Gregoire Boulouis1, Andreas Charidimou1, Eitan Auriel1, Kellen E Haley1, Ellis S van Etten1, Panagiotis Fotiadis1, Yael Reijmer1, Alison Ayres1, Kristin M Schwab1, Sergi Martinez-Ramirez1, Jonathan Rosand2, Anand Viswanathan1, Joshua N Goldstein3, Steven M Greenberg1, M Edip Gurol4. 1. Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston, MA, USA. 2. Division of Neurocritical Care and Emergency Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. 3. Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston, MA, USA; Division of Neurocritical Care and Emergency Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Department of Emergency Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. 4. Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston, MA, USA. Electronic address: edip@mail.harvard.edu.
Abstract
BACKGROUND: The association between cerebral small vessel diseases (cSVD) and intracranial atherosclerosis is debated and conflicting results have been reported. We sought to investigate this association in patients with intracerebral hemorrhage (ICH), due to severe cSVD. METHODS: Consecutive ICH patients were divided into those meeting criteria for cerebral amyloid angiopathy (CAA) and those with deep hypertensive ICH consistent with hypertensive cSVD (HTN-SVD). White matter hyperintensity volumes (WMH) and microbleed counts (MB) were measured on MRI. CTA was rated for severity of intracranial carotid calcifications and for presence of >50% intracranial stenosis (ICS). Associations of intracranial atherosclerosis severity with type of SVD (CAA vs HTN-cSVD) and with imaging and clinical markers of cSVD burden were analyzed. RESULTS: The cohort included 253 CAA and 90 HTN-SVD patients. In multivariable models, the type of cSVD (CAA vs. HTN-cSVD) was not associated with calcification severity (OR=1.04, 95% CI [0.62-3.5], p=0.37) or presence of ICS (OR=0.84, 95% CI [0.21-2.74], p=0.78). We found no association between intracranial atherosclerosis (calcifications and stenoses) and parenchymal markers of cSVD severity (WMH and MB, adjusted p≥0.2 for all comparisons) and no association with presence of dementia before ICH (adjusted p≥0.2 for both comparisons). CONCLUSIONS: We found no association between intracranial atherosclerosis and parenchymal or clinical consequences of cSVD, suggesting that cSVDs while sharing some risk factors are not influenced by upstream larger vessel pathologies.
BACKGROUND: The association between cerebral small vessel diseases (cSVD) and intracranial atherosclerosis is debated and conflicting results have been reported. We sought to investigate this association in patients with intracerebral hemorrhage (ICH), due to severe cSVD. METHODS: Consecutive ICHpatients were divided into those meeting criteria for cerebral amyloid angiopathy (CAA) and those with deep hypertensive ICH consistent with hypertensive cSVD (HTN-SVD). White matter hyperintensity volumes (WMH) and microbleed counts (MB) were measured on MRI. CTA was rated for severity of intracranial carotid calcifications and for presence of >50% intracranial stenosis (ICS). Associations of intracranial atherosclerosis severity with type of SVD (CAA vs HTN-cSVD) and with imaging and clinical markers of cSVD burden were analyzed. RESULTS: The cohort included 253 CAA and 90 HTN-SVDpatients. In multivariable models, the type of cSVD (CAA vs. HTN-cSVD) was not associated with calcification severity (OR=1.04, 95% CI [0.62-3.5], p=0.37) or presence of ICS (OR=0.84, 95% CI [0.21-2.74], p=0.78). We found no association between intracranial atherosclerosis (calcifications and stenoses) and parenchymal markers of cSVD severity (WMH and MB, adjusted p≥0.2 for all comparisons) and no association with presence of dementia before ICH (adjusted p≥0.2 for both comparisons). CONCLUSIONS: We found no association between intracranial atherosclerosis and parenchymal or clinical consequences of cSVD, suggesting that cSVDs while sharing some risk factors are not influenced by upstream larger vessel pathologies.
Authors: Yunis Mayasi; Johanna Helenius; David D McManus; Richard P Goddeau; Adalia H Jun-O'Connell; Majaz Moonis; Nils Henninger Journal: J Neurol Neurosurg Psychiatry Date: 2017-05-27 Impact factor: 10.154
Authors: Michaël T J Peeters; Rik Houben; Alida A Postma; Robert J van Oostenbrugge; Leon J Schurgers; Julie Staals Journal: Front Neurol Date: 2019-12-20 Impact factor: 4.003