The value of plasma fibrillin-1 level in patients with spontaneous cerebral artery dissection

ObjectiveTo explore the value of plasma fibrillin-1 levels in patients with spontaneous cerebral artery dissection (sCeAD).MethodsA single-center prospective cohort of 99 consecutive patients with sCeAD between February 2013 and December 2015 were age and sex matched with 115 patients with non-sCeAD ischemic stroke and 20 healthy participants undergoing routine physical examination. The plasma fibrillin-1 level was measured with ELISA and compared among the 3 groups. The associations of fibrillin-1 with site, acuity, and severity of dissection, as well as clinical and radiographic prognosis of patients, were analyzed.ResultsOne hundred nine plasma samples from 99 patients with sCeAD, 115 from disease control patients, and 20 from healthy participants were collected. The plasma fibrillin-1 level of the dissection group (mean 85.56 ng/mL [95% confidence interval 81.53–89.59]) was higher than that of non-sCeAD ischemic stroke group (77.13 ng/mL [73.64–80.63], p = 0.015) or healthy controls (73.04 ng/mL [65.94–80.13], p = 0.029). Such differences were most prominent in the acute stage (97.64 ng/mL [91.64–103.64], 74.39 ng/mL [68.95–79.84], and 73.04 ng/mL [65.95–80.13], respectively). A cutoff value of 88.455 ng/mL was determined to differentiate acute dissection from nondissection stroke with a sensitivity of 0.778 and a specificity of 0.800. Higher fibrillin-1 level was detected in patients with more severe dissection radiographically (p < 0.001), while patients with lower fibrillin-1 concentration at baseline achieved better morphologic recovery on follow-up imaging tests (p = 0.003).ConclusionPlasma fibrillin-1 is a promising biomarker for aiding the diagnosis of acute sCeAD and may have potential value in lesion severity grading and radiographic prognosis prediction.Classification of evidenceThis study provides Class III evidence that patients with sCeAD have significantly higher levels of plasma fibrillin-1 than patients with ischemic stroke attributable to a cause other than sCeAD.

Download Full-text

A case of Marfan syndrome with ischemic stroke due to middle cerebral artery dissection

Neurology and Clinical Neuroscience ◽

10.1111/ncn3.12233 ◽

2018 ◽

Vol 6 (6) ◽

pp. 194-196

Author(s):

Tadashi Ozawa ◽

Akihiro Toyohara ◽

Younhee Kim ◽

Takafumi Mashiko ◽

Reiji Koide ◽

...

Keyword(s):

Ischemic Stroke ◽

Middle Cerebral Artery ◽

Marfan Syndrome ◽

Cerebral Artery ◽

Artery Dissection ◽

Cerebral Artery Dissection

Download Full-text

A case of middle cerebral artery dissection onset of ischemic stroke successfully diagnosed by MRA source images

Nosotchu ◽

10.3995/jstroke.36.366 ◽

2014 ◽

Vol 36 (5) ◽

pp. 366-369

Author(s):

Mitsuteru Shimohata ◽

Keiko Kitazawa ◽

Yasushi Ito ◽

Yumiko Watanabe ◽

Hajime Tanaka

Keyword(s):

Ischemic Stroke ◽

Middle Cerebral Artery ◽

Cerebral Artery ◽

Artery Dissection ◽

Cerebral Artery Dissection

Download Full-text

Abstract TMP106: Early Elevation of D-dimer Values Is Associated With Neurological Deterioration in Acute Ischemic Stroke due to Cerebral Artery Dissection

Stroke ◽

10.1161/str.47.suppl_1.tmp106 ◽

2016 ◽

Vol 47 (suppl_1) ◽

Author(s):

Kazuki Fukuma ◽

Masafumi Ihara ◽

Hiroshi Yamagami ◽

Masatoshi Koga ◽

Kazunori Toyoda ◽

...

Keyword(s):

Ischemic Stroke ◽

Aortic Dissection ◽

Acute Ischemic Stroke ◽

Anticoagulant Therapy ◽

Cerebral Artery ◽

Neurological Deterioration ◽

Artery Dissection ◽

Cerebral Artery Dissection ◽

D Dimer ◽

Early Elevation

Background and Purpose: Plasma D-dimer is a complementary diagnostic marker in patients with acute aortic dissection. However, it remains unknown whether monitoring of D-dimer is of diagnostic value for in-hospital management of cerebral artery dissection. The aim of this study was to identify the relationship between D-dimer and neurological deterioration in acute ischemic stroke due to cerebral artery dissection. Methods: We retrospectively studied 90 consecutive patients (60 men; mean age, 51.0 years) with ischemic stroke due to cerebral or cervical artery dissection who were admitted to our hospital within three weeks after the onset between Jan 2005 and May 2015. Plasma D-dimer values were measured at least on admission and within a week. Neurological deterioration (ND) was defined as an increase of ≥ 3 points in the National Institutes of Health Stroke Scale (NIHSS) score within 3 weeks after admission. D-dimer ratio (DDR, peak D-dimer between the 2nd and 7th hospital day / on admission) was measured as an index of D-dimer elevation at an early phase. Associations between ND and patient characteristics including D-dimer values and acute treatment regimen were examined. Results: Eight of the 90 patients (8.9%) presented ND, accompanied by progression of stenosis in cerebral artery dissection. None of them had aortic dissection, severe heart failure and active malignant tumor. Fifty-nine of the 90 patients (65.6%) received anticoagulant therapy, 33 (36.7%) antiplatelet therapy and 5 (5.6%) thrombolysis in the acute phase. The mean D-dimer value was 2.80±1.81 (standard deviation, SD) at the time of progression. In univariate analysis, DDR was higher in ND group (3.93±2.45 SD) than non-ND group (1.46±1.04 SD) (p<0.01), whereas the D-dimer value on admission was similar in 2 groups . Multivariate logistic regression analysis showed DDR was related to ND before [OR: 1.57; 95% CI: 1.15-2.38, p<0.01] and after controlling for thrombolysis, anticoagulant therapy and deep vein thrombosis [OR: 1.63; 95% CI: 1.14-2.62, p<0.01]. Conclusion: Early elevation of D-dimer values may predict neurological deterioration with progression of stenosis in acute ischemic stroke due to cerebral artery dissection

