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Bernadette Boden-Albala

Publications and source records attributed to Bernadette Boden-Albala.

At least 19 recordsLinked to original sources

Levels of acute phase proteins remain stable after ischemic stroke.

BACKGROUND: Inflammation and inflammatory biomarkers play an important role in atherosclerosis and cardiovascular disease. Little information is available, however, on time course of serum markers of inflammation after stroke. METHODS: First ischemic stroke patients > or =40 years old had levels of high-sensitivity C-reactive protein (hsCRP), serum amyloid A (SAA), and fibrinogen measured in plasma samples drawn at 1, 2, 3, 7, 14, 21 and 28 days after stroke. Levels were log-transformed as needed, and parametric and non-parametric statistical tests were used to test for evidence of a trend in levels over time. Levels of hsCRP and SAA were also compared with levels in a comparable population of stroke-free participants. RESULTS: Mean age of participants with repeated measures (n = 21) was 65.6 +/- 11.6 years, and 13 (61.9%) were men, and 15 (71.4%) were Hispanic. Approximately 75% of patients (n = 15) had mild strokes (NIH Stroke Scale score 0-5). There was no evidence of a time trend in levels of hsCRP, SAA, or fibrinogen for any of the markers during the 28 days of follow-up. Mean log(hsCRP) was 1.67 +/- 1.07 mg/L (median hsCRP 6.48 mg/L) among stroke participants and 1.00 +/- 1.18 mg/L (median 2.82 mg/L) in a group of 1176 randomly selected stroke-free participants from the same community (p = 0.0252). CONCLUSION: Levels of hsCRP are higher in stroke patients than in stroke-free subjects. Levels of inflammatory biomarkers associated with atherosclerosis, including hsCRP, appear to be stable for at least 28 days after first ischemic stroke.

Acute-Phase Reaction↗

Carotid plaque surface irregularity predicts ischemic stroke: the northern Manhattan study.

BACKGROUND AND PURPOSE: There is scant population-based evidence regarding extracranial carotid plaque surface irregularity and ischemic stroke. Using a prospective cohort design, we evaluated the association of carotid plaque surface irregularity and the risk of ischemic stroke in a multiethnic population. METHODS: High-resolution B-mode ultrasound of the carotid arteries was performed in 1939 stroke-free subjects (mean age 69+/-10.0 years; 59% women; 53% Hispanic, 25% black, 22% white). Plaque was defined as a focal protrusion 50% greater than the surrounding area and localized along the extracranial carotid tree (internal carotid artery/bifurcation vs common carotid artery). Plaque surface was categorized as regular or irregular. Cox proportional hazard models were used to assess the association of surface characteristics and the risk of ischemic stroke. RESULTS: Among 1939 total subjects, carotid plaque was visualized in 56.3% (1 plaque: 21.6%, >1 plaque: 34.7%, irregular plaque: 5.5%). During a mean follow up of 6.2 years after ultrasound examination, 69 ischemic strokes occurred. Unadjusted cumulative 5-year risks of ischemic stroke were: 1.3%, 3.0%, and 8.5% for no plaque, regular plaque, and irregular plaque, respectively. After adjusting for demographics, traditional vascular risk factors, degree of stenosis, and plaque thickness, presence of irregular plaque (vs no plaque) was independently associated with ischemic stroke (Hazard ratio, 3.1; 95% CI, 1.1 to 8.5). CONCLUSIONS: The presence of irregular carotid plaque independently predicted ischemic stroke in a multiethnic cohort. Plaque surface irregularities assessed by B-mode ultrasonography may help identify intermediate- to high-risk individuals beyond their vascular risk assessed by the presence of traditional risk factors.

Aged↗

Endothelial dysfunction is associated with carotid plaque: a cross-sectional study from the population based Northern Manhattan Study.

