo N, Svendsen F, Thomassen L, Helland CA. BioMed Research International, 2018 Apr 26;2018:6489276. The article is available at: http://hdl.handle.net/1956/19591
Paper IV: Impaired cerebrovascular reactivity may predict delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage. Bøthun ML, Haaland ØA, Moen G, Logallo N, Svendsen F, Thomassen L, Helland CA. Journal of the Neurological Sciences, 2019. Dec 15:2019:407:116539. The article is available at: http://hdl.handle.net/1956/21594