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Postacute myocardial infarction (AMI) readmissions are common among Medicare beneficiaries (≥65 years) and are associated with significant resource utilization. However, patterns of AMI readmissions for younger age groups in the United States are not known. In the Nationwide Readmissions Database, a nationally representative all-payer database of inpatient hospitalizations, we identified 212,171 index AMI hospitalizations in January to November 2013, weighted to represent 478,247 hospitalizations nationally (mean age 66.9 years, 38% women, 29% low income). This included 26,516 cases in the 18 to 44 age group, 183,703 in the 45 to 64 age group, and 268,027 in the ≥65 age group. The overall 30-day readmission rate was 14.5% and varied across age groups (9.7% [18 to 44], 11.2% [45 to 64], and 17.3% [≥65]). The cumulative cost of 30-day readmissions was $1.1 billion, of which $365 million was spent on those <65 years of age. In multivariable hierarchical models, the risk of readmission was higher in women and in low-income patients, but the effect varied by age (p value for age-gender and age-income interactions <0.05) and was more prominent in the younger age groups. Further, patients in all age groups continue to have a high hospitalization burden beyond the typical 30-day readmission period, with an overall 24% post-AMI 90-day readmission rate. In conclusion, readmissions in young and middle-aged AMI survivors pose a substantial burden on patients and on U.S. health-care resources. Women and low-income patients with AMI, particularly those in younger age groups, are more frequently readmitted, and readmissions continue to burden the health-care system beyond the typical 30-day window. Future investigations would need to be targeted toward a better understanding and improvement of the rehospitalization burden for vulnerable patient groups.

To determine the association between cardiorespiratory fitness and sedentary behavior, independent of exercise activity. We included 2223 participants (aged 12-49 years; 1053 females [47%]) without known heart disease who had both cardiovascular fitness testing and at least 1 day of accelerometer data from the National Health and Nutrition Examination Survey 2003-2004. From accelerometer data, we quantified bouts of exercise as mean minutes per day for each participant. Sedentary time was defined as less than 100 counts per minute in mean minutes per day. Cardiorespiratory fitness was derived from a submaximal exercise treadmill test. Multivariable-adjusted linear regression analyses were performed with fitness as the dependent variable. Models were stratified by sex, adjusted for age, body mass index, and wear time, and included sedentary and exercise time. An additional hour of daily exercise activity time was associated with a 0.88 (0.37-1.39; P<.001) metabolic equivalent of task (MET) higher fitness for men and a 1.37 (0.43-2.31; P=.004) MET higher fitness for women. An additional hour of sedentary time was associated with a −0.12 (−0.02 to −0.22; P=.03) and a −0.24 (−0.10 to −0.38; P<.001) MET difference in fitness for men and women, respectively. After adjustment for exercise activity, sedentary behavior appears to have an inverse association with fitness. These findings suggest that the risk related to sedentary behavior might be mediated, in part, through lower fitness levels.

Low mid-life fitness is associated with higher risk for heart failure (HF). However, it is unclear to what extent this HF risk is modifiable and mediated by the burden of cardiac and noncardiac comorbidities. We studied the effect of cardiac and noncardiac comorbidities on the association of mid-life fitness and fitness change with HF risk. Linking individual subject data from the Cooper Center Longitudinal Study (CCLS) with Medicare claims files, we studied 19,485 subjects (21.2% women) who survived to receive Medicare coverage from 1999 to 2009. Fitness estimated by Balke treadmill time at mean age of 49years was analyzed as a continuous variable (in metabolic equivalents [METs]) and according to age- and sex-specific quintiles. Associations of mid-life fitness and fitness change with HF hospitalization after age of 65 years were assessed by applying a proportional hazards recurrent events model to the failure time data with each comorbidity entered as time-dependent covariates. After 127,110 person years of Medicare follow-up, we observed 1,038 HF hospitalizations. Higher mid-life fitness was associated with a lower risk for HF hospitalization (hazard ratio [HR] 0.82 [0.76-0.87] per MET) after adjustment for traditional risk factors. This remained unchanged after further adjustment for the burden of Medicare-identified cardiac and noncardiac comorbidities (HR 0.83 [0.78-0.89]). Each 1 MET improvement in mid-life fitness was associated with a 17% lower risk for HF hospitalization in later life (HR 0.83 [0.74-0.93] per MET). Mid-life fitness is an independent and modifiable risk factor for HF hospitalization at a later age.

