Small Vessel Infarcts Research Articles

Stroke in Asymptomatic Trypanosoma cruzi-Infected Patients

Background: The knowledge about the natural history of stroke in Chagas disease is incomplete. Methods: Vascular risk factors and stroke subtypes of asymptomatic Trypanosoma cruzi-infected patients with no clinical evidence of heart failure were assessed. They were compared with chronic chagasic cardiomyopathy patients who suffered a stroke and with a control group of 60 T. cruzi-noninfected stroke patients. Eighty-six consecutive chagasic stroke patients (mean age: 57.4 years; 64% females) were studied. Results: 38.4% of chagasic stroke patients had asymptomatic T. cruzi infection. Smoking was more frequent in asymptomatic chagasic stroke patients (21.2 vs. 5.7%; p = 0.04). Prevalence of hypertension, diabetes and prior stroke was similar in both groups. Small-vessel infarction (15.6 vs. 3.8%) and large-vessel atherosclerosis (9.4 vs. 3.8%) were significantly more frequent in asymptomatic than in symptomatic T. cruzi-infected stroke patients (p = 0.001). Nevertheless, their frequency was even higher in T. cruzi-noninfected stroke patients (36.7 and 13.3%, respectively). Apical aneurysm (27.3%), left atrial dilatation (12.1%), left ventricle hypokinesia (9.4%) and right bundle branch block (36.4%) were also detected in asymptomatic T. cruzi-infected stroke patients. Conclusions: Ischemic stroke may be the first manifestation of Chagas disease in asymptomatic patients with mild left ventricle dysfunction. Other noncardioembolic stroke subtypes can occur in asymptomatic T. cruzi-infected patients.

Inverse Relationship Between Cerebrovascular Lesions and Severity of Lewy Body Pathology in Patients With Lewy Body Diseases

Cerebrovascular pathology is a major cause of stroke and mortality. Studies on prevalence of cerebrovascular pathologies in dementia with Lewy bodies (DLBs) and Parkinson disease (PD) patients are scarce and contradictory. We aimed to determine the prevalence and severity of cerebrovascular pathologies in DLB and PD and to analyze their relationship to LB pathology. The prevalence and severity of atherosclerosis in the circle of Willis, cerebral amyloid angiopathy, cerebral infarcts, hemorrhages, small-vessel disease, white matter lesions, including the Consortium to Establish a Registry for Alzheimer Disease (CERAD) protocol as well as Braak neurofibrillary tangle stages for AD pathology were analyzed in autopsy-verified DLB (n = 13), PD (n = 102), and control subjects (n = 53). In all patient groups, the extent of LB pathology was inversely correlated to the severity of most vascular pathologies (atherosclerosis, infarcts, and small-vessel disease; all p < 0.05). By contrast, cerebral amyloid angiopathy, CERAD, and Braak neurofibrillary tangle stages were positively correlated with LB pathology (p < 0.05). Whereas the overall prevalence and severity of small-vessel disease, infarcts, hemorrhages, and white matter lesions were comparable among both disease groups, the extents of atherosclerosis, cerebral amyloid angiopathy, CERAD, and Braak neurofibrillary tangle stages were significantly higher in DLB than in those of PD patients (p < 0.05). Microinfarcts were statistically more prevalent in each patient group than in controls, whereas gross infarcts predominated in controls (p < 0.05 each). In conclusion, DLB and PD patients with advanced LB pathology were less likely to show severe cerebrovascular disease or history of stroke.

