02903nas a2200421 4500008004100000022001400041245011100055210006900166260001300235300001100248490000800259520175200267653002502019653000902044653001902053653002402072653003002096653002802126653001102154653001102165653002002176653000902196653001502205653003302220653002402253653000902277653001702286653001302303100001602316700001902332700001502351700001702366700001602383700001802399700001402417700001502431856003502446 1999 eng d a0002-934300aOral anticoagulation in patients with atrial fibrillation: adherence with guidelines in an elderly cohort.0 aOral anticoagulation in patients with atrial fibrillation adhere c1999 Feb a165-710 v1063 a

PURPOSE: To determine adherence with practice guidelines in a population-based cohort of elderly persons aged 70 years or older with atrial fibrillation.

SUBJECTS AND METHODS: This was a cross-sectional analysis of a subgroup of participants in the Cardiovascular Health Study, a prospective observational study involving four communities in the United States. Subjects were participants with atrial fibrillation on electrocardiogram at one or more yearly examinations from 1993 to 1995. The outcome measure was self-reported use of warfarin in 1995.

RESULTS: In 1995, 172 (4.1%) participants had atrial fibrillation together with information regarding warfarin use and no preexisting indication for its use. Warfarin was used by 63 (37%) of these participants. Of the 109 participants not reporting warfarin use, 92 (84%) had at least one of the clinical risk factors (aside from age) associated with stroke in patients with atrial fibrillation. Among participants not taking warfarin, 47% were taking aspirin. Several characteristics were independently associated with warfarin use, including age [odds ratio (OR) = 0.6 per 5-year increment, 95% CI 0.5-0.9], a modified mini-mental examination score <85 points [OR = 0.3, 95% confidence interval (CI) 0.1-0.9], and among patients without prior stroke, female sex (OR = 0.5, 95% CI 0.2-1.0).

CONCLUSIONS: Despite widely publicized practice guidelines to treat patients who have atrial fibrillation with warfarin, most participants who had atrial fibrillation were at high risk for stroke but were not treated with warfarin. More studies are needed to determine why elderly patients with atrial fibrillation are not being treated with warfarin.

10aAdministration, Oral10aAged10aAnticoagulants10aAtrial Fibrillation10aCerebrovascular Disorders10aCross-Sectional Studies10aFemale10aHumans10aLogistic Models10aMale10aOdds Ratio10aPractice Guidelines as Topic10aProspective Studies10aRisk10aRisk Factors10aWarfarin1 aWhite, R, H1 aMcBurnie, M, A1 aManolio, T1 aFurberg, C D1 aGardin, J M1 aKittner, S, J1 aBovill, E1 aKnepper, L uhttps://chs-nhlbi.org/node/59003636nas a2200397 4500008004100000022001400041245015700055210006900212260001600281300001200297490000800309520249400317653002102811653000902832653001102841653002202852653001102874653001402885653000902899653002602908653002602934653003002960653003202990653000903022653001703031653002103048100001503069700001703084700001603101700001503117700002103132700001603153700001403169700002003183856003503203 1999 eng d a0003-992600aTraditional risk factors and subclinical disease measures as predictors of first myocardial infarction in older adults: the Cardiovascular Health Study.0 aTraditional risk factors and subclinical disease measures as pre c1999 Jun 28 a1339-470 v1593 a

BACKGROUND: Risk factors for myocardial infarction (MI) have not been well characterized in older adults, and in estimating risk, we sought to assess the individual and joint contributions made by both traditional risk factors and measures of subclinical disease.

METHODS: In the Cardiovascular Health Study, we recruited 5888 adults aged 65 years and older from 4 US centers. At baseline in 1989-1990, participants underwent an extensive examination that included traditional risk factors such as blood pressure and fasting glucose level and measures of subclinical disease as assessed by electrocardiography, carotid ultrasonography, echocardiography, pulmonary function, and ankle-arm index. Participants were followed up with semiannual contacts, and all cardiovascular events were classified by the Morbidity and Mortality Committee. The main analytic technique was the Cox proportional hazards model.