Download Full-text

Intravenous Recombinant Tissue Plasminogen Activator Thrombolysis in Acute Ischemic Stroke due to Middle Cerebral Artery Dissection

Journal of Stroke and Cerebrovascular Diseases ◽

10.1016/j.jstrokecerebrovasdis.2012.02.003 ◽

2012 ◽

Vol 21 (8) ◽

pp. 915.e7-915.e9 ◽

Cited By ~ 8

Author(s):

Ryosuke Doijiri ◽

Chiaki Yokota ◽

Rieko Suzuki ◽

Kazunori Toyoda ◽

Kazuo Minematsu

Keyword(s):

Ischemic Stroke ◽

Middle Cerebral Artery ◽

Acute Ischemic Stroke ◽

Plasminogen Activator ◽

Tissue Plasminogen Activator ◽

Cerebral Artery ◽

Recombinant Tissue Plasminogen Activator ◽

Artery Dissection ◽

Tissue Plasminogen ◽

Cerebral Artery Dissection

Download Full-text

Intracranial Cerebral Artery Dissection of Anterior Circulation as a Cause of Convexity Subarachnoid Hemorrhage

Cerebrovascular Diseases ◽

10.1159/000430945 ◽

2015 ◽

Vol 40 (1-2) ◽

pp. 45-51 ◽

Cited By ~ 16

Author(s):

Kazuki Fukuma ◽

Masafumi Ihara ◽

Tomotaka Tanaka ◽

Yoshiaki Morita ◽

Kazunori Toyoda ◽

...

Keyword(s):

Ischemic Stroke ◽

Subarachnoid Hemorrhage ◽

Cerebral Artery ◽

Internal Carotid ◽

Border Zone ◽

Artery Dissection ◽

Early Reperfusion ◽

Cerebral Magnetic Resonance Imaging ◽

Vertebrobasilar Artery ◽

Cerebral Artery Dissection

Background: Convexity subarachnoid hemorrhage (cSAH), defined as intrasulcal bleeding restricted to hemispheric convexities, has several etiologies: reversible cerebral vasoconstriction syndrome, cerebral amyloid angiopathy, and internal carotid artery (ICA) stenosis or occlusion. However, it remains unknown whether cerebral artery dissection causes cSAH. Methods: We retrospectively investigated patients admitted to our hospital between 2005 and 2013 with ischemic stroke or transient ischemic attack caused by cerebral artery dissection. Cerebral artery dissection was diagnosed by cervical or cerebral magnetic resonance imaging (MRI) or computed tomography (CT) showing a wall hematoma. CT angiography, ultrasonography, or intra-arterial digital-subtraction angiography detected cerebral artery dissection if a double lumen, string sign, intimal flap, or dissecting aneurysm was observed at a nonbifurcation site. We used CT or MRI to detect cSAH, which was defined as blood collection restricted to one or few cerebral sulci without extending to the basal cisterns, ventricles, or Sylvian and interhemispheric fissures. Demographic, neuroimaging, treatment, and prognostic data were collected. Results: In total, 82 patients were diagnosed with ischemic stroke caused by cerebral artery dissection. The following arteries were affected: the ICA (9 patients), anterior cerebral artery (ACA; 12 patients), middle cerebral artery (MCA; 12 patients), vertebral artery (37 patients), basilar artery (5 patients), posterior cerebral artery (2 patients), and posterior inferior cerebellar artery (4 patients). In addition, 1 patient presented with simultaneous dissection in both the vertebral and internal carotid arteries, and 6 patients (7%) presented with cSAH (3 men and 3 women, age 39-67 years). The MCA was dissected in four cases and the ACA in two cases, with cSAH frequencies of 33 (4 of 12) and 17% (2 of 12), respectively, in those vessels. Artery dissection in the vertebrobasilar artery system was not responsible for cSAH (0 of 48). In all the MCA dissection cases, cSAH occurred in the arterial border zone between the ACA and MCA territories. Although 2 patients showed early reperfusion with temporary cSAH enlargement, cSAH was self-limiting. Antithrombotic treatment did not complicate the clinical course when used in 4 patients during acute or subacute phases. All patients achieved a 3-month poststroke modified Rankin Scale of 0-2. Conclusion: Our data suggest that cSAH caused by intracranial cerebral artery dissection is not rare. Further investigations are needed to elucidate the precise mechanism underlying cSAH in cerebral artery dissection.

Download Full-text