Glycemic Status Underlies Increased Arterial Stiffness and Impaired Endothelial Function in Migrant South Asian Stroke Survivors Compared to European Caucasians

The pathophysiology of an increased risk of cerebrovascular disease mortality among South Asians (SA) remains unclear. Indices of arterial stiffness and endothelial dysfunction are independent markers of vascular disease, having both prognostic and diagnostic implications. We hypothesized that there are ethnic variations in indices of arterial stiffness and endothelial dysfunction between SA and European Caucasian (EC) stroke patients, which may underline a poorer prognosis in the former, and further investigated promoters of vessel wall abnormalities. Using a cross-sectional approach, a total of 100 SA stroke survivors were prospectively recruited from the ongoing West Birmingham Stroke Project. Indices of vessel wall characteristics (arterial stiffness and endothelial function [change in reflective index]) were measured noninvasively using the digital volume pulse analysis technique in a temperature-controlled environment, using a direct standardized approach. SA stroke subjects were compared to 60 EC stroke survivors, 60 SA with risk factors, and 73 healthy controls. Among stroke patients, both ethnic groups were comparable for cardiovascular risk profile, except for more diabetes mellitus in SA (P=0.007) subjects and a higher prevalence of atrial fibrillation in EC (P=0.04) subjects. According to the TOAST and Bamford classifications, SA subjects had more small vessel (P=0.04) and lacunar infarctions (P=0.01). SA subjects had higher measurements of arterial stiffness (P<0.001) and impaired endothelial-dependent vascular function (change in reflective index %; P<0.001). On univariate analysis, endothelial function was negatively correlated with fasting plasma glucose (r=-0.4; P<0.001) and total cholesterol level (r=-0.2; P<0.001). On multivariate analysis, glycemic status was independently associated with impaired endothelial function (P=0.008) and increased arterial stiffness (P<0.001) among SA subjects. SA stroke survivors had more small vessel disease-related cerebrovascular events compared to EC subjects. Underlying glycemic status in SA subjects had an adverse impact on the vascular system, leading to abnormal vessel wall characteristics.

Small Vessel Infarcts and Microbleeds Associated with Radiation Exposure

Small Vessel Infarcts and Microbleeds Associated with Radiation Exposure

Diffusion-weighted imaging of encephalopathy related to idiopathic hypereosinophilic syndrome

Encephalopathy related to idiopathic hypereosinophilic syndrome (HES encephalopathy) is a rare (but well-documented) syndrome. Magnetic resonance imaging (MRI) findings of HES encephalopathy, particularly diffusion-weighted images (DWI) findings, have not been reported. We report a case of HES encephalopathy in a 79-year-old male presenting with a focal neurological deficit and cognitive function disorders. Eosinophil number was >20,000/mm 3. Initial DWI revealed multiple high-signal lesions that were clearer than on T2-weighted images. After corticosteroid therapy, symptoms improved and MRI-identified lesions decreased. This is the first report demonstrating DWI findings of HES encephalopathy. We suggest that lesions identified on MRI may be related to a combination of demyelination, inflammation and/or even small-vessel infarction due to local intimal lesions and clotting, secondary to eosinophilic toxicity. Investigation using DWI should therefore be done in patients with HES encephalopathy even if T2-weighted images are normal.

Levels and value of platelet activation markers in different subtypes of acute non-cardio-embolic ischemic stroke

Introduction Platelet activation and its interaction with leukocytes are important in the pathophysiology of ischemic stroke. This study aimed to evaluate the value of platelet activation and platelet-leukocyte interaction in different subtypes of acute, non-cardio-embolic ischemic stroke. Methods Fifty-four patients with acute, non-cardio-embolic ischemic stroke, including 32 small-vessel and 22 large-vessel diseases, were evaluated. Platelet activation markers (CD62P, CD63, and CD40L) and platelet-leukocyte interaction were measured by flow cytometry at different time points (< 48 hours and Days 7, 30, and 90 post-ischemic stroke). Markers were also evaluated in 28 other stroke patients in the convalescent stage (3 to 9 months after acute stroke) and in 28 control subjects. Results Patients with ischemic stroke had significantly increased circulating CD62P, CD63, platelet-monocyte interaction, and platelet-lymphocyte interaction in the acute stage compared with the convalescent stage and control groups. Levels of CD62P and CD63 were significantly higher in the large-vessel disease group than in the small-vessel disease group, and differences in CD62P were significant even at one month. The CD40L level in the poor outcome group was significantly higher than that in the good outcome group. Stroke patients with diabetes mellitus and large-vessel disease were associated with poor outcome. Conclusions Patients with large-vessel cerebral infarction elicit higher platelet activation and platelet-leukocyte interaction compared to small-vessel infarction. Further large scale trials are warranted to evaluate the relationship between platelet activation markers and outcome in stroke patients under different anti-platelet therapies, and to clarify optimal treatment.

