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Elkhair, Ahamed

Mayo Clinic

Mayo Clinic

Citations 6

Hemispheric Cortical Atrophy ipsilateral to Carotid Stenosis (N5.001)
Demirer, Mutlu , Anisetti, Bhrugun , Elkhair, Ahamed, Youssef, Hossam , Barrett, Kevin M. , Ertekin‐Taner, Nilüfer , Brott, Thomas G. , Youseff, Hossam , Lin, Michelle , Middlebrooks, Erik H. , Okromelidze, Lela , Meschia, James F.

Neurology | December 6, 2023 | Volume: 98 | Issue: 18_supplement | Pages: No page available

10.1212/wnl.98.18_supplement.3124 Get It

Age-Related Macular Degeneration is Associated with Cerebral Amyloid Angiopathy (S35.003)
Anisetti, Bhrugun , Elkhair, Ahamed, Youssef, Hossam , Lin, Michelle

Neurology | December 6, 2023 | Volume: 98 | Issue: 18_supplement | Pages: No page available

10.1212/wnl.98.18_supplement.2860 Get It

Differential Effect of Stroke Types on Cerebral White Matter Disease Progression (S45.001)
Elkhair, Ahamed, Youssef, Hossam , Anisetti, Bhrugun , Salem, Amr , Mateti, Nihas, Youseff, Hossam , Lin, Michelle

Neurology | April 28, 2023 | Volume: 100 | Issue: 17_supplement_2 | Pages: No page available

10.1212/wnl.0000000000203696 Get It

Abnormal Left Ventricular Geometry is Associated with Cerebral White Matter Disease (S36.005)
Salem, Amr , Mateti, Nihas, Demirer, Mutlu , Anisetti, Bhrugun , Youssef, Hossam , Elkhair, Ahamed, Youseff, Hossam , Adedinsewo, Demilade , Meschia, James F. , Lin, Michelle

Neurology | April 28, 2023 | Volume: 100 | Issue: 17_supplement_2 | Pages: No page available

10.1212/wnl.0000000000203017 Get It

Abstract WMP76: Carotid Revascularization Slows Hemispheric White Matter Disease Progression
Demirer, Mutlu , Craver, Emily C. , Middlebrooks, Erik H. , Anisetti, Bhrugun , Youssef, Hossam , Elkhair, Ahamed, Okromelidze, Leila, Barrett, Kevin M. , Ertekin‐Taner, Nilüfer , Brott, Thomas G. , Middlebrooks, Erik H , Youseff, Hossam , Lin, Michelle , Meschia, James F.

Stroke | February 2, 2023 | Volume: 54 | Issue: Suppl_1 | Pages: No page available

10.1161/str.54.suppl_1.wmp76 Get It

Introduction: Carotid revascularization is known to prevent stroke in patients with high-grade carotid stenosis, but whether carotid revascularization may slow the progression of hemispheric WMD in patients with carotid stenosis to prevent cognitive decline have not been well described. Methods: We conducted a longitudinal study involving patients age ≥40 years with carotid stenosis on ultrasound from 2011-2015 with serial brain MRI scans at least 1 year apart followed for radiographic and clinical outcomes to 2020. Severity of carotid stenosis was defined as moderate 50-69%, high-grade 70-99%, or occluded. Hemispheric WMD volume was quantified from axial T2 FLAIR images. Patients were stratified by revascularization status. Primary outcome was change in WMD volume per year ipsilateral or contralateral to the index carotid. Hemispheric differences in the annual rate of WMD progression (cc/yr) were compared between revascularized vs not revascularized using multivariable linear regression analysis adjusted for variables that differed between revascularization status. Results: Of the 150 patients, moderate stenosis was present in 37.3%, high-grade stenosis in 42.0%, and carotid occlusion in 20.7%. Mean age was 71±10 years, 36.7% were female. Seventy-three (48.7%) had carotid revascularization with a median follow-up of 5.1 years. Baseline WMD volume was 4.86cc ipsilateral and 4.39cc contralateral to the index carotid. Patients who underwent revascularization trended to have slower WMD progression in the hemisphere ipsilateral to the index carotid compared to those not revascularized (0.32cc/yr vs 0.63 cc/yr, p=0.340). The same trend was not observed in the contralateral hemisphere. In adjusted models, carotid revascularization was associated with a 0.33 cc per year decrease in WMD progression between hemispheres compared to those not revascularized (β= -0.33, p=0.070). Conclusions: In this study with a median follow-up of 5 years, we found that carotid revascularization resulted in a 50% reduction in the annual rate of WMD progression. Intervention trials should test whether carotid revascularization slows WMD progression in patients with cognitive impairment to prevent further cerebrovascular events and cognitive decline.
Abstract TMP81: The Relationship Between Carotid Stenosis And Silent Cerebrovascular Disease
Demirer, Mutlu , Middlebrooks, Erik H. , Anisetti, Bhrugun , Youssef, Hossam , Elkhair, Ahamed, Barrett, Kevin M. , Brott, Thomas G. , Middlebrooks, Erik H , Youseff, Hossam , Lin, Michelle , Meschia, James F.

Stroke | February 3, 2022 | Volume: 53 | Issue: Suppl_1 | Pages: No page available

10.1161/str.53.suppl_1.tmp81 Get It

Introduction: Patients with carotid stenosis may have silent cerebrovascular disease due to chronic hypoperfusion and atheroembolism. If so, progression of silent disease may be preventable through revascularization. We aim to evaluate the association between carotid stenosis/occlusion and cerebral small vessel disease (SVD) burden ipsilateral to the cervical carotid stenosis. Methods: Patients age ≥40 years with carotid stenosis or occlusion on carotid ultrasound who underwent MRI brain and intracranial angiogram with gradable SVD on MRI from 2011-2015 were included. Severity of carotid stenosis was defined using NASCET criteria as 50-69% (moderate), 70-99% (high-grade), or occluded. WMH volume was quantified using an automated artificial intelligence algorithm applied to axial T2 FLAIR images. Images were also scored for presence of chronic lacune, cerebral microbleeds (CMB), and silent infarcts using STRIVE criteria. Differences in WMD volume between hemispheres ipsilateral and contralateral to the carotid stenosis were calculated, and prevalence of SVD and silent infarct were compared across severities of carotid stenosis. Results: Of the 183 patients, mean age was 71±10 years and 38% were female. Moderate and severe stenosis was present in 36% and 46.5%, respectively, and 18% had carotid occlusion. Mean WMH volume was 7271±522mm 3 . Patients with carotid stenosis had greater WMH volume ipsilateral to the side of carotid stenosis than the contralateral side (mean difference 224±206mm 3 ), and higher severity of stenosis was associated with greater hemispheric difference in WMH volume (moderate vs high; 164±274mm 3 vs 743±309 mm 3 , p=0.009). Silent infarcts were more prevalent in high-grade carotid stenosis than moderate grade (moderate vs high, 10.8% vs 36.5%; p=0.002). There were no differences in either lacunae or CMBs across severities. Conclusions: Greater than one third of patients with high-grade carotid stenosis had ipsilateral silent brain infarction, and the volume of WMH was greater on the side of carotid stenosis. Future analyses should consider the potential yield of screening for carotid atherosclerosis in patients with varying degrees of hemispheric WMH asymmetry.