Dataset Information

Revised Framingham Stroke Risk Profile to Reflect Temporal Trends.

ABSTRACT:

Background

Age-adjusted stroke incidence has decreased over the past 50 years, likely as a result of changes in the prevalence and impact of various stroke risk factors. An updated version of the Framingham Stroke Risk Profile (FSRP) might better predict current risks in the FHS (Framingham Heart Study) and other cohorts. We compared the accuracy of the standard (old) and of a revised (new) version of the FSRP in predicting the risk of all-stroke and ischemic stroke and validated this new FSRP in 2 external cohorts, the 3C (3 Cities) and REGARDS (Reasons for Geographic and Racial Differences in Stroke) studies.

Methods

We computed the old FSRP as originally described and a new model that used the most recent epoch-specific risk factor prevalence and hazard ratios for individuals ≥55 years of age and for the subsample ≥65 years of age (to match the age range in REGARDS and 3C studies, respectively) and compared the efficacy of these models in predicting 5- and 10-year stroke risks.

Results

The new FSRP was a better predictor of current stroke risks in all 3 samples than the old FSRP (calibration χ² of new/old FSRP: in men: 64.0/12.1, 59.4/30.6, and 20.7/12.5; in women: 42.5/4.1, 115.4/90.3, and 9.8/6.5 in FHS, REGARDS, and 3C, respectively). In the REGARDS, the new FSRP was a better predictor among whites compared with blacks.

Conclusions

A more contemporaneous, new FSRP better predicts current risks in 3 large community samples and could serve as the basis for examining geographic and racial differences in stroke risk and the incremental diagnostic utility of novel stroke risk factors.

SUBMITTER: Dufouil C

PROVIDER: S-EPMC5504355 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature

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Publications

Revised Framingham Stroke Risk Profile to Reflect Temporal Trends.

Dufouil Carole C Beiser Alexa A McLure Leslie A LA Wolf Philip A PA Tzourio Christophe C Howard Virginia J VJ Westwood Andrew J AJ Himali Jayandra J JJ Sullivan Lisa L Aparicio Hugo J HJ Kelly-Hayes Margaret M Ritchie Karen K Kase Carlos S CS Pikula Aleksandra A Romero Jose R JR D'Agostino Ralph B RB Samieri Cécilia C Vasan Ramachandran S RS Chêne Genevieve G Howard George G Seshadri Sudha S

Circulation 20170203 12

<h4>Background</h4>Age-adjusted stroke incidence has decreased over the past 50 years, likely as a result of changes in the prevalence and impact of various stroke risk factors. An updated version of the Framingham Stroke Risk Profile (FSRP) might better predict current risks in the FHS (Framingham Heart Study) and other cohorts. We compared the accuracy of the standard (old) and of a revised (new) version of the FSRP in predicting the risk of all-stroke and ischemic stroke and validated this ne ...[more]

PMID: 28159800

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Project description:Background and purposeLimited data exist on the performance of the revised Framingham Stroke Risk Score (R-FSRS) and the R-FSRS in conjunction with nontraditional risk markers. We compared the R-FSRS, original FSRS, and the Pooled Cohort Equation for stroke prediction and assessed the improvement in discrimination by nontraditional risk markers.MethodsSix thousand seven hundred twelve of 6814 participants of the MESA (Multi-Ethnic Study of Atherosclerosis) were included. Cox proportional hazard, area under the curve, net reclassification improvement, and integrated discrimination increment analysis were used to assess and compare each stroke prediction risk score. Stroke was defined as fatal/nonfatal strokes (hemorrhagic or ischemic).ResultsAfter mean follow-up of 10.7 years, 231 of 6712 (3.4%) strokes were adjudicated (2.7% ischemic strokes). Mean stroke risks using the R-FSRS, original FSRS, and Pooled Cohort Equation were 4.7%, 5.9%, and 13.5%. The R-FSRS had the best calibration (Hosmer-Lemeshow goodness-of-fit, χ2=6.55; P=0.59). All risk scores were predictive of incident stroke. C statistics of R-FSRS (0.716) was similar to Pooled Cohort Equation (0.716), but significantly higher than the original FSRS (0.653; P=0.01 for comparison with R-FSRS). Adding nontraditional risk markers individually to the R-FSRS did not improve discrimination of the R-FSRS in the area under the curve analysis, but did improve category-less net reclassification improvement and integrated discrimination increment for incident stroke. The addition of coronary artery calcium to R-FSRS produced the highest category-less net reclassification improvement (0.36) and integrated discrimination increment (0.0027). Similar results were obtained when ischemic strokes were used as the outcome.ConclusionsThe R-FSRS downgraded stroke risk but had better calibration and discriminative ability for incident stroke compared with the original FSRS. Nontraditional risk markers modestly improved the discriminative ability of the R-FSRS, with coronary artery calcium performing the best.