BACKGROUND: Impaired vascular function occurs early in atherogenesis. Brachial flow mediated dilatation (FMD) is a non-invasive measure of vascular function and may be an important marker of preclinical atherosclerosis. Data on the association between FMD and carotid plaque in multi-ethnic populations are limited. The objective of this study was to determine whether endothelial dysfunction is independently associated with carotid plaque in a community of northern Manhattan. METHODS: In the population-based Northern Manhattan Study (NOMAS), high-resolution B-mode ultrasound images of the brachial and carotid arteries were obtained in 643 stroke-free subjects (mean age 66 years; 55% women; 65% Caribbean-Hispanic, 17% African-American, 16% Caucasian). Brachial FMD was measured during reactive hyperemia. Maximum carotid plaque thickness (MCPT) was measured at the peak plaque prominence. RESULTS: The mean brachial FMD was 5.78 +/- 3.83 %. Carotid plaque was present in 339 (53%) subjects. The mean MCPT was 1.68 +/- 0.82 mm, and the 75th percentile was 2.0 mm. Reduced FMD was significantly associated with increased MCPT. After adjusting for demographics, vascular risk factors, and education, each percent of FMD decrease was associated with a significant 0.02 mm increase in MCPT (p = 0.028). In a dichotomous adjusted model, blunted FMD was associated with an increased risk of MCPT > or = 2.0 mm (OR, 1.11 for every 1% decrease in FMD; 95% CI, 1.03-1.19). CONCLUSION: Decreased brachial FMD is independently associated with carotid plaque. Non-invasive evaluation of endothelial dysfunction may be a useful marker of preclinical atherosclerosis and help to individualize cardiovascular risk assessment beyond traditional risk factors.

Aged↗

The association between endothelial dysfunction and cardiovascular outcomes in a population-based multi-ethnic cohort.

BACKGROUND: Brachial artery flow-mediated dilation (FMD) may predict cardiovascular events in selected high-risk patients. Whether FMD testing predicts cardiovascular events in asymptomatic, lower risk individuals from the general population is unknown. METHODS AND RESULTS: As a part of a multi-ethnic, prospective cohort study, the Northern Manhattan Study, we examined FMD by high-resolution ultrasonography in 842 community participants who were free of stroke or myocardial infarction. Lower FMD levels predicted cardiovascular events (myocardial infarction, stroke and vascular death) at 36 months of follow-up (hazard ratio (HR)=1.12 for every 1% decrease in FMD, 95% CI 1.01-1.25, p=0.03). The risk of events in patients with FMD in the lower two tertiles (FMD<7.5%) was significantly higher than those in the highest tertile (HR=3.28, 95% CI 1.07-10.06, p=0.04 for lowest versus highest tertile, and HR=3.05, 95% CI 1.03-9.66, p=0.04 for middle versus highest tertile). In a multivariate analysis including cardiovascular risk factors, the increase in risk associated with FMD was no longer statistically significant. CONCLUSIONS: Non-invasive FMD testing predicts incident cardiovascular events in this multi-ethnic, population-based sample, but its predictive value is not independent of cardiovascular risk factors.

Aged↗

Prognostic implications of left ventricular mass among Hispanics: the Northern Manhattan Study.

Hispanics may carry a similar burden of increased left ventricular mass (LVM) as non-Hispanic blacks but whether LVM portends a worse outcome among Hispanics is largely unknown. We prospectively evaluated 1081 Hispanics enrolled in the Northern Manhattan Study during the period of 1993 to 2001. Subjects were aged > or =40 years and free of prior myocardial infarction or stroke. LVM was defined echocardiographically and indexed for height(2.7). Cox proportional hazards models were used to assess the risk of vascular events with adjustments for age, gender, systolic blood pressure, diabetes, and smoking. LVM averaged 48.4+/-15 gm/ht(2.7) and on multivariate analysis was significantly associated with the combined end point of myocardial infarction, stroke, or vascular death (adjusted hazard ratio 1.34 per SD change in LVM [95% CI 1.10 to 1.63]). During a mean of 57 months of follow-up, 74 vascular events occurred. The annual rate of vascular events was 21.8 per 1000 patient-years in the highest quartile of LVM and 8.6 per 1000 patient-years in the lowest quartile (P=0.007). These data demonstrate in a large population-based sample that increased LVM yields independent prognostic information among Hispanics, predicting a higher incidence of events attributable to vascular disease in this understudied population. Our findings identify the Hispanic population with increased LVM as a high-risk subgroup.

