Silent and clinically overt stroke in older Japanese subjects with white-coat and sustained hypertension.

OBJECTIVES: We investigated whether white-coat hypertension is a risk factor for stroke in relation to silent cerebral infarct (SCI) in an older Japanese population. BACKGROUND: It remains uncertain whether white-coat hypertension in older subjects is a benign condition or is associated with an increased risk of stroke. METHODS: We studied the prognosis for stroke in 958 older Japanese subjects (147 normotensives [NT], 236 white-coat hypertensives [WCHT] and 575 sustained hypertensives [SHT]) in whom ambulatory blood pressure monitoring was performed in the absence of antihypertensive treatment. In 585 subjects (61%), we also assessed SCI using brain magnetic resonance imaging. RESULTS: Silent cerebral infarcts were found in 36% of NT (n = 70), 42% of WCHT (n = 154), and 53% of SHT (n = 361); multiple SCIs (the presence of > or =2 SCIs) were found in 24% of NT, 25% of WCHT and 39% of SHT. During a mean 42-month follow-up period, clinically overt strokes occurred in 62 subjects (NT: three [2.0%]; WCHT: five [2.1%]; SHT: 54 [9.4%]), with 14 fatal cases (NT: one [0.7%]; WCHT: 0 [0%]; SHT: 13 [2.3%]). A Cox regression analysis showed that age (p = 0.0001) and SHT (relative risk, [RR] [95% confidence interval, CI]: 4.3 [1.3-14.2], p = 0.018) were independent stroke predictors, whereas WCHT was not significant. When we added presence/absence of SCI at baseline into this model, the RR (95% CI) for SCI was 4.6 (2.0-10.5) (p = 0.003) and that of SHT was 5.5 (1.8-18.9) versus WCHT (p = 0.004) and 3.8 (0.88-16.7) versus NT (p = 0.07). CONCLUSIONS: In older subjects the incidence of stroke in WCHT is similar to that of NT and one-fourth the risk in SHT. Although SCI is a strong predictor of stroke, the difference in stroke prognosis between SHT and WCHT was independent of SCI. It is clinically important to distinguish WCHT from SHT even after assessment of target organ damage in the elderly.     

Subclinical arterial damage in untreated masked hypertensive subjects detected by home blood pressure measurement

BACKGROUND: Masked hypertension (MHT: normal office blood pressure [BP] + elevated BP out of the office) is a significant predictor of target organ damage and cardiovascular disease. The purpose of this study was to investigate the subclinical arterial damage in unmedicated subjects with MHT detected by home BP measurement. METHODS: We recruited 282 subjects not taking antihypertensive medication, who had at least one of the following five cardiovascular risk factors: high BP, hyperlipidemia, diabetes mellitus, current smoking, and chronic kidney disease. Furthermore, we classified them into four groups (normotension [NT], white-coat hypertension [WCHT], MHT, and sustained hypertension [SHT]) by office BP (140/90 mm Hg) and home BP (135/85 mm Hg) measurements. Arterial damage was evaluated by measuring carotid intima-media thickness (IMT) and brachial-ankle pulse wave velocity (baPWV). RESULTS: Subjects with MHT had a higher prevalence of habitual alcohol drinkers than the other groups, and higher pulse rates at home than those with NT and WCHT. After adjustment for covariates, carotid IMT was the highest in MHT among the four groups (mean: 1.01 v 0.83 mm for NT, 0.86 mm for WCHT, and 0.91 mm for SHT, all P < .01). The baPWV was also significantly higher in MHT than NT and WCHT (mean: 1940 v 1663 and 1733 cm/sec, all P < .01), whereas the difference between MHT and SHT (2023 cm/sec) was not significant. CONCLUSIONS: This study shows that masked hypertensives detected by home BP are at higher risk for increased arterial damage than normotensives or white-coat hypertensives, and potentially than sustained hypertensives.     

Relationship between aortic stiffness and cardiovascular risk factors in a population of normotensives, white-coat normotensives, white-coat hypertensives, sustained hypertensives and diabetic patients.

