Effects of Statins on Progression of Subclinical Brain Infarct

Fu, Jian Hui; Mok, Vincent; Lam, Wynnie W M; Wong, Adrian; Chu, Winnie C.W.; Xiong, Yunyun; Ng, Ping Wing; Tsoi, Tak Hon; Yeung, Vincent; Wong, Ka Sing

doi:10.1159/000313614

Cited by 30 publications

(27 citation statements)

References 49 publications

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“…Although the evolution of MCA stenosis was not different between the two groups, the rates of progression of cerebral white matter lesions, subclinical brain infarcts, all-cause mortality, and any clinical events were significantly lower in the simvastatin-treated group 94,95,96 .…”

Section: Risk Factor Controlmentioning

confidence: 75%

“…In the randomized, double-blind Regression of Cerebral Artery Stenosis (ROCAS) study 94,95 , 132 Chinese patients with asymptomatic MCA stenosis and increased LDL cholesterol (3·00-5·00 mmol/L) were randomized to simvastatin 20mg/day or placebo for 2 years. Although the evolution of MCA stenosis was not different between the two groups, the rates of progression of cerebral white matter lesions, subclinical brain infarcts, all-cause mortality, and any clinical events were significantly lower in the simvastatin-treated group 94,95,96 .…”

Section: Risk Factor Controlmentioning

confidence: 99%

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Stroke Caused by Atherosclerosis of the Major Intracranial Arteries

Banerjee¹,

Chimowitz²

2017

Journal of Vascular Surgery

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Our goal in this review is to discuss the pathophysiology, diagnosis and treatment of stroke caused by atherosclerosis of the major intracranial arteries. References for the review were identified by searching PubMed for related studies published from 1955 to June 2016 using search terms "intracranial stenosis" and "intracranial atherosclerosis". Reference sections of published randomized clinical trials and previously published reviews were searched for additional references. Intracranial atherosclerotic disease (ICAD) is a highly prevalent cause of stroke that is associated with a high risk of recurrent stroke. It is more prevalent among blacks, Hispanics and Asians compared with whites. Diabetes, hypertension, metabolic syndrome, smoking, hyperlipidemia and a sedentary lifestyle are the major modifiable risk factors associated with ICAD. Randomized clinical trials comparing aggressive management (dual antiplatelet treatment for 90 days followed by aspirin monotherapy and intensive management of vascular risk factors) with intracranial stenting plus aggressive medical management have shown medical management alone to be safer and more effective for preventing stroke. As such, aggressive medical management has become the standard of care for symptomatic patients with ICAD. Nevertheless, there are subgroups of patients who are still at high risk of stroke despite being treated with aggressive medical management. Future research should aim to establish clinical, serologic, and imaging biomarkers to identify high-risk patients, and clinical trials evaluating novel therapies should be focused on these patients.

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Section: Risk Factor Controlmentioning

confidence: 75%

Section: Risk Factor Controlmentioning

confidence: 99%

Stroke Caused by Atherosclerosis of the Major Intracranial Arteries

Banerjee¹,

Chimowitz²

2017

Journal of Vascular Surgery

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“…These findings are especially timely given evidence that statins may prevent incident subclinical infarcts. (40) Future studies are needed to examine the impact of preventive treatment in asymptomatic persons, including those with even the smallest abnormalities.…”