The clinical spectrum of freezing of gait in atypical parkinsonism

Freezing of gait (FOG), commonly seen in advanced Parkinson's disease (PD), has been classified as its fifth cardinal feature. However, its presence frequently leads to a misdiagnosis of PD. FOG is actually more common in atypical parkinsonism (AP): including vascular Parkinsonism (VP), progressive supranuclear palsy (PSP), multiple system atrophy (MSA), corticobasal degeneration (CBD), dementia with Lewy bodies (DLB), and higher level gait disorders (HLGDs). VP is the result of multiple small vessel infarcts (lacunar state or Binswanger's disease), particularly involving the frontal, parietal, and basal ganglia regions. Approximately 50% have FOG (often referred to as lower body parkinsonism). FOG is also common in neurodegenerative forms of AP, present in 45-57%. Of these, FOG is present in 53% of PSP, 54% MSA, 54% DLB, 25% CBD, and 40% HLGD. It is generally seen in the late stages. There are two syndromes closely associated with AP that are dominated by FOG; pure akinesia (PA) and primary progressive freezing gait (PPFG). PA is characterized by akinesia of gait (including FOG), writing, and speech. Tremor, rigidity, dementia, and response to levodopa are notably absent. PPFG is defined by early FOG (often the initial feature) that progresses to include postural instability. It is accompanied by bradykinesia, rigidity, postural tremor, dementia, and levodopa unresponsiveness. Both syndromes are heterogeneous but PSP seems to be the most common cause. CBD and DLB can also present as PPFG. FOG is a common feature of AP and although typically occurring late in disease may also be an early symptom.

Single-Nucleotide Polymorphisms of MMP-2 Gene in Stroke Subtypes

Background: Matrix metalloproteinases (MMP) are expressed after ischemic stroke. These proteases are responsible for a higher incidence of hemorrhages, are correlated to size of infarction and influence the effects of recombinant tissue plasminogen activator treatment. We therefore evaluated single nucleotide polymorphisms (SNP) of MMP-2 in different subtypes of stroke patients in an association study using a case-control design. Methods: 197 stroke patients were divided according to modified TOAST criteria (small vessel disease, large vessel disease, hemorrhagic stroke and asymptomatic carotid artery stenosis) and compared to 143 controls. Clinical data like age, sex, risk factors and diagnostic results including MRI or cranial CT scans and ultrasound evaluations of intra- and extracranial arteries were obtained. Genotypes of MMP-2 (12 SNP) were compared to controls and DNA samples were analyzed by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) analysis. Logistic regression analysis was performed for small vessel disease to test for interactions between markers and defined clinical risk factors. Additionally, MMP-2 serum levels obtained in the first 24 h after stroke were measured. Results: From the MMP-2 gene, 5 markers (rs1030868, rs2241145, rs2287074, rs2287076, rs7201) showed a significant association with small vessel infarcts (p < 0.05) and rs7201:g.C was identified as an independent risk factor by multivariable logistic regression analysis. MMP-2 protein levels were significantly lower in this group (174 ± 48 ng/dl) versus controls (214 ± 56 ng/dl). For other stroke subtypes, no significant association with MMP-2 SNP could be found. Conclusion: Our study demonstrates an association of the MMP-2 gene with the development of lacunar stroke, and no association of MMP-2 with other stroke subtypes.