OBJECTIVE: To evaluate the relationship between carotid-femoral pulse wave velocity (PWV) and office and ambulatory blood pressure (ABP) and other cardiovascular risk factors and to determine the discriminatory value of PWV in a large population including normotensive subjects (NT), white-coat normotensives (masked hypertension) (WCNT), and white-coat hypertensives (WCHT) compared to a group of treated and untreated hypertensive patients. METHODS: The study population included a total of 688 subjects aged from 18 to 80 years, with no previous cardiovascular events, who underwent 24 h ABP monitoring, biochemical evaluation and determination of PWV and left ventricular mass index (LVMI). Subjects were classified as true normotensives (NT, n=132; normal office and ABP values), WCNT (n=39; office BP < 140/90 and daytime BP > or =135 or > or =85 mmHg), WCHT (n=87; office BP > or =140 or > or =90 and daytime BP < 135/85 mmHg). Untreated (UT-HT, n=154) and treated (T-HT, n=171) hypertensive patients and type 2 diabetic patients (DM, n=102) were also studied. RESULTS: Values of PWV (m/s) in all groups were, in ascending order: NT (8.9 +/- 0.2) < WCHT (9.9 +/- 0.2) < T-HT (11.4 +/- 0.2) = WCNT (11.5 +/- 0.4) < UT-HT (11.9 +/- 0.3) < DM (12.6 +/- 0.4) (ANOVA, p = 0.043), and of LVMI (g/m2): NT (59 +/- 2) = WCHT (63 +/- 2) < WCNT (73 +/- 3) = T-HT (75 +/- 3) = UT-HT (77 +/- 3) < DM (84 +/- 4) (ANOVA, p < 0.05). The percentage of subjects with PWV values below the median (10.7 m/s) was higher (p < 0.02) in NT (81.8%) and WCHT (72.6%) than in UT-HT (49.2%), T-HT (43.6%), WCNT (47.6%) and DM (27.7%). In multiple regression analysis, taking PWV as the dependent variable, age (all groups), 24h systolic BP (UT-HT, T-HT, WCNT and DM) and 24h diastolic BP (NT and WCHT) were the variables that independently influenced the PWV value. CONCLUSIONS: Higher values of PWV occur in clinical situations associated with higher cardiovascular risk. This is in agreement with risk stratification based on ABP values but not on office BP values. Lower PWV and LVMI values occur in NT and WCHT subjects, supporting a low cardiovascular risk in these groups. By contrast, higher PWV values were associated with higher ABP values in DM, hypertensive patients and white-coat normotensives, i.e. clinical situations that are associated with higher cardiovascular risk, who in the present study also exhibited higher LVMI than subjects with normal ABP values.     

Blood pressure on arising, morning blood pressure surge and blood pressure variability in white coat hypertensives and in matched normotensives and sustained hypertensives.

INTRODUCTION: It is still controversial whether subjects with white-coat hypertension (WCHT) exhibit higher cardiovascular risk compared to normotensive subjects (NT). In subjects with WCHT it is not known whether the abnormal blood pressure (BP) reaction in the office also occurs at other times of day, particularly on arising and immediately after waking, i.e. the times at which the majority of cardiovascular events are reported to occur. OBJECTIVE AND METHODS: To evaluate with 24h ambulatory BP measurement the values of morning BP surge, BP on arising and BP variability in subjects with WCHT in comparison with age-, gender- and weight-matched normotensives (BP) and untreated sustained hypertensives (BP). RESULTS: Groups of BP, WCHT and BP were matched for age, gender and body weight: BP: n=69, age 49 +/- 7 years, 54 % female, BMI 26 +/- 1, casual BP 126/79 +/- 5/4 mmHg, daytime BP 124/80 +/- 6/6 mmHg; WCHT: n=74, age 52 +/- 8 years, 57% female, BMI 26 +/- 2, casual BP 152/95 +/- 7/7 mmHg, daytime BP 126/80 +/- 5/6 mmHg; HT: n=79, age 53 +/- 7 years, 56% female, BMI 27 +/- 2, casual BP 154/97 +/- 9/8 mmHg, daytime BP 143/89 +/- 12/10 mmHg. Of the three groups, subjects with WCHT exhibited BP on arising (121/81 +/- 13/8 mmHg) similar to that of NTs (120/80 +/- 13/9 mmHg, NS), both significantly lower than that of HTs (137/92 +/- 17/10 mmHg, p < 0.01), suggesting the absence of an alerting BP reaction in WCHT at that time. By contrast, subjects with WCHT showed higher values of systolic morning BP surge vs. NTs (25 +/- 10 vs. 22 +/- 11 mmHg, p < 0.05), both lower than that observed in hypertensives (33 +/- 11 mmHg, p < 0.01 vs. NT and WCHT) and greater daytime variability (systolic BP standard variation), i.e. 12 2 vs. 10 +/- 2 mmHg, p < 0.05, both lower than that observed in hypertensives (14 +/- 3 mmHg, p < 0.01 vs. NT and WCHT). CONCLUSIONS: Although subjects with WCHT did not show any alerting blood pressure reaction on arising, morning BP surge and BP variability were greater in these subjects than in control normotensives, although lower than sustained hypertensives. Although this is still speculative, we cannot exclude the possibility that even a slight increase in morning BP surge might in the long term constitute an additional load on the circulation that could increase cardiovascular risk in subjects with WCHT compared to matched normotensives.     