Adult↗

Alcohol intake, carotid plaque, and cognition: the Northern Manhattan Study.

BACKGROUND AND PURPOSE: Moderate alcohol intake has been associated with better cognitive performance, implicating vascular and neurodegenerative processes. Few studies to clarify the importance of vascular disease have included direct measures of atherosclerosis or minority populations at higher risk of vascular disease and dementia. METHODS: The Northern Manhattan Study includes stroke-free community based Hispanic (54%), black (25%), and white (22%) participants. We performed a cross-sectional study of alcohol intake and performance on the Mini-Mental State Examination (MMSE) in subjects with sonographic measurement of maximal carotid plaque thickness and adjusted for sociodemographic and vascular risk factors. RESULTS: The median MMSE score was 27 (interquartile range 24 to 29; n=2215). Reported alcohol intake was divided into 5 groups: never (n=509), past (n=494), <1 drink/week (n=300), 1/week to < or =2 drinks/day (n=796), and >2 drinks/day (n=116). Drinking 1 drink weekly up to 2 daily was associated with better performance on the MMSE (odds ratio=1.19; 95% CI, 1.10 to 1.26) compared with nondrinkers in women (P< or =0.0001) but not in men, adjusting for sociodemographic and vascular risk factors. Maximal carotid plaque thickness (mean 1.1 mm; SD 1.2 mm) was not associated with alcohol intake and did not mediate the relationship between alcohol and cognition. CONCLUSIONS: Moderate alcohol consumption was independently associated with better cognitive performance in women from this multiethnic sample. Carotid plaque was not a mediator of this association suggesting alcohol may impact cognition through a separate vascular or degenerative pathway.

Black or African American↗

Short sleep duration as a risk factor for hypertension: analyses of the first National Health and Nutrition Examination Survey.

Depriving healthy subjects of sleep has been shown to acutely increase blood pressure and sympathetic nervous system activity. Prolonged short sleep durations could lead to hypertension through extended exposure to raised 24-hour blood pressure and heart rate, elevated sympathetic nervous system activity, and increased salt retention. Such forces could lead to structural adaptations and the entrainment of the cardiovascular system to operate at an elevated pressure equilibrium. Sleep disorders are associated with cardiovascular disease, but we are not aware of any published prospective population studies that have shown a link between short sleep duration and the incidence of hypertension in subjects without apparent sleep disorders. We assessed whether short sleep duration would increase the risk for hypertension incidence by conducting longitudinal analyses of the first National Health and Nutrition Examination Survey (n=4810) using Cox proportional hazards models and controlling for covariates. Hypertension incidence (n=647) was determined by physician diagnosis, hospital record, or cause of death over the 8- to 10-year follow-up period between 1982 and 1992. Sleep durations of < or =5 hours per night were associated with a significantly increased risk of hypertension (hazard ratio, 2.10; 95% CI, 1.58 to 2.79) in subjects between the ages of 32 and 59 years, and controlling for the potential confounding variables only partially attenuated this relationship. The increased risk continued to be significant after controlling for obesity and diabetes, which was consistent with the hypothesis that these variables would act as partial mediators. Short sleep duration could, therefore, be a significant risk factor for hypertension.

Adult↗

Factors associated with in-hospital mortality after administration of thrombolysis in acute ischemic stroke patients: an analysis of the nationwide inpatient sample 1999 to 2002.