Project description:BackgroundEndogenous sex hormones in postmenopausal women have been associated with risk of cardiovascular diseases. The aim of this study was to determine the association between endogenous sex hormones and the revised Framingham Stroke Risk Profile (rFSRP) in postmenopausal women.MethodsThis is an observational cross-sectional study on the Vara-Skövde cohort, a Swedish population-based study for longitudinal surveillance of the development and progress of type 2 diabetes and hypertension. The participants were physically examined in 2002-2005 and sex hormones were analysed with liquid chromatography-tandem mass spectrometry assay (LC-MS/MS). Women who were ≥55 years old, with estradiol levels below 20 pg/mL, not using hormonal therapy, and with no self-reported history of stroke, were included (N = 133). The outcome variable was rFSRP. Regression analyses of log-transformed rFSRP were fitted against levels of sex hormones (17-α-OH-progesterone, estrone, estradiol, progesterone, dihydrotestosterone, dehydroepiandrosterone, testosterone and androstenedione), adjusting for body mass index (BMI) or waist-to-hip ratio (WHR), C-reactive protein (CRP) and cholesterol level.ResultsLevels of estrone and estradiol were positively associated with rFSRP in the crude model (estrone β = 0.208, 95% CI = 0.081;0.336, P = 0.002; estradiol β = 0.170, CI = 0.034;0.305, P = 0.015). Adjustments for BMI revealed significant positive associations between progesterone (β = 0.155 95% CI = 0.025;0.285, P = 0.020), estrone (β = 0.167, 95% CI = 0.037;0.297, P = 0.013) and 17-α-OH-progesterone (β = 0.146, 95% CI = 0.014; 0.277, P = 0.030) and rFSRP, and adjustments for WHR revealed a significant positive association between testosterone and rFSRP (β = 0.152, CI = 0.026;0.278, p = 0.018).ConclusionsIncrease of estrone was associated with higher rFSRP, also in the fully adjusted model, whereas progesterone, 17-α-OH-progesterone and testosterone were significant only in the models adjusting for BMI and WHR respectively. Larger studies studying stroke events are warranted to confirm these findings.Clinical trial numberNot applicable.

