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Objective: Greater parity has been associated with cardiovascular disease risk. We sought to find whether the effects on cardiac remodeling and heart failure risk are clear.Methods: We examined the association of number of live births with echocardiographic measures of cardiac structure and function in participants of the Framingham Heart Study (FHS) using multivariable linear regression. We next examined the association of parity with incident heart failure with preserved (HFpEF) or reduced (HFrEF) ejection fraction using a Fine-Gray subdistribution hazards model in a pooled analysis of n = 12,635 participants in the FHS, the Cardiovascular Health Study, the Multi-Ethnic Study of Atherosclerosis, and Prevention of Renal and Vascular Endstage Disease. Secondary analyses included major cardiovascular disease, myocardia infarction and stroke.Results: Among n = 3931 FHS participants (mean age 48 ± 13 years), higher numbers of live births were associated with worse left ventricular fractional shortening (multivariable β -1.11 (0.31); P = 0.0005 in ≥ 5 live births vs nulliparous women) and worse cardiac mechanics, including global circumferential strain and longitudinal and radial dyssynchrony (P < 0.01 for all comparing ≥ 5 live births vs nulliparity). When examining HF subtypes, women with ≥ 5 live births were at higher risk of developing future HFrEF compared with nulliparous women (HR 1.93, 95% CI 1.19–3.12; P = 0.008); by contrast, a lower risk of HFpEF was observed (HR 0.58, 95% CI 0.37–0.91; P = 0.02).Conclusions: Greater numbers of live births are associated with worse cardiac structure and function. There was no association with overall HF, but a higher number of live births was associated with greater risk for incident HFrEF.

Depression is common among patients with heart failure (HF) and can impact patients' outcomes. In this study, we evaluated the rates of psychotherapy referrals for patients with HF with depression.Using the National Ambulatory Medical Care Survey from 2008 to 2018, we examined visits for patients with depression and concurrent HF or coronary artery disease. We estimated the likelihood of referral for psychotherapy using survey weights to provide nationally representative estimates. Among 1797 visits for patients with HF or coronary artery disease and depression, only 9.4% (95% confidence interval 7.2%-12.2%) were referred for psychotherapy, including mental health counseling and stress management. Rates of referral were lowest among patients with depression and HF at 7.5% (95% confidence interval 4.1%-13.2%). The odds of referral decreased over the years from 2008 to 2018 (odds ratio per additional year 0.87, 95% confidence interval 0.77-0.98, P = .022), with referral rates in 2008 of 12.8% compared with 4.8% in 2018.In this nationally representative study of ambulatory visits, patients with HF and depression were referred for psychotherapy in only 7.5% of visits and referral rates have decreased over the years. Magnifying the value of psychotherapy and increasing referral rates are essential steps to improve care for patients with HF with depression.

Background: It is unclear to what extent following a standard performance protocol will help reduce gaps in cardiovascular health among sexes, racial/ethnic groups, and geographic regions in United States hospitals. Method: Based on the Get With The Guidelines Coronary Artery Disease (GWTG-CAD) registry linked with Medicare inpatient data, we included 49,358 patients, age 65 years or older, from 366 US hospitals from 2003 to 2009. Our primary outcome was 3-year all-cause mortality. Exposures included sex, race/ethnicity, and geographic region. Our mediator was a composite score of quality of care, defined as the total number of performance measures the patient received divided by total number of performance measures the patient was eligible for. Logistic regression with generalized estimating equations and mediation analysis were used. Results: During 3 years of follow-up, 16,130 deaths were identified. Compared with men, women were less likely to receive optimal care at discharge (adjusted odds ratio (aOR)=0.92, 95% Confidence Interval (CI): 0.88-0.95, p Conclusion: Compared with men, women were less likely to receive optimal care at discharge which was associated with higher mortality. The observed sex disparity in mortality could potentially be reduced or even eliminated by providing equitable and optimal care. In contrast, the higher mortality observed in black patients could not be accounted for by differences in the quality of care measured in this study. We did not observe differences in care or outcomes by geographic region.