ROSTRAL MIDBRAIN INFARCTION PRODUCING ISOLATED LATEROPULSION

A distinct syndrome characterized by lateropulsion arises from lacunar infarctions of the paramedian tegmentum of the rostral midbrain. Only a few reports are available, and in little more than a handful was the infarct documented with modern imaging techniques. We describe two cases and review the pertinent literature. ### Case reports. #### Patient 1. Over the course of 2 months, a 76-year-old man had several small vessel infarctions in various vascular territories. He had been anticoagulated with warfarin for chronic atrial fibrillation but his International Normalized Ratio was subtherapeutic during his first two hospitalizations for these events. He recovered without neurologic deficit and was discharged after warfarin adjustment and initiation of acetylsalicylic acid. He returned to the hospital 2 weeks later complaining of imbalance. On admission, his blood pressure was 161/74 mm Hg and his heartbeat was irregular at a rate of 78/minute. He was afebrile. Signs of meningeal irritation were absent. He was alert and oriented with fluent language. There were no abnormalities of conjugate gaze or pupil function, cyclotropia or head tilt. Gait and stance were wide based. There was lateropulsion to the left, both sitting and standing. MRI findings are shown in the figure. Duplex ultrasonography of neck vessels and echocardiography were unrevealing. After reversal of anticoagulation, a lumbar puncture was performed (protein 128 mg/dL, glucose 40 mg/dL …

Diagnosis of Lacunar Infarcts within 6 Hours of Onset by Clinical and CT Criteria Versus MRI

The diagnosis of small deep infarcts (SDIs) based on clinical and noncontrast CT findings is often employed to triage stroke patients for emergent endovascular interventions. Few studies have evaluated the accuracy of <6 hours presentation with lacunar clinical syndromes in predicting the presence of a SDI and the absence of large vessel occlusion. Consecutive patients were identified with symptoms suggestive of acute stroke, diffusion-weighted magnetic resonance imaging (DW-MRI) and CT performed within 6 hours of onset, and absence of hemorrhage on imaging. Patients were given a diagnosis of SDI if they met the defined clinical and CT criteria. Diagnoses of large vessel occlusion absent (LVOA) and final diagnoses of SDI versus non-SDI incorporated hyperacute multimodal MRI data. Of 64 patients, 15 were diagnosed as SDI at <6 hours based on clinical/CT criteria. Fourteen of 15 patients (93%) had a final diagnosis of LVOA. Ten of 15 (67%) had a final MR-DWI-confirmed diagnosis of SDI. Clinical/CT diagnosis of SDI showed sensitivity of 44%, specificity 97%, positive predictive value (PPV) 93%, and negative predictive value (NPV) of 61% in predicting LVOA and sensitivity 83%, specificity 90%, PPV 67%, and NPV 96% compared to the final diagnosis of SDI. Most patients incorrectly diagnosed with SDIs harbored small cortical branch infarcts. Diagnoses of SDI <6 hours from symptom onset based on a classic lacunar syndrome and CT criteria show only modest predictive value in predicting the presence of a small-vessel territory infarct but perform fairly well in identifying patients without large-vessel occlusions amenable to endovascular therapy.

Genetic Variant-Associated Endothelial Dysfunction Behind Small-Vessel Cerebral Circulatory Disorders: A New Pathomechanism Behind Common Cerebral Phenotypes

An increasing body of evidence suggests that different genetic factors, such as angiotensin-converting enzyme (ACE) I/D, angiotensin II type-1 receptor (AT1R) A1166C, methylenetetrahydrofolate reductase (MTHFR) C677T and ENOS G894T variants are associated with an endothelial dysfunction (ED). EDs are relatively new phenomena that are presumed to contribute to vasoregulatory malfunctions at the small-vessel level. Ever more clinical observations indicate that the above genetic variants are also associated with cerebral small-vessel disorders. This article reviews the knowledge available on the roles of ED- associated genetic variants in cerebral circulatory disorders, and suggests that EDs can be causative factors for different common cerebral pathologies such as leukoaraiosis or/and small-vessel infarcts. Newly-developed drugs involving phosphodiesterase type-5 inhibitors, which improve the endothelial functions, may comprise a new approach to the treatment and prevention of small-vessel cerebral circulatory disorders.