Section: Discussionmentioning

confidence: 99%

Small Brain Lesions and Incident Stroke and Mortality

et al. 2015

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Background Although cerebral lesions ≥3mm on imaging are associated with incident stroke, lesions < 3mm are typically ignored. Objective To examine stroke risks associated with subclinical brain lesions by size (< 3 mm only, lesions ≥3 mm only, both < 3 mm and ≥3 mm) and white matter hyperintensities (WMH). Design Community cohort, Atherosclerosis Risk in Communities (ARIC) Study Setting Two ARIC sites with magnetic resonance imaging (MRI) data (1993–95) Participants 1,884 (99%) adults (50–73 years, 40% men; 50% black) with MRI and no prior stroke; average 14.5 years follow-up. Measurements MRI lesions: none (n=1611), < 3 mm only (n=50), ≥3 mm only (n=185), or both < 3 and ≥3 mm lesions (n=35); WMH score (0–9 scale). Outcomes: incident stroke (n=157), overall mortality (n=576), stroke mortality (n=50). Hazard Ratios (HR) estimated with proportional hazards models. Results Compared to no lesions, stroke risk was tripled with lesions < 3mm only (HR=3.47, 95% CI:1.86-6.49), doubled with lesions ≥3 mm only (HR=1.94, 95% CI:1.22-3.07), and was 8-fold higher with both < 3 mm and ≥3 mm-sized lesions (HR=8.59, 95% CI:4.69-15.73). Stroke risk doubled with WMH ≥3 (HR=2.14, 95% CI:1.45-3.16). Stroke mortality risk tripled with lesions < 3 mm only (HR=3.05, 95% CI:1.04-8.94), doubled with lesions ≥3 mm (HR=1.9, 95% CI:1.48-2.44) and was seven-times higher with both lesion sizes (HR=6.97, 95% CI:2.03-23.93). Limitations Few stroke events (n=147), especially hemorrhagic (n=15); limited numbers of participants with only lesions ≤3mm (n=50) or with both lesions ≤3mm and 3–20mm (n=35). Conclusions Very small cerebrovascular lesions may be associated with increased risks of stroke and mortality; having both < 3 mm and ≥3 mm lesions may represent a particularly striking risk increase. Larger studies are needed to confirm findings and provide more precise estimates.

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“…As the population continues to age the clinical manifestations of subclinical cerebrovascular disease will take on a greater role, and so will the importance of identifying risk factors and potential treatment targets. At this time the data has been inconclusive on the utility of statins in preventing an increase in WMH volumes[38, 39], or SBI[40], though the efficacy in preventing clinical stroke is clear[6]. Further research is needed in identifying risk factors for subclinical cerebrovascular disease, and how these modifiable diseases are influenced by an individual’s genetic profile.…”

Section: Discussionmentioning

confidence: 99%

Lipid Profile Components and Subclinical Cerebrovascular Disease in the Northern Manhattan Study

et al. 2014

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Background: Subclinical cerebrovascular disease has been associated with multiple adverse events related to aging, including stroke and dementia. The modifiable risk factors for subclinical cerebrovascular disease beyond hypertension have not been well characterized. Our objective was to examine the association between baseline, and changes over time, in lipid profile components and subclinical cerebrovascular disease on magnetic resonance imaging (MRI). Methods: Fasting plasma lipids were collected on participants in the Northern Manhattan Study, a prospective cohort study examining risk factors for cardiovascular disease in a multiethnic elderly urban-dwelling population. A subsample of the cohort underwent brain MRI between 2003 and 2008 (a median of 6.2 years, range = 0-14, after enrollment), when repeat fasting lipids were obtained. We used lipid profile components at the time of initial enrollment (n = 1,256 with lipids available) as categorical variables, as well as change in clinical categories over the two measures (n = 1,029). The main outcome measures were (1) total white matter hyperintensity volume (WMHV) using linear regression and (2) silent brain infarcts (SBI) using logistic regression. Results: None of the plasma lipid profile components at the time of enrollment were associated with WMHV. The association between baseline lipids and WMHV was, however, modified by apolipoprotein E (apoE) status (χ² with 2 degrees of freedom, p = 0.03), such that among apoE4 carriers those with total cholesterol (TC) ≥200 mg/dl had a trend towards smaller WMHV than those with TC <200 mg/dl (difference in logWMHV -0.19, p = 0.07), while there was no difference among apoE3 carriers. When examining the association between WMHV and change in lipid profile components we noted an association with change in high-density lipoprotein cholesterol (HDL-C, >50 mg/dl for women, >40 mg/dl for men) and TC. A transition from low-risk HDL-C (>50 mg/dl for women, >40 mg/dl for men) at baseline to high-risk HDL-C at the time of MRI (vs. starting and remaining low risk) was associated with greater WMHV (difference in logWMHV 0.34, p value 0.03). We noted a similar association with transitioning to a TC ≥200 mg/dl at the time of MRI (difference in logWMHV 0.25, p value 0.006). There were no associations with baseline or change in lipid profile components with SBI. Conclusions: The association of plasma lipid profile components with greater WMHV may depend on apoE genotype and worsening HDL and TC risk levels over time.

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Effects of Statins on Progression of Subclinical Brain Infarct

Cited by 30 publications

References 49 publications

Stroke Caused by Atherosclerosis of the Major Intracranial Arteries

Stroke Caused by Atherosclerosis of the Major Intracranial Arteries

Small Brain Lesions and Incident Stroke and Mortality

Lipid Profile Components and Subclinical Cerebrovascular Disease in the Northern Manhattan Study

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