RESULTS: At baseline, 1967 men and 2979 women had no history of an MI. After follow-up for an average of 4.8 years, there were 302 coronary events, which included 263 patients with MI and 39 with definite fatal coronary disease. The incidence was higher in men (20.7 per 1000 person-years) than women (7.9 per 1000 person-years). In all subjects, the incidence was strongly associated with age, increasing from 7.8 per 1000 person-years in subjects aged 65 to 69 years to 25.6 per 1000 person-years in subjects aged 85 years and older. Glucose level and systolic blood pressure were associated with the incidence of MI, but smoking and lipid measures were not. After adjustment for age and sex, the significant subclinical disease predictors of MI were borderline or abnormal ejection fraction by echocardiography, high levels of intimal-medial thickness of the internal carotid artery, and a low ankle-arm index. Forced vital capacity and electrocardiographic left ventricular mass did not enter the stepwise model. Excluding subjects with clinical cardiovascular diseases such as prior angina or congestive heart failure at baseline had little effect on these results. Risk factors were generally similar in men and women.

CONCLUSIONS: After follow-up of 4.8 years, systolic blood pressure, fasting glucose level, and selected subclinical disease measures were important predictors of the incidence of MI in older adults. Uncontrolled high blood pressure may explain about one quarter of the coronary events in this population.

10aAge Distribution10aAged10aFemale10aFollow-Up Studies10aHumans10aIncidence10aMale10aMultivariate Analysis10aMyocardial Infarction10aPredictive Value of Tests10aProportional Hazards Models10aRisk10aRisk Factors10aSex Distribution1 aPsaty, B M1 aFurberg, C D1 aKuller, L H1 aBild, D, E1 aRautaharju, P, M1 aPolak, J, F1 aBovill, E1 aGottdiener, J S uhttps://chs-nhlbi.org/node/59303152nas a2200337 4500008004100000022001400041245008600055210006900141260001300210300001100223490000700234520223900241653000902480653002802489653001902517653001502536653001102551653001702562653001402579653000902593653003202602653002402634653000902658653001802667100002202685700001702707700001702724700001802741700002002759856003502779 2001 eng d a1047-279700aHypertension, heart rate, use of antihypertensives, and incident prostate cancer.0 aHypertension heart rate use of antihypertensives and incident pr c2001 Nov a534-420 v113 a

PURPOSE: Recent studies have reported conflicting results on a possible relationship between hypertension, heart rate, and prostate cancer. A model has been developed suggesting that high blood pressure and high heart rate may both be markers for increased central sympathetic nervous activity, which may result in androgen-mediated stimulation of prostate cancer growth.

METHODS: In this study we examined the associations between hypertension, heart rate, use of antihypertensive medications, and incident prostate cancer in a cohort of 2442 men. Data from the Cardiovascular Health Study (CHS), an NHLBI-sponsored observational study of adults age 65 or older in four U.S. communities, were analyzed using Cox proportional hazards regression. Seated systolic and diastolic blood pressures were measured using a standardized protocol at the initial clinical examination and annually at follow-up visits. Medications data were transcribed by trained interviewers from prescription medication containers brought into the clinic by participants.

RESULTS: A total of 209 cases of incident prostate cancer were identified from either an ICD-9 code of 185 in hospital medical records (n = 130) or by self-report from annual surveillance interviews (n = 79). An average of 5.6 years of follow-up was available for analyses. No associations between blood pressure measures at entry into the study and prostate cancer were found, although these results may have been affected by subsequent treatment of hypertension. An association between resting heart rate (HR) equal to or greater than 80 beats per minute and incident prostate cancer was found compared to men with a rate of less than 60 beats per minute (HR: 1.6, 95% confidence interval [CI]: 1.03-2.5). An inverse association was found between risk of incident prostate cancer and use of any antihypertensive medication (HR: 0.7, 95% CI: 0.5-0.9). A test of heterogeneity found no difference between use of the specific classes of antihypertensive medication and the association with prostate cancer risk.