Deep white matter lesions on MRI, and not silent brain infarcts are related to headache and dizziness of non-specific cause in non-stroke Japanese subjects

OBJECTIVE: Silent or asymptomatic cerebrovascular disease is believed to be an important risk factor for symptomatic stroke and vascular dementia. Although non-specific complaints such as mild to moderate headache and/or dizziness may also be caused by silent stroke, which remains a topic of controversy. METHODS: To investigate the relationship between silent brain infarcts and non-specific complaints, we assessed findings on magnetic resonance images using a common protocol in the following three groups of subjects; Group 1:78 subjects with non-specific complaints, Group 2:47 subjects with vascular risk factors, and Group 3:75 normal subjects without any subjective complaints or vascular risk factors. In addition to silent stroke, deep white matter lesions on MRI were also evaluated. All subjects were recruited from 12 institutes of the study group located at various parts of Japan. RESULTS: Silent brain infarcts were demonstrated in 44%, 43%, and 20% of subjects in Groups 1, 2, and 3, respectively. In Group 1, the average number of infarcts per individual who had silent brain infarction was 1.8, which was significantly fewer than 3.8 in Group 2 or 3.5 in Group 3 (p<0.0167). White matter lesions were found in 68%, 49%, and 11% in Groups 1, 2, and 3, respectively, indicating that non-specific complaints are more closely related to deep white matter lesions than to silent infarct lesions. Such white matter lesions were found more frequently in subjects with depressive state than in non-depressed subjects (67% vs. 39%, p=0.0155). CONCLUSION: The present results suggest that deep white matter lesions, rather than silent brain infarcts, appear to be important in producing headache and/or dizziness of non-specific cause and also to be related to the depressive state.     

Longitudinal changes in brain magnetic resonance imaging findings in children with sickle cell disease

Children with sickle cell anemia (HbSS) are at high risk for neurologically overt cerebral infarcts associated with stroke and neurologically silent cerebral infarcts correlated with neuropsychometric deficit. We used complete magnetic resonance imaging (MRI) histories from 266 HbSS children, aged 6 through 19 years, who were enrolled in the Cooperative Study of Sickle Cell Disease (CSSCD) to examine silent infarct prevalence, localization, recurrence, and progression. We report a baseline prevalence of 21.8%, marginally higher than previously reported due to improved imaging technologies. Although we observed no overall sex difference in prevalence, most lesions in girls occurred before age 6, whereas boys remained at risk until age 10. Silent infarcts were significantly smaller and less likely to be found in the frontal or parietal cortex than were infarcts associated with stroke. Children with silent infarct had an increased incidence of new stroke (1.03/100 patient-years) and new or more extensive silent infarct (7.06/100 patient-years) relative to stroke incidence among all children in our cohort (0.54/100 patient-years). Both events were substantially less frequent than the risk of stroke recurrence among children not provided chronic transfusion therapy. Although chronic transfusion is known to decrease occurrence of new silent infarcts and strokes in children with elevated cerebral arterial blood flow velocity, further study is required to determine its risk-benefit ratio in children with silent infarct and normal velocities. Until safe and effective preventive strategies against infarct recurrence are discovered, MRI studies are best reserved for children with neurologic symptoms, neuropsychometric deficits, or elevated cerebral artery velocities.     