ObjectiveThis study aimed to examine the association of midlife fitness and body mass index (BMI) with incident dementia later in life.Design and participantsA cohort study of 6428 individuals (mean age 50.9±7.6 years) from the Cooper Center Longitudinal Study.MeasuresCardiorespiratory fitness and BMI were assessed twice (1970–1999) during visits to the Cooper Clinic, a preventive medicine clinic in Dallas, Texas. These measures were examined as continuous and categorical variables. As continuous variables, fitness and BMI were examined at baseline (averaged of two examinations) and as absolute change between exams (mean time 2.1±1.8 years). Variables were categorised: unfit versus fit and normal versus overweight/obese. Medicare claims data were used to obtain all-cause dementia incidence (1999–2009). Mean follow-up between midlife examinations and Medicare surveillance was 15.7 ((SD=6.2) years. Multivariable models were used to assess the associations between fitness, BMI and dementia.ResultsDuring 40 773 person years of Medicare surveillance, 632 cases of dementia were identified. After controlling for BMI and covariates, each 1-metabolic equivalent increment in fitness was associated with 5% lower (HR 0.95; 95% CI 0.90 to 0.99) dementia risk. In comparison, after controlling for fitness and covariates, each 1 kg/m2 increment in BMI was associated with a 3.0% (HR 1.03; 95% CI 1.00 to 1.07) higher risk for dementia, yet without significance (p=0.051). Similar findings were observed when the exposures were categorised. Changes in fitness and BMI between examinations were not related to dementia. Jointly, participants who were unfit and overweight/obese had the highest (HR 2.28 95% CI 1.57 to 3.32) dementia risk compared with their fit and normal weight counterparts.ConclusionLower midlife fitness is a risk marker for dementia irrespective of weight status. Being unfit coupled with overweight/obese status might increase one’s risk for dementia even further.

Several magnetic resonance imaging (MRI) studies have reported that antidepressant medications are strongly linked to brain microstructural alterations. Notably, external capsule alterations have been reported to be a biological marker for therapeutic response. However, prior studies did not investigate whether a change in the neurite density or directional coherence of white matter (WM) fibers underlies the observed microstructural alterations. This MRI-based case–control study examined the relationship between patients’ current use of antidepressant medications and advanced measurements of external capsule WM microstructure derived from multishell diffusion imaging using neurite orientation dispersion and density imaging (NODDI). The study compared a group of thirty-five participants who were taking antidepressant medications comprising selective serotonin reuptake inhibitors (SSRIs) (n = 25) and serotonin and norepinephrine reuptake inhibitors (SNRIs) with a control group of thirty-five individuals matched in terms of age, sex, race, and atherosclerotic cardiovascular risk factors. All participants were selected from the Dallas Heart Study phase 2, a multi-ethnic, population-based cohort study. A series of multiple linear regression analyses were conducted to predict microstructural characteristics of the bilateral external capsule using age, sex, and antidepressant medications as predictor variables. There was significantly reduced neurite density in the bilateral external capsules of patients taking SSRIs. Increased orientation dispersion in the external capsule was predominantly seen in patients taking SNRIs. Our findings suggest an association between specific external capsule microstructural changes and antidepressant medications, including reduced neurite density for SSRIs and increased orientation dispersion for SNRIs.

