19 research outputs found
Fasting and postchallenge glycemia and cardiovascular disease risk. The Framingham Offspring Study
WSTĘP. Celem pracy było zbadanie słuszności hipotezy, według
której hiperglikemia na czczo (FHG, fasting hyperglycemia) i glikemia 2 godziny po obciążeniu glukozą (2hPG, 2-h postchallenge glycemia)
niezależnie zwiększają ryzyko chorób sercowo-naczyniowych (CVD, cardiovascular
disease).
MATERIAŁ I METODY. W latach 1991-1995 autorzy przebadali 3370
uczestników badania Framingham Offspring Study, u których nie występowały objawy
kliniczne CVD (choroba wieńcowa, udar mózgu lub chromanie przestankowe)
ani cukrzyca, wymagająca leczenia farmakologicznego. Okres obserwacji pod kątem występowania CVD wynosił 4 lata. W celu oceny ryzyka związanego z FHG (stężenie glukozy na czczo ł 7,0 mmol/l) i 2hPG niezależnie od
wpływu standardowych czynników ryzyka CVD, zastosowano model regresji proporcjonalnego
ryzyka Coxa.
WYNIKI. Średni wiek badanych wynosił 54 lata, 54% chorych stanowiły
kobiety. Uprzednio nierozpoznaną cukrzycę stwierdzono u 3,2% na podstawie FHG,
a u 4,9% (164 osoby), opierając się na wartościach FHG lub 2hPG ł
11,1 mmol/l. Spośród tych 164 chorych u 55 (33,5%) 2hPG było ł
11,1 mmol/ przy prawidłowym FHG, ale stanowiły one jedynie 1,7% z 3261 badanych
bez FHG. W czasie 12 242 pacjentolat obserwacji wystąpiło 118 incydentów CVD.
W oddzielnych modelach, skorygowanych względem płci i standardowych czynników
ryzyka chorób sercowo-naczyniowych, ryzyko względne (RR, relative risk) CVD dla
glikemii na czczo (FPG, fasting plasma glucose) większej lub równej 7,0 mmol/l
wynosiło 2,8 (95% przedział ufności 1,6–5,0), a dla wzrostu 2hPG o 2,1 mmol/l
- 1,2 (1,1–1,3). W modelu wspólnym RR dla FHG zmalało i wynosiło 1,5 (0,7–3,6),
podczas gdy RR dla 2hPG pozostało istotnie podwyższone (1,1; 1,02–1,3). Analiza
statystyczna c dla modelu obejmującego jedynie standardowe czynniki ryzyka CVD
wyniosła 0,744; po dołączeniu FHG - 0,746, a po dodaniu FHG i 2hPG - 0,752.
WNIOSKI. Glikemia po doustnym obciążeniu glukozą jest niezależnym
czynnikiem ryzyka chorób sercowo-naczyniowych, ale wartość predykcyjna 2hPG jest
niewielka w stosunku do standardowych czynników ryzyka CVD.INTRODUCTION. To test the hypothesis that fasting
hyperglycemia (FHG) and 2-h postchallenge glycemia
(2hPG) independently increase the risk for cardiovascular
disease (CVD).
MATERIAL AND METHODS. During 1991–1995, we
examined 3,370 subjects from the Framingham
Offspring Study who were free from clinical CVD (coronary heart disease, stroke, or intermittent claudication)
or medication-treated diabetes, and we followed
them for 4 years for incident CVD events. We
used proportional-hazards regression to assess the
risk associated with FHG (fasting plasma glucose
≥ 7.0 mmol/l) and 2hPG, independent of the risk
predicted by standard CVD risk factors.
RESULTS. Mean subject age was 54 years, 54% were
women, and previously undiagnosed diabetes was
present in 3.2% by FHG and 4.9% (164) by FHG or
a 2hPG ≥ 11.1 mmol/l. Of these 164 subjects,
55 (33.5%) had 2hPG ≥ 11.1 without FHG, but these
55 subjects represented only 1.7% of the 3,261 subjects
without FHG. During 12,242 person-years of
follow-up, there were 118 CVD events. In separate
sex- and CVD risk-adjusted models, relative risk (RR)
for CVD with fasting plasma glucose ≥ 7.0 mmol/l
was 2.8 (95% CI 1.6–5.0); RR for CVD per 2.1 mmol/l
increase in 2hPG was 1.2 (1.1–1.3). When modeled
together, the RR for FHG decreased to 1.5 (0.7–3.6),
whereas the RR for 2hPG remained significant (1.1,
1.02–1.3). The c-statistic for a model including CVD
risk factors alone was 0.744; with addition of FHG,
it was 0.746, and with FHG and 2hPG, it was 0.752.
