02209nas a2200193 4500008004100000022001400041245011400055210006900169260001600238520157000254100002001824700002101844700002001865700002901885700002201914700002001936700002301956856003601979 2017 eng d a1464-368500aComparing methods to address bias in observational data: statin use and cardiovascular events in a US cohort.0 aComparing methods to address bias in observational data statin u c2017 Sep 083 a

Background: The theoretical conditions under which causal estimates can be derived from observational data are challenging to achieve in the real world. Applied examples can help elucidate the practical limitations of methods to estimate randomized-controlled trial effects from observational data.

Methods: We used six methods with varying design and analytic features to compare the 5-year risk of incident myocardial infarction among statin users and non-users, and used non-cardiovascular mortality as a negative control outcome. Design features included restriction to a statin-eligible population and new users only; analytic features included multivariable adjustment and propensity score matching.

Results: We used data from 5294 participants in the Cardiovascular Health Study from 1989 to 2004. For non-cardiovascular mortality, most methods produced protective estimates with confidence intervals that crossed the null. The hazard ratio (HR) was 0.92, 95% confidence interval: 0.58, 1.46 using propensity score matching among eligible new users. For myocardial infarction, all estimates were strongly protective; the propensity score-matched analysis among eligible new users resulted in a HR of 0.55 (0.29, 1.05)-a much stronger association than observed in randomized controlled trials.

Conclusions: In designs that compare active treatment with non-treated participants to evaluate effectiveness, methods to address bias in observational data may be limited in real-world settings by residual bias.

1 aKaiser, Paulina1 aArnold, Alice, M1 aBenkeser, David1 aHazzouri, Adina, Zeki Al1 aHirsch, Calvin, H1 aPsaty, Bruce, M1 aOdden, Michelle, C uhttps://chs-nhlbi.org/node/750202117nas a2200217 4500008004100000022001400041245012100055210006900176260001300245300001000258490000700268520143400275100002001709700001901729700002501748700002201773700002401795700002101819700002301840856003601863 2020 eng d a1873-258500aThe association of prediagnosis social support with survival after heart failure in the Cardiovascular Health Study.0 aassociation of prediagnosis social support with survival after h c2020 Feb a73-770 v423 a

PURPOSE: Although social support has been shown to be associated with survival among persons with cardiovascular disease, little research has focused on whether social support, measured before the onset of heart failure, can enhance survival after diagnosis. The objective of this study was to assess the association between prediagnosis social support and postdiagnosis survival among older adults with heart failure.

METHODS: We obtained the data from the Cardiovascular Health Study, which included noninstitutionalized adults aged 65 years or older from four sites in the United States with primary enrollment in 1989-1990. We used two measures of social support, the Lubben Social Network Scale and the Interpersonal Support Evaluation List. The analytic data set included 529 participants with a social support measure within two years before diagnosis of heart failure.

RESULTS: After adjustment for demographic covariates, cardiovascular risk factors, and general health status, mortality rates were lower among participants in the highest tertile of social network scores (HR 0.74, 95% CI: 0.59, 0.93) and the middle tertile (HR 0.73 [0.58, 0.90]), compared with the lowest tertile. Results with interpersonal support were null.

CONCLUSIONS: These findings suggest that prediagnosis structural social support may modestly buffer heart failure patients from mortality.

1 aKaiser, Paulina1 aAllen, Norrina1 aDelaney, Joseph, A C1 aHirsch, Calvin, H1 aCarnethon, Mercedes1 aArnold, Alice, M1 aOdden, Michelle, C uhttps://chs-nhlbi.org/node/828502707nas a2200241 4500008004100000022001400041245011900055210006900174260001600243520193300259100002902192700002002221700002002241700002002261700002002281700002402301700001902325700001902344700002102363700001902384700002602403856003602429 2021 eng d a1758-535X00aStatins and cognitive decline in the Cardiovascular Health Study: A comparison of different analytical approaches.0 aStatins and cognitive decline in the Cardiovascular Health Study c2021 Jul 313 a

BACKGROUND: Despite their well-established benefits for the prevention of cardiovascular disease, robust evidence on the effects of statins on cognition is largely inconclusive. We apply various study designs and analytical approaches to mimic randomized controlled trial (RCT) effects from observational data.

METHODS: We used observational data from 5,580 participants enrolled in the Cardiovascular Health Study from 1989/90 to 1999/2000. We conceptualized the cohort as an overlapping sequence of non-randomized trials. We compared multiple selection (eligible population, prevalent users, new-users) and analytic approaches (multivariable adjustment, inverse probability treatment weights, propensity score matching) to evaluate the association between statin use and 5-year change in global cognitive function, assessed using the Modified Mini-Mental State (3MS) examination.

RESULTS: When comparing prevalent users to non-users (N=2,772), statin use was associated with slower cognitive decline over 5 years (adjusted annual change in 3MSE = 0.34 points/year; 95% CI:0.05;0.63). Compared to prevalent user design, estimates from new user designs (e.g. comparing eligible statin initiators to non-initiators) were attenuated showing either null or negative association, though not significant. For example, in a propensity score-matched sample of statin-eligible individuals (N=454), annual 3MS change comparing statin initiators to non-initiators was -0.21 points/year (95% CI:-0.81;0.39).

CONCLUSIONS: The association of statin use and cognitive decline is attenuated towards the null when using rigorous analytical approaches that more closely mimic RCTs. Point estimates, even within the same study, may vary depending on the analytical methods used. Further studies that leverage natural or quasi experiments around statin use are needed to replicate our findings.

1 aHazzouri, Adina, Zeki Al1 aJawadekar, Neal1 aGrasset, Leslie1 aKaiser, Paulina1 aKezios, Katrina1 aCalonico, Sebastian1 aGlymour, Maria1 aHirsch, Calvin1 aArnold, Alice, M1 aVaradhan, Ravi1 aOpoodden, Michelle, C uhttps://chs-nhlbi.org/node/8840