BACKGROUND AND PURPOSE: The prospective trials evaluating the safety and efficacy of intravenous tissue plasminogen activator have generally been conducted at academic medical centers and community hospitals with an institutional commitment to stroke care. Relatively little is known about the safety of this therapy as it is used in the community. We therefore examined outcomes in acute stroke patients treated with thrombolysis using the largest discharge database available in the United States for the years 1999 to 2002. METHODS: Data were derived from the Nationwide Inpatient Sample for the years 1999 to 2002. Using the appropriate International Classification of Disease-Clinical Modification, 9th revision, codes, patients admitted through the emergency room with a primary diagnosis of acute ischemic stroke were selected for analysis. From these patients, those coded as receiving thrombolysis were identified. Multivariate logistic regression was performed on the thrombolysis and nonthrombolysis cohorts to identify independent predictors of in-hospital mortality from among those clinical elements available in the database. RESULTS: We identified 2594 patients treated with thrombolysis from a group of 248,964 patients admitted through the emergency room with a primary diagnosis of acute ischemic stroke. The thrombolysis cohort had a higher in-hospital mortality rate compared with the nonthrombolysis patients (11.4% versus 6.8%). The rate of intracerebral hemorrhage was 4.4% for the thrombolysis cohort and 0.4% for nonthrombolysis patients. Multivariate logistic regression showed advanced age, Asian/Pacific Islander race, congestive heart failure, and atrial fibrillation/flutter to be independent predictors of in-hospital mortality after thrombolysis. Thrombolysis volume, overall ischemic stroke volume, and teaching status were not significant predictors of in-hospital mortality after thrombolysis. CONCLUSIONS: Thrombolysis, as it is used in the community, has a safety profile that is similar to that observed in the large, prospective clinical trials.

Adult↗

Current understanding of multiple risk factors as the metabolic syndrome: distillation or deconstruction.

The "metabolic syndrome" is a new term that defines the clustering of vascular risk factors, such as hyperlipidemia, obesity, elevated blood pressure, and elevated blood glucose. Controversy exists regarding the use of the term, which raises the question of whether the unique grouping of vascular risk factors adds more clinical risk then the additive effect of multiple risk factors viewed as separate but important entities. Whatever the answer, the metabolic syndrome constitutes a major public health problem with over 47 million persons in the United States meeting criteria for the metabolic syndrome. Although studies have demonstrated that the metabolic syndrome is a risk factor for overall mortality as well as cardiovascular events, the relationship between the metabolic syndrome and ischemic stroke has not been well characterized. Two large cross-sectional studies report an association between metabolic syndrome and increased risk of a history of stroke. One large multiethnic prospective study found the metabolic syndrome to be significantly associated with an increased risk of ischemic stroke after adjustment for sociodemographics and other cardiovascular risk factors. This study estimated that the metabolic syndrome may account for 19% of ischemic strokes including 30% of stroke in women and over 40% of stroke in Hispanics. Despite debate about the utility of its definition, there is evidence to suggest that the metabolic syndrome is an important risk factor for ischemic stroke, with differential effects by gender and race-ethnicity. Further, the metabolic syndrome has important clinical and public health implications by helping to easily identify individuals at greatest risk of vascular events.

Cardiovascular Diseases↗

Moderate alcohol consumption reduces risk of ischemic stroke: the Northern Manhattan Study.

BACKGROUND AND PURPOSE: Moderate alcohol consumption is protective against coronary disease, but its relationship to ischemic stroke (IS) is controversial. METHODS: Stroke-free participants > or =40 years of age identified by random-digit dialing were enrolled in a prospective cohort study between 1993 and 2001. Alcohol consumption was assessed through in-person interview and categorized as none in the past year, > or =1 drink in past month to < or =2 per day (moderate drinkers), and >2 drinks daily. Lifetime drinking was also assessed. Cox proportional hazard regression modeling was used to assess hazard ratios and their 95% CIs for the association of drinking with risk of stroke and vascular events. RESULTS: Mean age among participants (n=3176) was 69.1+/-10.3 years; 62.8% were women, 20.8% were non-Hispanic white, 24.5% non-Hispanic black, and 52.4% were Hispanic. No alcohol in the previous year was present in 62.3%, and 32.5% drank moderately. After adjusting for other risk factors compared with those who did not drink in the past year, moderate drinkers had a reduced risk of IS (0.67; 95% CI, 0.46 to 0.99) and IS, myocardial infarction, or vascular death (0.74; 95% CI, 0.59 to 0.94). Results were similar when never-drinkers were used as referent group. Reduction in risk was seen for nonatherosclerotic IS subtypes, and results stratified by age, sex, and race-ethnicity were similar. CONCLUSIONS: Moderate alcohol consumption is associated with decreased risk of IS in a multiethnic population. This effect is independent of other risk factors and holds for nonatherosclerotic stroke subtypes.