The combination of homozygous MTHFR 677T and angiotensin II type-1 receptor 1166C variants confers the risk of small-vessel-associated ischemic stroke

Previous studies have suggested that both angiotensin II type-1 receptor (AT1R) 1166C and methylenetetrahydrofolate reductase (MTHFR) 677T variants can have disadvantageous effects on the small-vessel circulation under certain conditions. The purpose of this study was to analyze the possible consequences of the simultaneous distribution of these two genetic variants in different types of ischemic stroke. The genetic and clinical data on 357 ischemic stroke patients and 263 control subjects were analyzed by using univariate and logistic statistical approaches. Neither the MTHFR 677T nor the AT1R 1166C genetic variant alone conferred the risk of any subtype of ischemic stroke. The combination of the homozygous MTHFR 677TT genotype and at least one AT1R 1166C allele occurred more frequently in the ischemic stroke patients (8.68%) than in the controls (4.56%, p < 0.05). Specific subclassification of the patients revealed an accumulation of this combination in small-vessel-associated ischemic stroke (12.2%, p < 0.01); multivariate logistic regression analysis of the data confirmed this association, with an odds ratio of 2.66 (95% confidence interval, 1.28-7.89; p < 0.05). These findings suggest that the combination of these two genetic factors can contribute to the development of small-vessel cerebral infarcts. Although the exact mechanism of action is not known, addition of the unfavourable effects on the endothelial function can be presumed.

Pablo Lavados: improving stroke care in Chile

Pablo Lavados: improving stroke care in Chile

Incidence, case-fatality rate, and prognosis of ischaemic stroke subtypes in a predominantly Hispanic-Mestizo population in Iquique, Chile (PISCIS project): a community-based incidence study

Incidence of ischaemic stroke subtypes, classified by cause, seems to vary between communities. We aimed to prospectively ascertain the incidence of first-ever ischaemic stroke in a predominantly Hispanic-Mestizo population in the northern desertic region of Chile. Between July, 2000, and June, 2002, all patients with possible stroke or transient ischaemic attacks were identified from multiple overlapping sources and were rapidly assessed by two field neurologists. All identified patients were diagnosed by at least two stroke neurologists according to Trial of Org 10172 in Acute Stroke Treatment (TOAST) definitions and were followed up at 6 months. Annual incidence rates were age adjusted to WHO, European, and US populations by the direct method to allow comparisons. A total of 239 ischaemic strokes were identified, of which 185 (77%) were first-ever cases. 151 (82%) patients were hospitalised, of whom only 70 (38%) were assessed within 6 h of symptom onset. The mean age of patients was 66.4 years (SD 14.9) and 56% were men. The crude annual incidence rates (per 100 000) according to stroke subtype were: cardioembolic, 9.3; large-artery disease, 2.0; small-vessel disease, 15.8; other determined cause, 0.2; and undetermined cause, 17.4. Hypertension was the most common cardiovascular risk factor in all subtypes and atrial fibrillation was the most common cause of cardioembolic stroke. Case fatality at 30 days was highest in cardioembolic strokes (28%) and lowest in small-vessel disease (0%). Dependency or death at 6 months was also highest in cardioembolic strokes (62%) and lowest in small-vessel disease (21%). Incidence and prognosis of small vessel and cardioembolic infarction was similar to that in other populations and incidence of large-artery atherothrombotic infarction was lower than in most previous reports. Hypertension and atrial fibrillation were the most common risk factor and cause, respectively, of ischemic stroke in this population. These findings should help the national stroke programme in the prevention of cardioembolic stroke, increase access to specialists and acute brain imaging and vascular studies, and improve stroke care.