CONCLUSIONS. Postchallenge hyperglycemia is an
independent risk factor for CVD, but the marginal
predictive value of 2hPG beyond knowledge of standard
CVD risk factors is small
Prevalence and prognostic impact of subclinical cardiovascular disease in individuals with the metabolic syndrome and diabetes
Dostępne dane dotyczące występowania i znaczenia
prognostycznego subklinicznej postaci choroby
sercowo-naczyniowej (CVD), u pacjentów z zespołem
metabolicznym są ograniczone. W prezentowanej
pracy zbadano częstość występowania subklinicznej
choroby sercowo-naczyniowej u 1945 uczestników
próby Framingham Offspring Study (śr. wieku 58 lat,
59% uczestników stanowiły kobiety) z wykorzystaniem
elektrokardiografii, echokardiografii, ultra ultrasonografii
tętnic szyjnych, wskaźnika ciśnienia tętniczego
kostka–ramię oraz wydalania albumin
z moczem. W pracy oceniono w sposób prospektywny
częstość występowania subklinicznej choroby
sercowo-naczyniowej związanej z zespołem metabolicznym
i cukrzycą, w zależności od obecności
subklinicznej postaci tego schorzenia lub jej braku.
Przekrojowo u 51% z 581 uczestników z zespołem
metabolicznym zdiagnozowano subkliniczną formę
choroby sercowo-naczyniowej w przynajmniej jednym
z badań dodatkowych, co było częstsze niż
u chorych bez zespołu metabolicznego [iloraz szans
skorygowany pod względem wielu zmiennych 2,06
(95% CI: 1,67–2,55); p < 0,0001]. W trakcie dalszej
obserwacji klinicznej (śr. 7,2 lat) jawna klinicznie
choroba sercowo-naczyniowa rozwinęła się u 139
pacjentów, 59% tej liczby stanowiły osoby z zespołem
metabolicznym (10,2%). Uogólniając, występowanie
zespołu metabolicznego było związane ze zwiększonym ryzykiem występowania CVD [iloraz
ryzyka skorygowany pod względem wielu zmiennych
(HR, hazard ratio) 1,61 (95% CI: 1,12–2,33)]. U pacjentów
z zespołem metabolicznym oraz subkliniczną
postacią choroby sercowo-naczyniowej zaobserwowano
zwiększone ryzyko wystąpienia jawnej klinicznie
postaci choroby sercowo-naczyniowej [2,67
(1,62–4,41) w porównaniu z chorymi bez zdiagnozowanego
zespołu metabolicznego, cukrzycy lub
subklinicznej formy choroby sercowo-naczyniowej].
Zaobserwowano także mniejszy związek występowania
zespołu metabolicznego z rozwinięciem się
choroby sercowo-naczyniowej u pacjentów bez subklinicznej
postaci CVD [HR 1,59 (95% CI: 0,87–2,90)].
Podobne zmniejszenie ryzyka wystąpienia choroby
sercowo-naczyniowej u pacjentów bez subklinicznej
postaci CVD obserwowano u chorych na cukrzycę.
Występowanie subklinicznej formy CVD stanowiło
istotny predyktor rozwinięcia się jawnej klinicznie
choroby sercowo-naczyniowej u pacjentów bez zespołu
metabolicznego lub cukrzycy [1,93 (1,15–3,24)].
W niniejszym populacyjnym badaniu osób z zespołem
metabolicznym zaobserwowano częstsze występowanie
subklinicznej postaci miażdżycy, co prawdopodobnie
przyczynia się do wyższego ryzyka wystąpienia
jawnej klinicznie postaci CVD związanej
z tym schorzeniem.Data are limited regarding prevalence and prognostic
significance of subclinical cardiovascular disease
(CVD) in individuals with metabolic syndrome.