Aged↗

Association of increased body mass index and impaired endothelial function among Hispanic women.

We tested the hypothesis that an increased body mass index was similarly associated with impaired endothelial function as measured by flow-mediated dilation in a high-risk, Hispanic population of men and women living in northern Manhattan. The association of flow-mediated dilation and body mass index was significant in women (beta -0.16 +/- 0.04, p <0.0001) but not in men (beta -0.02 +/- 0.06, p = 0.72). This is the first study to demonstrate a gender-specific difference in endothelial function associated with body mass index.

Age Factors↗

Heritability of carotid artery distensibility in Hispanics: the Northern Manhattan Family Study.

BACKGROUND AND PURPOSE: Reduced arterial distensibility has been introduced as a novel risk factor for atherosclerosis. The importance of the genetic contribution to variation in distensibility is largely unknown. The purpose of this study was to estimate heritability of carotid distensibility. METHODS: The ongoing Northern Manhattan Family Study recruits high-risk Caribbean Hispanic families to study genetic effects on stroke/cardiovascular risk factors. The distensibility metrics (strain, stiffness, distensibility, and elastic modulus) were measured from the right common carotid artery, and the heritability for each was estimated. Variance component methods were used to estimate age- and sex-adjusted heritability. Correlations were calculated to evaluate the relationship between distensibility phenotypes and intimamedia thickness (IMT) at each carotid segment. RESULTS: The current data included 88 probands and 605 relatives from 88 families. Age- and sex-adjusted heritability was 25% for strain, 17% for distensibility, 20% for stiffness, and 20% for elastic modulus. Without adjustment for covariates, strong correlations were found between distensibility metrics and IMT: the absolute values of correlation coefficients were between 0.2 and 0.5, and all P values were <0.001. However, the correlation coefficients were reduced substantially after adjusting for age and sex. CONCLUSIONS: These results suggested that genetic factors explained a moderate proportion of the variability of carotid distensibility. The correlations between distensibility and IMT were mainly attributable to age and sex effects. The regulation of carotid distensibility and IMT may reflect different underlying genetic and environmental mechanisms.

Adolescent↗

Relation of plasma glucose and endothelial function in a population-based multiethnic sample of subjects without diabetes mellitus.

To determine whether endothelial dysfunction precedes the clinical diagnosis of diabetes mellitus, we investigated the relation of endothelial flow-mediated dilation (FMD) with fasting plasma glucose among a multiethnic population-based cohort of 579 nondiabetic subjects without previous myocardial infarction or stroke enrolled in the Northern Manhattan Study (age 66 +/- 9 years; 41% men, 16% white, 15% black, and 68% Hispanic). Impaired fasting glucose or prediabetic status, defined as a fasting glucose level of 100 to 125 mg/dl, was present in 95 subjects (16%). Endothelial function was determined using FMD during reactive hyperemia. Multiple linear regression analyses were used to assess the relation between plasma glucose and endothelial function after adjustment for potential confounders. FMD was significantly lower (4.9 +/- 3.8% vs 6.1 +/- 3.7%, p = 0.003) in those with impaired fasting glucose than in subjects with normal fasting glucose. Prediabetic status was significantly associated with impaired FMD (odds ratio 1.9, 95% confidence interval 1.1 to 3.1, p = 0.02). After adjustment for age, gender, body mass index, and hypertensive status, a higher fasting glucose was significantly associated with a lower FMD (beta = -0.024 +/- 0.012, p = 0.04) in a continuous linear relation. Thus, for each 10-mg/dl increase in plasma glucose, a 0.24% decrease occurred in FMD. Impaired FMD was present among prediabetics. An elevated fasting plasma glucose level is associated with impaired endothelial function among nondiabetics. These results further support the role of hyperglycemia in the pathogenesis of vascular dysfunction at different stages of diabetes development and the role of impaired fasting glucose as a risk factor for macrovascular disease.