Intracranial carotid artery calcification on head CT and its association with ischemic changes on brain MRI in patients presenting with stroke-like symptoms: retrospective analysis

Our purpose was to study the association between the intracranial arterial calcifications observed on head CT and brain infarcts demonstrated by MRI in patients presenting with acute stroke symptoms. Institutional review board approval was obtained for this retrospective study which included 65 consecutive patients presenting acutely who had both head CT and MRI. Arterial calcifications of the vertebrobasilar system and the intracranial cavernous carotid arteries (intracranial carotid artery calcification, ICAC) were assigned a number (1 to 4) in the bone window images from CT scans. These four groups were then combined into high calcium (grades 3 and 4) and low calcium (grades 1 and 2) subgroups. Brain MRI was independently evaluated to identify acute and chronic large-vessel infarcts (LVI) and small-vessel infarcts (SVI). The relationship between ICAC and infarcts was evaluated before and after adjusting for demographics and cardiovascular risk factors. Statistical analysis could not be performed for the vertebrobasilar system due to an insufficient number of patients in the high calcium group. Of the 65 patients, 46 (71%) had a high ICAC grade on head CT. They were older and had a higher prevalence of cardiovascular risk factors. Acute SVI (P = 0.006), chronic SVI (P = 0.006) and acute LVI (P = 0.04) were associated with a high ICAC grade. After adjustment for age and other risk factors, only acute SVI was associated with a high ICAC grade (P = 0.002). Although age emerged as the most important determinant of ischemic cerebral changes, there were rather complex interactions among multiple risk factors with different infarct types. A high ICAC grade demonstrated a correlation with acute SVI in our patients independent of these risk factors.

Is 15 mm Size Criterion for Lacunar Infarction Still Valid? A Study on Strictly Subcortical Middle Cerebral Artery Territory Infarction Using Diffusion-Weighted MRI

Background and Purpose: The ‘lacunar hypothesis’ has been challenged, since small (diameter <15 mm) subcortical infarcts can be produced by middle cerebral artery disease (MCAD) or cardioembolism (CE), while a larger infarct can occur without evidence of MCAD or CE. We sought to assess whether the lacunar hypothesis based on size is still valid. Methods: We studied 118 patients who were admitted within 72 h after stroke onset and had acute deep subcortical MCA territory infarcts detected by diffusion-weighted MRI, and who had undergone angiography (mostly MR angiography). Stroke mechanisms were arbitrarily categorized regardless of lesion size: (1) MCAD when there was a corresponding MCA lesion; (2) internal carotid artery disease (ICAD) when there was a significant (>50%) ipsilateral ICAD; (3) CE when there was emboligenic heart disease without MCAD or ICAD, and (4) small vessel disease (SVD) when there was neither CE nor MCAD. SVD was further divided into definite SVD (dSVD, longest diameter <15 mm) or probable SVD (pSVD, longest diameter ≧15 mm). Results: Seventy-three patients (62%) had SVD, of which 38 (32%) had pSVD and 35 (30%) dSVD. Thirty-three patients (28%) had MCAD, five (4%) CE, and seven (6%) ICAD. The infarct diameter in MCAD was not larger than in SVD (p = 0.35), and there was no difference in clinical features or risk factors between MCAD and SVD, or between pSVD and dSVD. CE was distinguished from SVD by its larger size and cortical symptoms. Conclusions: There are no clinical and lesion-size differences between MCAD and SVD, suggesting that there seems to be no rationale for the 15 mm size criterion for lacunar or small-vessel infarction.