We investigated prevalence of subclinical CVD in
1,945 Framingham Offspring Study participants
(mean age 58 years; 59% women) using electrocardiography,
echocardiography, carotid ultrasound,
ankle-brachial blood pressure, and urinary albumin
excretion. We prospectively evaluated the incidence
of CVD associated with metabolic syndrome and
diabetes according to presence versus absence of
subclinical disease. Cross-sectionally, 51% of 581
participants with metabolic syndrome had subclinical
disease in at least one test, a frequency higher
than individuals without metabolic syndrome [multivariable-
adjusted odds ratio 2.06 (95% CI: 1.67-
2.55); p < 0.0001). On follow-up (mean 7.2 years),
139 individuals developed overt CVD, including
59 with metabolic syndrome (10.2%). Overall, metabolic
syndrome was associated with increased CVD
risk [multivariableadjusted hazards ratio (HR) 1.61
(95% CI: 1.12-2.33)]. Participants with metabolic syndrome
and subclinical disease experienced increased
risk of overt CVD [2.67 (1.62-4.41) compared with those without metabolic syndrome, diabetes, or subclinical
disease], whereas the association of metabolic
syndrome with CVD risk was attenuated in
absence of subclinical disease [HR 1.59 (95% CI: 0.87–2.90)]. A similar attenuation of CVD risk in absence
of subclinical disease was observed also for diabetes.
Subclinical disease was a significant predictor
of overt CVD in participants without metabolic syndrome
or diabetes [1.93 (1.15-3.24)]. In our community-based sample, individuals with metabolic
syndrome have a high prevalence of subclinical atherosclerosis
that likely contributes to the increased
risk of overt CVD associated with the condition
2013 ACC/AHA guideline on the assessment of cardiovascular risk: A report of the American College of Cardiology/American heart Association Task Force on Practice Guidelines
1.1. Organization of the Work Group: The Risk Assessment Work Group (Work Group) was composed of 11 members and 5 ex-officio members, including internists, cardiologists, endocrinologists, and experts in cardiovascular epidemiology, biostatistics, healthcare management and economics, and guideline development. 1.2. Document Review and Approval: A formal peer review process, which included 12 expert reviewers and representatives of federal agencies, was initially completed under the auspices of the NHLBI. This document was also reviewed by 3 expert reviewers nominated by the ACC and the AHA when the management of the guideline transitioned to the ACC/AHA. The ACC and AHA Reviewers’ RWI information is published in this document (Appendix 2). This document was approved for publication by the governing bodies of the ACC and AHA and endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation, American Society for Preventive Cardiology, American Society of Hypertension, Association of Black Cardiologists, National Lipid Association, Preventive Cardiovascular Nurses Association, and WomenHeart: The National Coalition for Women With Heart Disease. 1.3. Charge to the Work Group: The Work Group was 1 of 3 work groups appointed by the NHLBI to develop its own recommendations and provide cross-cutting input to 3 Panels for updating guidelines on blood cholesterol, blood pressure (BP), and overweight/obesity. The Work Group was asked to examine the scientific evidence on risk assessment for initial ASCVD events and to develop an approach for quantitative risk assessment that could be used in practice and used or adapted by the risk factor panels (blood cholesterol, hypertension, and obesity) in their guidelines and algorithms. Specifically, the Work Group was charged with 2 tasks: 1) To develop or recommend an approach to quantitative risk assessment that could be used to guide care; and 2) To use systematic review methodology to pose and address a small number of questions judged to be critical to refining and adopting risk assessment in clinical practice
The Comprehensive Post-Acute Stroke Services (COMPASS) study: design and methods for a cluster-randomized pragmatic trial
Background: Patients discharged home after stroke face significant challenges managing residual neurological deficits, secondary prevention, and pre-existing chronic conditions. Post-discharge care is often fragmented leading to increased healthcare costs, readmissions, and sub-optimal utilization of rehabilitation and community services. The COMprehensive Post-Acute Stroke Services (COMPASS) Study is an ongoing cluster-randomized pragmatic trial to assess the effectiveness of a comprehensive, evidence-based, post-acute care model on patient-centered outcomes.
Methods: Forty-one hospitals in North Carolina were randomized (as 40 units) to either implement the COMPASS care model or continue their usual care. The recruitment goal is 6000 patients (3000 per arm). Hospital staff ascertain and enroll patients discharged home with a clinical diagnosis of stroke or transient ischemic attack. Patients discharged from intervention hospitals receive 2-day telephone follow-up; a comprehensive clinic visit within 2 weeks that includes a neurological evaluation, assessments of social and functional determinants of health, and an individualized COMPASS Care PlanTM integrated with a community-specific resource database; and additional follow-up calls at 30 and 60 days post-stroke discharge. This model is consistent with the Centers for Medicare and Medicaid Services transitional care management services provided by physicians or advanced practice providers with support from a nurse to conduct patient assessments and coordinate follow-up services. Patients discharged from usual care hospitals represent the control group and receive the standard of care in place at that hospital. Patient-centered outcomes are collected from telephone surveys administered at 90 days. The primary endpoint is patient-reported functional status as measured by the Stroke Impact Scale 16. Secondary outcomes are: caregiver strain, all-cause readmissions, mortality, healthcare utilization, and medication adherence. The study engages patients, caregivers, and other stakeholders (including policymakers, advocacy groups, payers, and local community coalitions) to advise and support the design, implementation, and sustainability of the COMPASS care model.