Silent cerebral infarction: a potential risk for pneumonia in the elderly

OBJECTIVE: To determine whether patients who have silent cerebral infarction are more likely to develop pneumonia than are controls without silent cerebral infarction. DESIGN: We examined 269 community-residing participants of the senior day-care centre without history of previous stroke, and then followed them over a two-year period to assess pneumonia. On the basis of computerized tomography scans, they were divided into two groups: no infarction (n = 102) and cerebral hemispheric infarction (n = 167). Cerebral infarcts were further divided into deep and superficial infarcts. RESULTS: The incidence of pneumonia was significantly higher in subjects with silent cerebral infarction (19.8%) than in controls (4. 9%) (odds ratio, 4.67 [95% CI, 1.87-11.67]; P < 0.01). Deep infarcts were more closely associated with the incidence of pneumonia (29.1%) than superficial infarcts (7.6%) (odds ratio, 5.00 [CI, 1.91-13.08]; P < 0.01). CONCLUSIONS: Elderly subjects with silent cerebral infarction were more likely to develop pneumonia than were controls without silent cerebral infarction. Amongst hemispheric silent cerebral infarcts, those located in the deep brain structures may be an important predictor of the development of pneumonia.     

Prognosis of "masked" hypertension and "white-coat" hypertension detected by 24-h ambulatory blood pressure monitoring 10-year follow-up from the Ohasama study

OBJECTIVES: We sought to investigate the prognosis in subjects with "white-coat" hypertension (WCHT) and "masked" hypertension (MHT), in which blood pressure (BP) is lower in clinical measurements than during ambulatory monitoring. BACKGROUND: The prognostic significance of WCHT remains controversial, and little is known about MHT. METHODS: We obtained 24-h ambulatory BP and "casual" BP (i.e., obtained in clinical scenarios) values from 1,332 subjects (872 women, 460 men) > or =40 years old in a representative sample of the general population of a Japanese community. Survival and stroke morbidity were then followed up for a mean duration of 10 years. RESULTS: Composite risk of cardiovascular mortality and stroke morbidity examined using a Cox proportional hazards regression model for subjects with WCHT (casual BP > or =140/90 mm Hg, daytime BP <135/85 mm Hg; relative hazards [RH])1.28; 95% confidence interval [CI] 0.76 to 2.14) was no different from risk for subjects with sustained normal BP (casual BP <140/90 mm Hg, daytime BP <135/85 mm Hg). However, risk was significantly higher for subjects with MHT (casual BP <140/90 mm Hg, daytime BP > or =135/85 mm Hg; RH 2.13; 95% CI 1.38 to 3.29) or sustained hypertension (casual BP > or =140/90 mm Hg, daytime BP > or =135/85 mm Hg; RH 2.26; 95% CI 1.49 to 3.41) than for subjects with sustained normal BP. Similar findings were observed for cardiovascular mortality and stroke morbidity among subgroups by gender, use of antihypertensive medication, and risk factor level (all p for heterogeneity >0.2). CONCLUSIONS: Conventional BP measurements may not identify some individuals at high or low risk, but these people may be identifiable by the use of ambulatory BP.     

U-curve relationship between orthostatic blood pressure change and silent cerebrovascular disease in elderly hypertensives: orthostatic hypertension as a new cardiovascular risk factor

OBJECTIVES: The study investigated the clinical significance and mechanism of orthostatic blood pressure (BP) dysregulation in elderly hypertensive patients. BACKGROUND: Although orthostatic hypotension (OHYPO), often found in elderly hypertensive patients, has been recognized as a risk factor for syncope and cardiovascular disease, both the clinical significance and the mechanism of orthostatic hypertension (OHT) remain unclear. METHODS: We performed a head-up tilting test and brain magnetic resonance imaging (MRI) in 241 elderly subjects with sustained hypertension as indicated by ambulatory BP monitoring. We classified the patients into an OHT group with orthostatic increase of systolic blood pressure (SBP) of >or=20 mm Hg (n = 26), an OHYPO group with orthostatic SBP decrease of >or=20 mm Hg (n = 23), and a normal group with neither of these two patterns (n = 192). RESULTS: Silent cerebral infarcts were more common in the OHT (3.4/person, p < 0.0001) and OHYPO groups (2.7/person, p = 0.04) than in the normal group (1.4/person). Morning SBP was higher in the OHT group than in the normal group (159 vs. 149 mm Hg, p = 0.007), while there were no significant differences of these ambulatory BPs between the two groups during other periods. The OHT (21 mm Hg, p < 0.0001) and OHYPO (20 mm Hg, p = 0.01) groups had higher BP variability (standard deviation of awake SBP) than the normal group (17 mm Hg). The associations between orthostatic BP change and silent cerebrovascular disease remained significant after controlling for confounders, including ambulatory BP. The orthostatic BP increase was selectively abolished by alpha-adrenergic blocking, indicating that alpha-adrenergic activity is the predominant pathophysiologic mechanism of OHT. CONCLUSIONS: Silent cerebrovascular disease is advanced in elderly hypertensives having OHT. Elderly hypertensives with OHT or OHYPO may have an elevated risk of developing hypertensive cerebrovascular disease.     