Type of stroke after transient monocular blindness or retinal infarction of presumed arterial origin

Background: Retinal infarction and transient monocular blindness (TMB) are associated with an increased risk of future ischaemic stroke. Little information is available on the type of subsequent ischaemic strokes that may occur (anterior or posterior circulation and small vessel or large vessel). Aim: To analyse the type of stroke after TMB. Methods: Patients with transient or permanent retinal ischaemia were selected from three prospective studies: the Dutch TIA Trial, the Dutch Amaurosis Fugax Study and the European/Australian Stroke Prevention in Reversible Ischaemia Trial. On follow-up the type of stroke was classified according to the supply territory and the type of vessel involved. Results: 654 patients were included. During a mean follow-up of 5.2 years, 42 patients were found to have had a cerebral or retinal infarct, of which 27 occurred in the carotid territory ipsilateral to the symptomatic eye, 9 in the territory of the contralateral carotid artery and 6 were infratentorial strokes. Thirty patients had a large-vessel infarct, four had a small-vessel infarct and eight had a retinal infarct. Characteristics associated with a notable increased risk for subsequent stroke or retinal infarction were age ⩾65 years, a history of stroke, a history of intermittent claudication, diabetes mellitus, Rankin score ⩾3, more than three attacks of retinal ischaemia and any degree of ipsilateral carotid stenosis on duplex ultrasonography observation. Conclusion: Ischaemic strokes after TMB or retinal infarction were found to be mainly large-vessel infarcts in the territory of the ipsilateral carotid artery. TMB and retinal infarction are probably manifestations of large-vessel disease.

Type of stroke after transient monocular blindness or retinal infarction of presumed arterial origin

Background: Retinal infarction and transient monocular blindness (TMB) are associated with an increased risk of future ischaemic stroke. Little information is available on the type of subsequent ischaemic strokes that...

Angiotensin II type-1 receptor A1166C polymorphism is associated with increased risk of ischemic stroke in hypertensive smokers.

Recent observations revealed a novel role of angiotensin-converting enzyme 2 and the angiotensin II type-1 receptor (AT1R) in lung injury, thereby extending knowledge about the functions of the angiotensin system. Angiotensin II, whose target is the AT1R, is a potent vasoconstrictor. Accordingly, an imbalance leading to enhanced activity of the angiotensin II-AT1R axis is postulated to contribute to both circulatory disturbances and lung injury. In this context, a functional single-nucleotide polymorphism, AT1R A1166C, which leads to enhanced responsiveness of the AT1R, has been postulated as a candidate susceptibility factor for ischemic stroke. The aim of our study was to investigate its occurrence in ischemic stroke and to analyze its possible synergistic associations with clinical risk factors. Genetic and clinical data on 308 consecutive patients with acutely developing ischemic stroke were analyzed. A total of 272 stroke and neuroimaging alteration-free subjects served as a control group. Univariate and logistic regression statistical approaches were used. Alone, the AT1R 1166C allele did not pose a risk of stroke. In hypertensive smokers, however, it was associated with an increased risk of ischemic stroke (OR 22.3, 95% CI 5.8–110.2, p<0.001). Further subgroup analysis revealed the same association for both small-vessel (OR 24.3, 95% CI 6.1–121.1, p<0.001) and large-vessel (OR 21.3, 95% CI 4.6–81.1, p<0.001) infarction. On a pathophysiological basis, our results suggest the possibility that the AT1R A1166C polymorphism might give rise to ischemic stroke indirectly via an unfavorable effect on the cardiorespiratory function.

Stroke Etiology among Haitians Living in Miami

The black Caribbean population continues to grow in the US and little is known about stroke etiologies in that community. We examined stroke subtypes in 175 consecutive Haitian-born patients living in Miami, admitted for acute stroke. Ischemic stroke was diagnosed in 72%. Small vessel occlusion was the most frequent stroke subtype. There was a high prevalence of hypertension, medication noncompliance and intracranial atherosclerosis. Hypertension was the only cardiovascular risk factor significantly associated with small vessel infarction when compared with non-small vessel infarcts.