CONCLUSIONS: These data tend to support the hypothesized causal pathway between vascular disease markers and prostate cancer.

10aAged10aAntihypertensive Agents10aCohort Studies10aHeart Rate10aHumans10aHypertension10aIncidence10aMale10aProportional Hazards Models10aProstatic Neoplasms10aRisk10aUnited States1 aFitzpatrick, A, L1 aDaling, J, R1 aFurberg, C D1 aKronmal, R, A1 aWeissfeld, J, L uhttps://chs-nhlbi.org/node/66603296nas a2200409 4500008004100000022001400041245013600055210006900191260001300260300001300273490000700286520212000293653005102413653000902464653002202473653002802495653003002523653001102553653001102564653001402575653002302589653000902612653001602621653003002637653001502667653002402682653000902706653001702715100001702732700001602749700001602765700001502781700001902796700001702815700001802832856003602850 2012 eng d a1945-719700aLipoprotein-associated phospholipase A2 (Lp-PLA2) and future risk of type 2 diabetes: results from the Cardiovascular Health Study.0 aLipoproteinassociated phospholipase A2 LpPLA2 and future risk of c2012 May a1695-7010 v973 a

INTRODUCTION: Lipoprotein-associated phospholipase A2 (Lp-PLA(2)) has been consistently associated with cardiovascular disease (CVD) risk factors and predictive of CVD outcomes; furthermore, it is consistently higher among type 2 diabetics than nondiabetics. However, the relationships of circulating Lp-PLA(2) mass and activity with incident type 2 diabetes mellitus have not been examined. Therefore, the purpose of this study was to determine the association of Lp-PLA(2) mass and activity with type 2 diabetes among older adults.

METHODS: We conducted analyses of Lp-PLA(2) and prevalent and incident diabetes among 5474 men and women from the Cardiovascular Health Study (1989-2007). Lp-PLA(2) mass and activity were measured in baseline plasma. Diabetes status was ascertained annually with medication inventories and repeated blood glucose measurements. Generalized linear and Cox proportional hazards models were used to adjust for confounding factors including body mass index and inflammation.

RESULTS: At baseline, the top two quintiles of Lp-PLA(2) activity were significantly associated with prevalent type 2 diabetes with a multivariable relative risk = 1.35 [95% confidence interval (CI) = 1.11-1.63] for quintile 4, and relative risk = 1.33 (95% CI = 1.07-1.66) for quintile 5. Among participants free of diabetes at baseline, we found a significant positive association with both the homeostatic model assessment for insulin resistance and β-cell function per SD increase in Lp-PLA(2) activity (P values for both <0.01). In prospective analyses, the risk of incident type 2 diabetes was significantly higher among those in the highest quintile of Lp-PLA(2) activity [multivariable hazard ratio = 1.45 (95% CI = 1.01-2.07)] compared with the lowest quintile. Lp-PLA(2) mass was not significantly associated with incident type 2 diabetes.

DISCUSSION: Lp-PLA(2) activity is positively associated with insulin resistance and predicts incident type 2 diabetes among older adults independent of multiple factors associated with diabetes pathogenesis.

10a1-Alkyl-2-acetylglycerophosphocholine Esterase10aAged10aAged, 80 and over10aCardiovascular Diseases10aDiabetes Mellitus, Type 210aFemale10aHumans10aIncidence10aInsulin Resistance10aMale10aMiddle Aged10aPredictive Value of Tests10aPrevalence10aProspective Studies10aRisk10aRisk Factors1 aNelson, T, L1 aBiggs, M, L1 aKizer, J, R1 aCushman, M1 aHokanson, J, E1 aFurberg, C D1 aMukamal, K, J uhttps://chs-nhlbi.org/node/1369