Greater change of orthostatic blood pressure is related to silent cerebral infarct and cardiac overload in hypertensive subjects.

Greater change of postural blood pressure (BP) is often seen in elderly hypertensives and is recognized as a risk factor for cognitive decline and poorer cerebrovascular outcome, but its clinical significance still remains to be clarified. We performed a head-up tilting test, ambulatory BP monitoring, and brain MRI in 59 hypertensives and 27 normotensive subjects. We measured plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) levels at rest to assess cardiac burden. The 59 hypertensive patients were classified into 3 groups: an orthostatic hypertension (OHT) group with orthostatic increase in systolic BP (SBP) > or = 10 mmHg (n=16); an orthostatic hypotension (OHYPO) group with orthostatic SBP decrease < or = -10 mmHg (n=18); and an orthostatic normotension (ONT) group with neither of these two patterns (n=25). A group of 27 normotensive subjects (NT) was also included as a control. Plasma BNP (72 +/- 92 vs. 29 +/- 24 pg/ml, p < 0.05) and BNP/ANP ratio (4.6 +/- 3.3 vs. 2.4 +/- 1.5, p < 0.05) were significantly higher in the OHYPO than in the NT group. The BNP/ANP ratio was also higher in the OHT than in the NT group (5.1 +/- 3.9 vs. 2.4 +/- 1.5, p < 0.01). The number of silent cerebral infarct (SCI), prevalence of SCI and number of multiple SCIs was the highest in the OHT group, followed in order by the OHYPO, ONT and NT groups. Blood pressure and left ventricular mass index were not significantly different among the 3 hypertensive groups. In conclusion, hypertensive patients with greater change of postural BP (OHT and OHYPO) were shown to have increased risk of advanced silent brain lesions and greater cardiac burden.     

Silent cerebral infarcts in basal ganglia are advanced in congenital protein C-deficient heterozygotes with hypertension

Congenital protein C deficiency is now widely recognized as a genetic risk for venous thrombosis. However, it remains uncertain whether this condition also confers risk for arterial thrombosis. We evaluated the association of congenital protein C deficiency with hypertension and silent cerebrovascular disease using brain magnetic resonance imaging (MRI) (T1- and T2-weighted and proton density images) in a large family pedigree of protein C deficiency diagnosed by gene analysis, compared with 46 non-pedigree related control subjects with normal protein C levels (≥ 75%) who were selected from among 55 asymptomatic hypertensive subjects matched for age and cardiovascular risk factors. Of the 58 living subjects in this pedigree, we measured plasma protein C levels in 45 subjects, and found 2 cerebral infarctions in the 24 heterozygotic subjects, whereas there was no stroke in the 21 normal homozygotic subjects. We performed brain MRI in 14 asymptomatic hypertensive subjects without any cardiovascular disease and in two patients with cerebral infarction, and found 28 cerebral infarcts (two corresponded to the patient neurologic deficits and 26 were silent). All were lacunar infarcts < 10 cm in size. A total of 25 silent lacunar infarcts were found in nine heterozygotic subjects, whereas only one was found in the seven normal homozygotic subjects (2.8 v 0.14 lacunes per person, P = .002). No advanced white matter hyperintense lesions in T2-weighted images were found in either group. The prevalence of silent lacunar infarcts in the heterozygotic subjects was also significantly higher than that in normal control subjects (1.0 per person, P = .01). Concerning the distribution of silent infarcts, the number of lacunes located in the basal ganglia was higher in the heterozygotic subjects (2.3 per person, P < .001) than in the seven normal homozygotic subjects (0.14 per person) or in the control group (0.28 per person), whereas the number of lacunes in the white matter was not different among the groups. In conclusion, congenital protein C deficiency may accelerate the progression of silent cerebral infarct formation in hypertension, particularly in the basal ganglia, and may be a potential risk for stroke or vascularly induced dementia.     