Project description:Companion animals and humans are known to share extraintestinal pathogenic Escherichia coli (ExPEC), but the extent of E. coli sequence types (STs) that cause extraintestinal diseases in dogs is not well understood. Here, we generated whole-genome sequences of 377 ExPEC collected by the University of Melbourne Veterinary Hospital from dogs over an 11-year period from 2007 to 2017. Isolates were predominantly from urogenital tract infections (219, 58.1%), but isolates from gastrointestinal specimens (51, 13.5%), general infections (72, 19.1%), and soft tissue infections (34, 9%) were also represented. A diverse collection of 53 STs were identified, with 18 of these including at least five sequences. The five most prevalent STs were ST372 (69, 18.3%), ST73 (31, 8.2%), ST127 (22, 5.8%), ST80 (19, 5.0%), and ST58 (14, 3.7%). Apart from ST372, all of these are prominent human ExPEC STs. Other common ExPEC STs identified included ST12, ST131, ST95, ST141, ST963, ST1193, ST88, and ST38. Virulence gene profiles, antimicrobial resistance carriage, and trends in plasmid carriage for specific STs were generally reflective of those seen in humans. Many of the prominent STs were observed repetitively over an 11-year time span, indicating their persistence in the dogs in the community, which is most likely driven by household sharing of E. coli between humans and their pets. The case of ST372 as a dominant canine lineage observed sporadically in humans is flagged for further investigation. IMPORTANCE Pathogenic E. coli that causes extraintestinal infections (ExPEC) in humans and canines represents a significant burden in hospital and veterinary settings. Despite the obvious interrelationship between dogs and humans favoring both zoonotic and anthropozoonotic infections, whole-genome sequencing projects examining large numbers of canine-origin ExPEC are lacking. In support of anthropozoonosis, we found that most STs from canine infections are dominant human ExPEC STs (e.g., ST73, ST127, ST131) with similar genomic traits, such as plasmid carriage and virulence gene burden. In contrast, we identified ST372 as the dominant canine ST and a sporadic cause of infection in humans, supporting zoonotic transfer. Furthermore, we highlight that, as is the case in humans, STs in canine disease are consistent over time, implicating the gastrointestinal tract as the major community reservoir, which is likely augmented by exposure to human E. coli via shared diet and proximity.

Project description:BackgroundThe remaining lifetime risk (RLR) is the probability of developing an outcome over the remainder of one's lifespan at any given age. The RLR for atherosclerotic cardiovascular disease (ASCVD) in three 20-year periods were assessed using data from a single community-based cohort study of predominantly White participants.MethodsLongitudinal data from the Framingham study in 3 epochs (epoch 1, 1960-1979; epoch 2, 1980-1999; epoch 3, 2000-2018) were evaluated. The RLR of a first ASCVD event (myocardial infarction, coronary heart disease death, or stroke) from 45 years of age (adjusting for competing risk of death) in the 3 epochs were compared overall, and according to the following strata: sex, body mass index, blood pressure and cholesterol categories, diabetes, smoking, and Framingham risk score groups.ResultsThere were 317 849 person-years of observations during the 3 epochs (56% women; 94% White) and 4855 deaths occurred. Life expectancy rose by 10.1 years (men) to 11.9 years (women) across the 3 epochs. There were 1085 ASCVD events over the course of 91 330 person-years in epoch 1, 1330 ASCVD events over the course of 107 450 person-years in epoch 2, and 775 ASCVD events over the course of 119 069 person-years in epoch 3. The mean age at onset of first ASCVD event was greater in the third epoch by 8.1 years (men) to 10.3 years (women) compared with the first epoch. The RLR of ASCVD from 45 years of age declined from 43.7% in epoch 1 to 28.1% in epoch 3 (P<0.0001), a finding that was consistent in both sexes (RLR [epoch 1 versus epoch 3], 36.3% versus 26.5% [women]; 52.5% versus 30.1% [men]; P<0.001 for both). The lower RLR of ASCVD in the last 2 epochs was observed consistently across body mass index, blood pressure, cholesterol, diabetes, smoking, and Framingham risk score strata (P<0.001 for all). The RLR of coronary heart disease events and stroke declined in both sexes (P<0.001).ConclusionsOver the past 6 decades, mean life expectancy increased and the RLR of ASCVD decreased in the community-based, predominantly White Framingham study. The residual burden of ASCVD underscores the importance of continued and effective primary prevention efforts with better screening for risk factors and their effective treatment.

Dataset Information

Revised Framingham Stroke Risk Profile to Reflect Temporal Trends.

Background

Methods

Results

Conclusions

Publications

Revised Framingham Stroke Risk Profile to Reflect Temporal Trends.

Similar Datasets

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