Hui-Meng Chang

South Asian Patients With Ischemic Stroke Intracranial Large Arteries Are the Predominant Site of Disease

Background and Purpose— South Asians are the most prevalent ethnic group in the world. Intracranial disease is the most common vascular lesion worldwide. Methods— We prospectively studied 200 consecutive ethnic South Asian patients with acute ischemic stroke in Singapore. Results— Intracranial large-artery disease was prevalent among 54% of all stroke subtypes and was independently associated with hypertension and higher serum erythrocyte sedimentation rate. Conclusions— Among ethnic South Asian patients with ischemic stroke, intracranial large arteries are the predominant site of disease.

Severity of CIND and MCI predict incidence of dementia in an ischemic stroke cohort

Background: The utility of poststroke cognitive status, namely dementia, cognitive impairment no dementia (CIND), mild cognitive impairment (MCI), and no cognitive impairment (NCI), in predicting dementia has been previously examined. However, no studies to date have compared the ability of subtypes of MCI and CIND to predict dementia in a poststroke population. Methods: A cohort of ischemic stroke patients underwent neuropsychological assessment annually for up to 5 years. Dementia was defined using the DSM-IV criteria. Univariate and multivariable Cox proportional regression was performed to determine the ability of MCI subtypes, CIND severity, and individual domains of impairment to predict dementia. Results: A total of 362 patients without dementia were followed up for a mean of 3.4 years (17% drop out), with 24 developing incident dementia. Older age, previous and recurrent stroke, and CIND and MCI subtypes were significant predictors of dementia. In multivariable analysis controlling for treatment allocation, patients who were older, had previous or recurrent stroke, and had either CIND moderate or multiple domain MCI with amnestic component were at elevated risk for dementia. In multivariable domain analysis, recurrent strokes, age, and previous strokes, verbal memory, and visual memory were significant predictors of dementia. Receiver operating characteristic curve analysis showed that CIND moderate (area under the curve: 0.893) and multiple domain MCI with amnestic component (area under the curve: 0.832) were significant predictors of conversion to dementia. All other classifications of cognitive impairment had areas under the curve less than 0.7. Conclusion: Stroke patients with cognitive impairment no dementia (CIND) moderate are at higher risk of developing dementia, while CIND mild patients are not at increased risk of developing dementia.

The Prognostic Effects of Poststroke Cognitive Impairment No Dementia and Domain-Specific Cognitive Impairments in Nondisabled Ischemic Stroke Patients

Background and Purpose— There is some evidence that poststroke dementia, cognitive impairment no dementia (CIND), and mild cognitive impairment predict for poor outcomes such as dementia, death, and institutionalization. However, few studies have examined the prognostic value of CIND, CIND severity, and domain impairments in a poststroke cohort. Methods— A cohort of ischemic stroke patients with baseline cognitive assessments 3 months poststroke were followed up annually for outcomes of dependency, vascular events, and death for up to 5 years. Univariate and multivariate Cox proportional regression was performed to determine the ability CIND, CIND severity, and domain impairments to predict dependency, vascular outcomes, and death. Results— Four-hundred nineteen patients without dementia (mean age 60±11 years, 32% female) were followed for a mean of 3.2 years. Older age, diabetes, more severe strokes, CIND-mild, and CIND-moderate were independently predictive of dependency. There were no independent predictors of recurrent vascular events. Older age, diabetes, and CIND-moderate were independently predictive of death. In analyses of individual cognitive domains, impairments in visuomotor speed were independently predictive of dependency. Conclusions— In poststroke patients, CIND predicts dependency and death, while CIND severity discriminates patients with poor survival. Impairments in visuomotor speed independently predict dependency. Clinical Trial Registration— URL: http://clinicaltrials.gov. Unique Identifier: NCT00161070.

Is uric acid protective or deleterious in acute ischemic stroke? A prospective cohort study

Contrasting observations have been made between serum urate and ischemic stroke outcomes in studies involving Caucasian populations. To assess the hypothesis that urate is associated with stroke outcomes, a prospective follow-up study was performed in a cohort of Asian patients with ischemic stroke. Patients diagnosed with transient ischemic attack, first or recurrent ischemic stroke were included in this study. Serum urate, measured using high-performance liquid chromatography, was correlated with 12-month functional and vascular stroke outcomes. Poor functional outcome was defined as a modified Rankin scale exceeding 2 and vascular outcome was defined as a composite of recurrent stroke, myocardial infarction or vascular death during the study period. A total of 503 patients of mean age 63 (SD 12) years were included. A U-shaped relationship between urate quartiles and poor functional outcomes was demonstrated. More patients with low (<280microM) and high (>410microM) urate levels had poor functional outcomes (36% and 27% respectively), compared to those with urate levels between 340 and 410microM (14%). No significant relationship was observed between urate and vascular outcomes. Depending on its level, serum urate may exhibit protective and deleterious effects on stroke outcomes.