Prevalence and clinical outcomes of white‐coat and masked hypertension: Analysis of a large ambulatory blood pressure database

The aim of this study was to analyze prevalence and clinical outcomes of the following clinical conditions: normotension (NT; clinic BP < 140/90 mm Hg; 24‐hour BP < 130/80 mm Hg), white‐coat hypertension (WCHT; clinic BP ≥ 140 and/or ≥90 mm Hg; 24‐hour BP < 130/80 mm Hg), masked hypertension (MHT; clinic BP < 140/90 mm Hg; 24‐hour BP ≥ 130 and/or ≥80 mm Hg), and sustained hypertension (SHT; clinic BP ≥ 140 and/or ≥90 mm Hg; 24‐hour BP ≥ 130 and/or ≥80 mm Hg) in a large cohort of adult untreated individuals. Systematic research throughout the medical database of Regione Lazio (Italy) was performed to estimate incidence of myocardial infarction (MI), stroke, and hospitalizations for HT and heart failure (HF). Among a total study sample of 2209 outpatients, 377 (17.1%) had NT, 351 (15.9%) had WCHT, 149 (6.7%) had MHT, and 1332 had (60.3%) SHT. During an average follow‐up of 120.1 ± 73.9 months, WCHT was associated with increased risk of hospitalization for HT (OR 95% CI: 1.927 [1.233‐3.013]; P = .04) and HF (OR 95% CI: 3.449 [1.321‐9.007]; P = .011). MHT was associated with an increased risk of MI (OR 95% CI: 5.062 [2.218‐11.550]; P < .001), hospitalization for HT (OR 95% CI: 2.553 [1.446‐4.508]; P = .001), and for HF (OR 95% CI: 4.214 [1.449‐12.249]; P = .008). These effects remained statistically significant event after corrections for confounding factors including age, BMI, gender, smoking, dyslipidaemia, diabetes, and presence of antihypertensive therapies.     

Silent cerebral infarcts occur despite regular blood transfusion therapy after first strokes in children with sickle cell disease

Children with sickle cell disease (SCD) and strokes receive blood transfusion therapy for secondary stroke prevention; despite this, approximately 20% experience second overt strokes. Given this rate of second overt strokes and the clinical significance of silent cerebral infarcts, we tested the hypothesis that silent cerebral infarcts occur among children with SCD being transfused for secondary stroke prevention. A prospective cohort enrolled children with SCD and overt strokes at 7 academic centers. Magnetic resonance imaging and magnetic resonance angiography of the brain were scheduled approximately every 1 to 2 years; studies were reviewed by a panel of neuroradiologists. Eligibility criteria included regularly scheduled blood transfusion therapy. Forty children were included; mean pretransfusion hemoglobin S concentration was 29%. Progressive cerebral infarcts occurred in 45% (18 of 40 children) while receiving chronic blood transfusion therapy; 7 had second overt strokes and 11 had new silent cerebral infarcts. Worsening cerebral vasculopathy was associated with new cerebral infarction (overt or silent; relative risk = 12.7; 95% confidence interval, 2.65-60.5, P = .001). Children with SCD and overt strokes receiving regular blood transfusion therapy experience silent cerebral infarcts at a higher rate than previously recognized. Additional therapies are needed for secondary stroke prevention in children with SCD.     

Short sleep duration is an independent predictor of stroke events in elderly hypertensive patients

Data relating habitual sleep duration to the risk of silent or overt stroke are sparse. We tested the hypothesis that short duration of sleep is associated with increased risk of silent cerebral infarct (SCI) and stroke events in hypertensive patients. We performed ambulatory BP monitoring in 1268 hypertensives (mean age: 70.4 years) and followed them for 50 months. Brain MRI was performed in 932 of these subjects for the assessment of SCI, and these subjects were analyzed in this study. Cox proportional hazard models were used to calculate the hazard ratios (HR) of sleep-duration-associated risk for cardiovascular events while controlling for significant covariates. In multivariable Cox regression analysis, a sleep duration <7.5 h was independently associated with the risk of stroke (HR = 2.21; P = 0.003). The presence of SCI was also associated with stroke events (HR = 2.60; P = 0.005). When the subjects were divided into an SCI(+) group and SCI(?) group, the short sleep duration was a significant predictor for incident stroke only in the SCI(+) group (HR = 2.52; P = 0.001). Shorter sleep duration was an independent risk for future incidence of stroke events in hypertensive patients, especially those with SCIs.     