Discussion: Given the high societal and economic burden of stroke, identifying a care model to improve recovery, independence, and quality of life is critical for stroke survivors and their caregivers. The pragmatic trial design provides a real-world assessment of the COMPASS care model effectiveness and will facilitate rapid implementation into clinical practice if successful
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Clinical Research in Primary Stroke Prevention: Needs, Opportunities, and Challenges
Most (∼70%) of strokes are first-ever strokes, and hence to substantially reduce the neurological burden, primary prevention is crucial. Here, highlights of the National Institute of Neurological Disorders and Stroke workshop ‘Stroke Risk Assessment and Future Stroke Primary Prevention Trials’ held January 12–13, 2004 are summarized. The Workshop discussions focused on stroke risk assessment; the high-risk vs. population-based approaches to primary prevention; desirable characteristics of candidate treatments and potential novel treatments, such as the ‘polypill’; subclinical disease as risk assessment tool and as surrogate outcome, and methodological issues in stroke primary prevention trials. The importance of assessing cognitive decline as an important consequence of covert and overt vascular injury of the brain was emphasized. The scientific or logistic barriers to stroke primary prevention trials are challenging, but are not insurmountable
Advertising Disclaimer Effects of Stenting for Atherosclerotic Renal Artery Stenosis on eGFR and Predictors of Clinical Events in the CORAL Trial
Background and objectives: Atherosclerotic renal artery stenosis may cause kidney function loss, but effects of stenting on eGFR and clinical events associated with CKD are uncertain. Our study objectives were to determine effects of stenting on eGFR and predictors of clinical events.
Design, setting, participants, & measurements: Participants (n=931) in the Cardiovascular Outcomes in Renal Artery Stenosis Trial (from May of 2005 to September of 2012) had \u3e60% atherosclerotic renal artery stenosis and systolic hypertension on two or more antihypertensive drugs and/or stage ≥3 CKD. The intervention was stenting versus no stenting on a background of risk factor management: renin-angiotensin system inhibition, statin, antiplatelet therapy, and smoking cessation education. The effect of stenting on eGFR by the serum creatinine-cystatin C Chronic Kidney Disease Epidemiology Collaboration equation was the prespecified analysis of kidney function. Predictors of eGFR and CKD outcomes (≥30% eGFR loss, ESRD, and death) and cardiovascular disease outcomes (stroke, myocardial infarction, heart failure, and death) controlling for eGFR and albuminuria were also determined.
Results: eGFR was 59±24 ml/min per 1.73 m2 (mean±SD) at baseline. Over 3 years, eGFR change, assessed by generalized estimating equations, was −1.5±7.0 ml/min per 1.73 m2 per year in the stent group versus −2.3±6.3 ml/min per 1.73 m2 per year in the medical therapy only group (P=0.18). eGFR predictors (multiple variable generalized estimating equations) were age, albuminuria, systolic BP, and diabetes (inverse associations) as well as men, total cholesterol, and HDL cholesterol (positive associations). CKD outcomes events occurred in 19% (175 of 931), and predictors (Cox proportional hazards models) included albuminuria (positive association), systolic BP (positive association), and HDL cholesterol (inverse association). Cardiovascular disease outcomes events occurred in 22% (207 of 931), and predictors included age, albuminuria, total cholesterol, prior cardiovascular disease, and bilateral atherosclerotic renal artery stenosis (positive associations).
Conclusions: Stenting did not influence eGFR in participants with atherosclerotic renal artery stenosis receiving renin-angiotensin system inhibition–based therapy. Predictors of clinical events were traditional risk factors for CKD and cardiovascular disease
Multivariate linear regression and generalized linear regression comparing smokers and non-smokers on baseline characteristics as the response adjusted for age, sex and ethnicity.
<p>Multivariate linear regression and generalized linear regression comparing smokers and non-smokers on baseline characteristics as the response adjusted for age, sex and ethnicity.</p
Baseline clinical characteristics comparisons by smoking status within the last year.
<p>Baseline clinical characteristics comparisons by smoking status within the last year.</p