We tested the ability of the Framingham Risk Score (FRS) and the online ATP III risk estimator to estimate risk and to predict 10-year and longer-term coronary heart disease (CHD) death in younger adults (age 18-39 years). Although prediction with individual risk factors has been tested in individuals <30 years, current multivariate risk prediction strategies have not been applied to prediction of clinical CHD in this age range. We included 10 551 male participants of the CHA study who were aged 18 to 39 years and free of baseline CHD and diabetes at enrollment from 1967 to 1973. Risk of CHD was estimated using both FRS and ATP III online risk estimator for each individual. Men were stratified into deciles according to the magnitude of predicted risk calculated from measured baseline risk factors (CHA-predicted risk). Observed CHD mortality rates for 10, 20, and 30 years of follow-up were compared with estimated risks. Death rates of CHD were low across 30 years of follow-up. The FRS remained <10% for all deciles of CHA-predicted risk in the 18- to 29-year-old cohort. Framingham-predicted risk reached 12% only in the 30- to 39-year-old cohort in the highest decile of CHA-predicted risk despite substantial risk factor burden. Neither method classified individuals <30 years as high risk despite substantial risk factor burden. Future clinical guidelines should consider alternative strategies to estimate and communicate risk in populations <30 years.

Previous studies have demonstrated ethnic/racial differences in cardiorespiratory fitness (CRF). However, the relative contributions of body mass index (BMI), lifestyle behaviors, socioeconomic status (SES), cardiovascular (CV) risk factors, and cardiac function to these differences in CRF are unclear. In this study, we included 2,617 Dallas Heart Study participants (58.6% women, 48.6% black; 15.7% Hispanic) without CV disease who underwent estimation of CRF using a submaximal exercise test. We constructed multivariable-adjusted linear regression models to determine the association between race/ethnicity and CRF, which was defined as peak oxygen uptake (ml/kg/min). Black participants had the lowest CRF (blacks: 26.3 ± 10.2; whites: 29.0 ± 9.8; Hispanics: 29.1 ± 10.0 ml/kg/min). In multivariate analysis, both black and Hispanic participants had lower CRF after adjustment for age and gender (blacks: Std β = −0.15; p value ≤0.0001, Hispanics: Std β = −0.05, p value = 0.01; ref group: whites). However, this association was considerably attenuated for black (Std β = −0.04, p value = 0.03) and no longer significant for Hispanic ethnicity (p value = 0.56) after additional adjustment for BMI, lifestyle factors, SES, and CV risk factors. Additional adjustment for stroke volume did not substantially change the association between black race/ethnicity and CRF (Std β = −0.06, p value = 0.01). In conclusion, BMI, lifestyle, SES, and traditional risk factor burden are important determinants of ethnicity-based differences in CRF.

The ability of HDL to accept cholesterol from macrophages (cholesterol efflux capacity) is a key part of reverse cholesterol transport. In nearly 3000 adults, higher quartiles of baseline cholesterol efflux capacity were associated with lower rates of cardiovascular events. A low level of high-density lipoprotein (HDL) cholesterol is a major independent risk factor for atherosclerotic cardiovascular disease. 1 However, in randomized, controlled trials, high-dose niacin or inhibitors of cholesteryl ester transfer protein did not improve cardiovascular outcomes despite significantly increasing the HDL cholesterol level. 2 – 5 Furthermore, genetic variants associated with HDL cholesterol levels are often not associated with cardiovascular disease. 6 These observations suggest that HDL cholesterol may not be causally associated with cardiovascular disease, and they highlight the potential limitations of using the HDL cholesterol level to assess risk or responses to therapies targeted at HDL cholesterol. HDL has numerous . . .

Data from more than 250,000 men and women in 18 cohort studies were used to calculate the lifetime risk of cardiovascular events, stratified according to risk-factor burden, with adjustment for the competing risk of death from noncardiovascular causes. In recent decades, clinical and public health efforts to reduce the burden of cardiovascular disease have emphasized the importance of calculating global, short-term (generally 10-year) risk estimates. 1 However, the majority of adults in the United States who are considered to be at low risk for cardiovascular disease in the short term are actually at high risk across their remaining lifespan. 2 , 3 Estimates of the lifetime risk of cardiovascular disease provide a more comprehensive assessment of the overall burden of the disease in the general population, now and in the future, because they take into account both the risk of cardiovascular . . .