急性皮质下小梗死的影像学特征：大动脉粥样硬化性与小动脉病变性卒中的比较

目的 探讨大动脉粥样硬化与小动脉病变所致皮质下小梗死（small subcortical infarction,SSI）的影像学差异。方法连续住院的急性SSI患者根据循证缺血性卒中病因分型（SSS- TOAST）标准分为大动脉粥样硬化性卒中组和小动脉闭塞性卒中组,比较其影像学特征。结果共 纳入118例急性SSI...     

Hyperinsulinemia and hemostatic abnormalities are associated with silent lacunar cerebral infarcts in elderly hypertensive subjects.

OBJECTIVES: We sought to study the association of the silent cerebral infarct (SCI), a predisposing condition of stroke, with hyperinsulinemia and hemostatic abnormalities in older hypertensive subjects. BACKGROUND: Hypertension is a powerful risk factor for stroke. However, the role of other risk factors for stroke in hypertensive subjects remains incompletely understood. METHODS: We performed brain magnetic resonance imaging and measured cardiovascular risk factors, by administering the 75-g oral glucose tolerance test and measuring plasma insulin and hemostatic variables, in 123 asymptomatic hypertensive subjects (mean age 69 years). RESULTS: At least one SCI was detected in 80 subjects (65%), and multiple SCIs were found in 48 subjects (39%). The presence of SCIs was associated with older age, higher levels of 24-h systolic blood pressure, 2-h insulin, thrombin-generation markers (prothrombin fragment 1+2 and thrombin-antithrombin complexes), plasminogen activator inhibitor-1 (PAI-1), D-dimer and von Willebrand factor (vWF), but not with plasmin-alpha2-plasmin complex (PIC) levels. The 2-h insulin area under the curve (AUC) was positively correlated with PAI-1 and vWF levels (p < 0.01), and the PAI-1 level was negatively correlated with the PIC level (p < 0.02). Multiple logistic regression analysis revealed that age and the 2-h insulin AUC were significantly associated with SCIs, particularly those located in the subcortical white matter, and hemostatic abnormalities were significantly associated with the presence of multiple SCIs, particularly those located in the basal ganglia. CONCLUSIONS: In older asymptomatic hypertensive subjects, hyperinsulinemia appears to be associated with lacunar-type SCIs, particularly those located in the subcortical white matter, and hemostatic abnormalities show an association with the presence of multiple SCIs, particularly those located in the basal ganglia.     

Carotid plaque echogenicity and types of silent CT-brain infarcts. Is there an association in patients with asymptomatic carotid stenosis?

BACKGROUND: The aim of this study was to identify the differences in echogenicity and the degree of stenosis of asymptomatic carotid plaques associated with different types of ipsilateral silent CT-brain infarcts. METHODS: Some 273 asymptomatic carotid plaques (218 patients) causing 50 to 99% stenosis were studied with high-resolution ultrasound. B-mode images were digitised and normalised by assigning certain grey values to blood and adventitia. The grey scale median (GSM) of the plaque in the normalised image was used to quantify echogenicity. Every patient had a CT-brain scan which an independent neuroradiologist read. The presence of 1) non-lacunar and 2) lacunar silent CT-brain infarcts ipsilateral to the carotid plaque was noted. RESULTS: The mean GSM of plaques associated with non-lacunar silent CT-brain infarcts was 19.6, of plaques associated with lacunar infarcts was 35.5 and of those associated with no infarcts was 32 (p=0.008, ANOVA). The mean degree of stenosis was 79%, 72% and 73% respectively (p = 0.1, ANOVA). Plaque echogenicity (p = 0.007) and not the degree of stenosis (p = 0.07) predicted the presence of non-lacunar silent CT-brain infarcts (logistic regression). CONCLUSIONS: Carotid bifurcation plaques, which are associated with non-lacunar silent CT-brain infarcts, are significantly more hypoechoic than those associated with lacunar or no infarcts. Plaques associated with lacunar silent infarcts and no infarcts have the same echogenicity and degree of stenosis. These findings suggest an embologenic mechanism of non-lacunar silent CT-brain infarcts that may have prognostic implications in patients with asymptomatic carotid stenosis. Prospective studies of asymptomatic carotid stenosis should assess the significance of 1) plaque echogenicity and 2) the presence of different types of silent CT-brain infarcts and atheroembolic stroke.     