Black or African American↗

Ischemic stroke subtype incidence among whites, blacks, and Hispanics: the Northern Manhattan Study.

BACKGROUND: Stroke incidence is greater in blacks than in whites; data on Hispanics are limited. Comparing subtype-specific ischemic stroke incidence rates may help to explain race-ethnic differences in stroke risk. The aim of this population-based study was to determine ischemic stroke subtype incidence rates for whites, blacks, and Hispanics living in one community. METHODS AND RESULTS: A comprehensive stroke surveillance system incorporating multiple overlapping strategies was used to identify all cases of first ischemic stroke occurring between July 1, 1993, and June 30, 1997, in northern Manhattan. Ischemic stroke subtypes were determined according to a modified NINDS scheme, and age-adjusted, race-specific incidence rates calculated. The annual age-adjusted incidence of first ischemic stroke per 100,000 was 88 (95% CI, 75 to 101) in whites, 149 (95% CI, 132 to 165) in Hispanics, and 191 (95% CI, 160 to 221) in blacks. Among blacks compared with whites, the relative rate of intracranial atherosclerotic stroke was 5.85 (95% CI, 1.82 to 18.73); extracranial atherosclerotic stroke, 3.18 (95% CI, 1.42 to 7.13); lacunar stroke, 3.09 (95% CI, 1.86 to 5.11); and cardioembolic stroke, 1.58 (95% CI, 0.99 to 2.52). Among Hispanics compared with whites, the relative rate of intracranial atherosclerotic stroke was 5.00 (95% CI, 1.69 to 14.76); extracranial atherosclerotic stroke, 1.71 (95% CI, 0.80 to 3.63); lacunar stroke, 2.32 (95% CI, 1.48 to 3.63); and cardioembolic stroke, 1.42 (95% CI, 0.97 to 2.09). CONCLUSIONS: The high ischemic stroke incidence among blacks and Hispanics compared with whites is due to higher rates of all ischemic stroke subtypes.

Black or African American↗

Leukocyte count is associated with reduced endothelial reactivity.

BACKGROUND: Leukocyte count has been associated with cardiovascular and cerebrovascular disease in several studies. We hypothesized that white blood cell count is associated with endothelial reactivity. METHODS AND RESULTS: Leukocyte count was measured in a sample of stroke-free community participants undergoing brachial artery testing for endothelial reactivity. Flow-mediated dilation (FMD) during reactive hyperemia was assessed in each subject using high-resolution B-mode ultrasound. Multivariate linear regression was used to calculate the effect of leukocyte count on endothelial reactivity after adjusting for potential confounding factors. Mean age of the 868 participants was 66.7+/-8.8 years; 57% were women. Mean leukocyte count was (6.1+/-1.8)x10(9)/L. Each unit increase in leukocyte count was associated with a mean 0.18% decrease in FMD (p = 0.01). After adjusting for other atherosclerosis risk factors, including age, sex, hypertension, diabetes, hyperlipidemia, and smoking, the relationship persisted (mean decrease in FMD per unit leukocyte count = 0.17%, p = 0.02). There was a linear decrease in FMD by quartile of leukocyte count (p = 0.0014). The effect of leukocyte count on FMD was greater for women, those under age 70, and non-diabetics. CONCLUSIONS: Relative elevations in leukocyte count are associated with a reduction in brachial artery endothelial reactivity. These findings are consistent with current hypotheses regarding the inflammatory or infectious etiology of risk of atherosclerosis and stroke, but also suggest interactions with demographic and other risk factors.