Microvascular Structure and Network in the Retina of Patients With Ischemic Stroke

Background and Purpose— Microvascular disease has been implicated in the pathogenesis of stroke. The retina provides a window to assess microcirculation noninvasively. We studied the association between quantitatively measured retinal microvascular characteristics and acute ischemic stroke. Methods— We conducted a case-control study with acute ischemic stroke patients recruited from a tertiary hospital in Singapore and controls from the Singapore Epidemiology of Eye Disease program matched by 10-year age strata, sex, and race. Strokes were classified using modified Trial of Org 10172 in Acute Stroke Treatment (TOAST) criteria. Retinal vascular parameters were measured from retinal fundus photographs using a computer program. Logistic regression models for stroke were constructed adjusting for age, sex, race, and additionally for smoking, hypertension, diabetes mellitus, and hypercholesterolemia. Results— We included 557 ischemic stroke cases (261 lacunar, 185 large artery, and 54 cardioembolic stroke) and 557 controls. After adjusting for vascular risk factors, decreased arteriolar fractal dimension (odds ratio [OR] per standard deviation [SD] decrease, 2.28; 95% confidence interval [CI], 1.80–2.87) and venular fractal dimension (OR per SD decrease, 1.80; 95% CI, 1.46–2.23), increased arteriolar tortuosity (OR per SD increase, 1.56; 95% CI, 1.25–1.95), and venular tortuosity (OR per SD increase, 1.49; 95% CI, 1.27–1.76), narrower arteriolar caliber (OR per SD decrease, 2.79; 95% CI, 2.21–3.53), and wider venular caliber (OR per SD increase, 1.57; 95% CI, 1.27–1.95) were associated with stroke. Stratification by stroke subtypes and further adjustment for retinopathy signs revealed similar results. Conclusions— Patients with ischemic stroke have a sparser and more tortuous microvascular network in the retina. These findings provide insight into the structure and pattern of microcirculation changes in stroke.

Retinal microvascular changes and subsequent vascular events after ischemic stroke.

Objectives: Retinal microvasculature changes are associated with vascular events including stroke in healthy populations. It is not known whether retinal microvascular changes predict recurrent vascular events after ischemic stroke. We examined the relationship between retinal microvascular signs and subsequent vascular events in a prospective cohort of 652 acute ischemic stroke patients admitted to a tertiary hospital in Singapore from 2005 to 2007. Methods: Retinal photographs taken within 1 week of stroke onset were assessed in a masked manner for quantitative and qualitative measures. Follow-up data over 2–4 years were obtained by standardized telephone interview and then were verified from medical records. Predictors of recurrent vascular events (cerebrovascular, coronary, vascular death, and composite vascular events) were determined using Cox regression models. Results: Follow-up data over a median of 29 months were obtained for 89% (652 patients) of the cohort. After adjustment for covariates including traditional risk factors and index stroke etiology, patients with severe arteriovenous nicking (AVN) were more likely to have a recurrent cerebrovascular event (hazard ratio [HR] 2.28, 95% confidence interval [CI] 1.20–4.33) compared with those without AVN. Patients with severe focal arteriolar narrowing (FAN) were more likely to have a recurrent cerebrovascular event (HR 2.75, 95% CI 1.14–6.63) or subsequent composite vascular event (HR 2.77, 95% CI 1.31–5.86) compared to those without FAN. Conclusions: Retinal microvascular changes predicted subsequent vascular events after ischemic stroke, independent of traditional risk factors and stroke subtype. Thus, retinal imaging has a potential role in predicting the risk of recurrent vascular events after ischemic stroke and in understanding novel vascular risk factors.

Reconsidering recent myocardial infarction as a contraindication for IV stroke thrombolysis

Objectives: We reviewed the literature on IV stroke thrombolysis for patients with recent myocardial infarction (MI). Methods: We searched PubMed and Ovid databases, relevant trials, and guidelines. Results: Only 5 thrombolyzed stroke patients with recent MI were reported to have cardiac tamponade. Pathological studies show MI healing is completed by 7 weeks. Conclusion: The time window from MI as a contraindication for IV stroke thrombolysis may be narrowed from 3 months in current guidelines to 7 weeks.