Different patterns of silent cerebral infarct in patients with coronary artery disease or hypertension

The aim of the present study was to clarify the differences in the progression and the characteristics of silent cerebral infarcts (SCI) between patients with coronary artery disease (CAD) and hypertensive patients. Silent cerebral infarcts, a powerful prognostic indicator for stroke, are frequently found in patients with CAD and in hypertensives. However, the differences in the characteristics of SCI and related risk factors between CAD and hypertensive patients have not been thoroughly investigated. We evaluated the number of SCI and their distribution using brain magnetic resonance imaging (T1- and T2-weighted images) in 107 patients with CAD (validated by coronary angiography) and 101 hypertensive patients without history of clinical stroke. The prevalence of multiple SCI (three or more infarcts per person) in patients with CAD and with hypertension was significantly higher than in hypertensives without CAD (46% v 21%; P = .001), whereas that of patients with CAD without hypertension was intermediate (31%). The patients with multi- (two- or three-vessel) vessel diseases (VD) had a significantly higher prevalence of multiple SCI than the hypertensives and the no-stenosis or 1-VD group (68.1% in the 3-VD group, 52.0% in the 2-VD group, 26.8% in the 1-VD group, and 21.0% in the no-stenosis group). Multiple logistic regression analysis revealed that in the CAD group, the number of involved coronary arteries was an independent determinant of SCI (P < .005), whereas in the hypertensive group, age was an independent determinant of SCI (P < .005). When we investigated the distribution of SCI, in the CAD group, SCI in the deep perforator territory (the basal ganglia and the thalamus) were independently associated with the number of involved coronary arteries (P < .005), whereas SCI in the white matter were independently associated with age only (P < .005). In conclusion, SCI were more advanced in the patients with multivessel CAD than in the hypertensive patients, and were more common in patients with CAD and hypertension than in those without hypertension. Coronary atherosclerosis was independently and specifically associated with SCI located in the deep perferator territory but not of SCI located in the white matter. The CAD-atherosclerosis and hypertension may be independently involved in the pathologic process of SCI.     

Silent infarcts in young children with sickle cell disease

Silent infarcts have been reported most commonly in school-aged children with homozygous sickle cell disease (SCD-SS) and are associated with neurocognitive deficits. However, the prevalence of silent infarcts in younger children with SCD-SS is not well defined. In this retrospective study, brain magnetic resonance imaging and angiography (MRI/A) studies performed before 6 years of age in a cohort of children with SCD-SS were analysed and the prevalence of abnormalities was calculated. Clinical and laboratory parameters were compared between the groups with and without silent infarcts. Sixty-eight of 96 children in the cohort had brain MRI/A performed prior to age 6 years. Of the 65 who were neurologically asymptomatic, 18 (27·7%, 95% CI 17·3–40·2%) had silent infarcts (mean age 3·7 ± 1·1 years, range 1·3–5·9 years). Factors associated with silent infarcts included cerebral vessel stensosis by magnetic resonance angiography, lower rates of vaso-occlusive pain and acute chest syndrome and lower haemoglobin levels. The prevalence of silent infarcts in young children with SCD-SS is similar to that of older children and anaemia and severe vasculopathy may be risk factors.     

Risk factors related to the occurrence of silent myocardial ischemia in Mexicans

BACKGROUND: Silent myocardial ischemia is a growing world health problem. It has been related to factors that promote an increase in myocardial oxygen demand or affect coronary vasomotor tone. Coronary artery disease has shown an increasing trend in Mexico in this century. HYPOTHESIS: The aim of the study was to estimate the strength of the association between some risk factors and the occurrence of silent myocardial ischemia. METHODS: A cross-sectional study was conducted and 249 individuals were screened by 24-h Holter electrocardiogram. Silent myocardial ischemia was diagnosed in patients with painless transient ST-segment depression. All subjects were interviewed for coronary risk factors and total serum cholesterol was measured. RESULTS: Silent ischemia was diagnosed in 115 patients (46%), who were older (59 +/- 9 vs. 57 +/- 11 years; p = 0.01). In a logistic regression analysis, a lower risk for silent ischemia was found in patients with thrombolysis [odds ratio (OR) 0.28; 95% confidence interval (CI 95%) 0.14-0.53], or those who followed their medical treatment (OR 0.16; CI 95% 0.04-0.68). The major risk factors were hypercholesterolemia (OR 1.6; CI 95% 0.9-2.9) and more severe coronary artery disease (OR 2.5; CI 95% 1.1-5.7). CONCLUSIONS: Some coronary risk factors are related to silent ischemia. It is still important to diagnose this entity, but modification of its related risk factors should be kept in mind to diminish its occurrence and its severe consequences.