Aged↗

Periodontal microbiota and carotid intima-media thickness: the Oral Infections and Vascular Disease Epidemiology Study (INVEST).

BACKGROUND: Chronic infections, including periodontal infections, may predispose to cardiovascular disease. We investigated the relationship between periodontal microbiota and subclinical atherosclerosis. METHODS AND RESULTS: Of 1056 persons (age 69+/-9 years) with no history of stroke or myocardial infarction enrolled in the Oral Infections and Vascular Disease Epidemiology Study (INVEST), we analyzed 657 dentate subjects. Among these subjects, 4561 subgingival plaque samples were collected (average of 7 samples/subject) and quantitatively assessed for 11 known periodontal bacteria by DNA-DNA checkerboard hybridization. Extensive in-person cardiovascular risk factor measurements, a carotid scan with high-resolution B-mode ultrasound, white blood cell count, and C-reactive protein values were obtained. In 3 separate analyses, mean carotid artery intima-media thickness (IMT) was regressed on tertiles of (1) burden of all bacteria assessed, (2) burden of bacteria causative of periodontal disease (etiologic bacterial burden), and (3) the relative predominance of causative/over other bacteria in the subgingival plaque. All analyses were adjusted for age, race/ethnicity, gender, education, body mass index, smoking, diabetes, systolic blood pressure, and LDL and HDL cholesterol. Overall periodontal bacterial burden was related to carotid IMT. This relationship was specific to causative bacterial burden and the dominance of etiologic bacteria in the observed microbiological niche. Adjusted mean IMT values across tertiles of etiologic bacterial dominance were 0.84, 0.85, and 0.88 (P=0.002). Similarly, white blood cell values increased across tertiles of etiologic bacterial burden from 5.57 to 6.09 and 6.03 cells x10(9)/L (P=0.01). C-reactive protein values were unrelated to periodontal microbial status (P=0.82). CONCLUSIONS: Our data provide evidence of a direct relationship between periodontal microbiology and subclinical atherosclerosis. This relationship exists independent of C-reactive protein.

Aged↗

Interleukin-2 levels are associated with carotid artery intima-media thickness.

OBJECTIVE: To show that serum interleukin levels are associated with carotid intima-media thickness (IMT). BACKGROUND: Inflammation is hypothesized to play a central role in atherogenesis, and serum markers of inflammation are predictive of cardiovascular disease. Interleukin-2, a pro-inflammatory cytokine produced largely by naive CD4 T cells and Th1 (pro-inflammatory) T cells, has been found in a high proportion of carotid plaques. METHODS: High-resolution ultrasound of the carotid arteries and serum cytokine levels were measured in stroke-free participants. The mean of the maximum IMT in bilateral bifurcation, common and internal carotid artery segments was measured. Serum levels of interleukin (IL)-1beta, IL-2, IL-6, C-reactive protein, tumor necrosis factor (TNF) alpha and TNF receptors were measured using enzyme-linked immunosorbent assay. RESULTS: IL-2 levels were significantly correlated with IMT (r=0.33, P<0.0001), but other cytokines were not. Each unit increase in IL-2 was significantly associated with a mean increase in IMT of 0.18 mm (P=0.0001). After adjusting for other atherosclerotic risk factors, the association was unchanged (mean increase in IMT per unit increase IL-2=0.18 mm, P<0.0001). Each standard deviation increase in the level of IL-2 was associated with an increased risk (adjusted odds ratio 1.80, 95% CI 1.12-2.89) for an IMT> or =1.0mm (75th percentile for IMT). CONCLUSION: Serum levels of IL-2, a pro-inflammatory cytokine, are associated with carotid artery IMT, a predictor of stroke and vascular disease. Serum inflammatory markers may provide a novel marker of atherosclerotic risk, and inflammation may provide a new therapeutic target for stroke prevention.

Aged↗