Retinal Vascular Caliber and Extracranial Carotid Disease in Patients With Acute Ischemic Stroke The Multi-Centre Retinal Stroke (MCRS) Study

Background and Purpose— Previous studies show that both retinal vascular caliber and carotid disease predict incident stroke in the general population, but the exact relationship between these 2 microvascular and macrovascular structural risk factors is unclear. We studied the relationship between retinal vascular caliber and carotid disease in patients presenting with acute ischemic stroke. Methods— We conducted a cross-sectional study of patients with acute ischemic stroke recruited from 3 centers (Melbourne, Sydney, Singapore). The caliber of retinal arterioles and venules was measured from digital retinal photographs. Severe extracranial carotid disease was defined as stenosis ≥75% or occlusion determined by carotid Doppler using North American Symptomatic Carotid Endarterectomy Trial-based criteria. Results— Among the 1029 patients with acute stroke studied, 7% of the population had severe extracranial carotid disease. Retinal venular caliber was associated with ipsilateral severe carotid disease (P<0.001 in multivariate models). Patients with wider retinal venular caliber were more likely to have severe ipsilateral carotid disease (multivariable-adjusted OR, 3.81; 95% CI, 1.80 to 8.07, comparing the largest and smallest venular caliber quartiles). The retinal venular caliber–carotid disease association remained significant in patients with large artery stroke. Conclusions— In patients with acute stroke, retinal venular widening was strongly associated with ipsilateral severe extracranial carotid disease. Our findings suggest concomitant retinal and cerebral microvascular disease may be present in patients with carotid stenosis or occlusion disease. The pathogenesis of stroke due to carotid disease may thus be partially mediated by microvascular disease.

Severe bruxism following basal ganglia infarcts: insights into pathophysiology

Bruxism characterized by clenching and grinding of teeth can lead to toothwear, headaches and depression. While bruxism has been associated with a number of neurological diseases, it has not been highlighted following cerebral infarction. An elderly man presented with an acute onset of tooth grinding and jaw clenching associated with dysarthria. His bruxism was worse during the day and resolved during sleep. He had frequent jaw aches, headaches and swallowing difficulty. Examination demonstrated the presence of dysarthria with jaw clenching and tooth grinding, producing persistent high pitch and loud squeaky sounds. A magnetic resonance imaging and angiography examination revealed a recent infarct in the right thalamus. In addition, chronic lacunar infarcts were present in the bilateral caudate nuclei with severe basilar artery stenosis. He was successfully treated with botulinum toxin. We discuss the pathophysiologic mechanisms of bruxism associated with basal ganglia infarcts. Dysfunction of the efferent and/or afferent thalamic or striatopallidal tracts may play a role in bruxism. Early recognition of bruxism following stroke could reduce unnecessary suffering since the condition can be effectively treated.

Associations of ankle-brachial index (ABI) with cerebral arterial disease and vascular events following ischemic stroke

OBJECTIVES Low ankle-brachial index (ABI), indicative of peripheral arterial disease (PAD), is a risk factor for stroke. ABI has been shown to be associated with cerebral arterial disease and prognosis following stroke. We studied the associations of the degree of ABI lowering with extracranial carotid disease (ECD), intracranial large artery disease (ICLAD), and subsequent vascular events in a prospective cohort of acute ischemic stroke patients. METHODS ABI, extracranial and intracranial cerebral arteries were assessed in a blinded manner. ABI was categorized into 0.9-1.3 (normal), 0.8-0.89 (mildly lowered) and <0.8 (severely lowered). Follow-up data at 1 year were obtained from standardized telephone interviews and verified with medical records. RESULTS Among the 1311 patients, 73% had normal ABI, 13% had ABI 0.8-0.89 and 13% had ABI <0.8. Compared to patients with normal ABI, those with ABI<0.8 had higher prevalence of severe ECD (15% vs. 5%, p = 0.006) and ICLAD (72% vs. 48%, p = 0.003), even after adjustment for age, gender, hypertension, diabetes, hyperlipidemia, smoking, ischemic heart disease and atrial fibrillation (severe ECD p < 0.001, ICLAD p < 0.001). At 1 year, patients with ABI <0.8 had a higher incidence of composite vascular events (19% vs. 11%, p = 0.02), stroke (15% vs. 10%, p = 0.06) and myocardial infarction (4% vs. 2%, p = 0.07) than patients with normal ABI. CONCLUSION Among ischemic stroke patients, large cerebral arterial disease and incidence of subsequent vascular events at 1 year were associated with severe ABI lowering <0.8, but not with mild ABI lowering (0.8-0.89).