Advanced glycation end products (AGEs) are compounds formed by the non-enzymatic glycation of proteins, lipids, and nucleic acids, and are thought to play a role in the pathogenesis of diseases across multiple organ systems. Carboxymethyl-lysine (CML) is a dominant AGE found in tissue proteins and in the circulation, and a commonly used AGE biomarker. Only a few epidemiological studies have evaluated the association between circulating CML and mortality risk, and none have evaluated the association between CML and cause-specific non-CVD mortality. We measured CML by ELISA on serum specimens collected from 3,373 Cardiovascular Health Study participants in 1996. Participants were followed for death through 2010, and cause of death was classified using death certificates, medical records, and proxy interview. We used Cox regression to estimate the relative risk of total and cause-specific mortality associated with circulating CML, adjusting for confounders (Models 1 & 2) and estimated glomerular filtration rate (eGFR) as a potential mediator (Model 3). We tested whether sex or diabetes modified the association between CML and mortality. The mean age among participants was 78 years and 60% were women. The mean CML level among participants was 629 ng/mL. Over median follow-up of 10 years, 2,322 deaths occurred (73.4 per 1,000 person-years). After adjustment for confounders (Models 1 & 2), CML was associated with an increased risk of death from CVD, dementia, infection, fracture/trauma, and renal failure (Table). Aside from renal failure, adjustment for eGFR attenuated the HR estimates modestly. There was no evidence for effect modification of the association of CML and all-cause mortality risk by sex or diabetes. In a cohort of community-dwelling older individuals, elevated circulating CML was associated with increased risk of mortality from cardiovascular causes, dementia, infection, fracture/trauma, and renal failure. A portion of the increased risk may be mediated through decreased renal function.

This study aimed to examine the possible antecedents of both dementia and sustained intact cognition at age 90 years among men who underwent a prospective, multidisciplinary assessment from ages 19 to 90 years, with little attrition.We conducted a prospective 20-year reassessment of 196 (out of 268) former Harvard college sophomores who survived until age 70 years. Since 1939, the study gathered measurements of childhood environment, dominant personality traits, objective mental and physical health over time, smoking in pack-years, alcohol abuse, and depression. Questionnaires were obtained every 2 years and physical exams every 5 years. Cognitive status was assessed at ages 80, 85, and 90 years.Despite addressing a wide variety of health, behavioral, and social factors over the lifespan, we observed few predictors with strong association with either intact cognition at age 90 years (n = 40) or dementia (n = 44). Univariate analysis revealed seven suggestive predictors of intact cognition at age 90 years or of dementia: warm childhood relationship with mother, exercise at age 60 years, high maternal education, young age of mother at subject's birth, low body mass index, good physical health at 60 years, and late retirement. Only the first three variables, warm childhood relationship with mother, exercise at age 60 years, and high maternal education, remained significant with logistic regression.In this prospective study of long-lived, highly educated men, several well-known putative predictors of Alzheimer's disease did not distinguish those who over the next 20 years developed dementia from those with unimpaired cognition until age 90 years.

Introduction: Fibroblast growth factor-23 (FGF-23) is a bone-derived phosphaturic hormone strongly associated with cardiovascular mortality and left ventricular hypertrophy among individuals with end-stage renal disease (ESRD). Whether the relationship between FGF-23 and cardiac dysfunction extends to participants without ESRD is not clearly established. Hypothesis: We tested whether FGF-23 is associated with left ventricular mass index (LVMI) and left ventricular ejection fraction (LVEF) in participants with coronary heart disease (CHD) and a broad range of kidney function in the Heart and Soul Study. Methods and Results: In cross-sectional analyses of 887 participants of the Heart and Soul Study, FGF-23 was positively associated with LVMI (2.09 g/m 2 , 95% confidence interval [CI] 0.15 to 4.03 per 1 standard-deviation [SD] higher ln FGF-23) and inversely associated with LVEF (-0.96%, CI -1.71% to -0.21%, per 1 SD higher ln FGF-23) after adjustment for age, CHD risk factors, microalbuminuria, and cystatin-based estimated glomerular filtration rate (eGFR). In multinomial logistic regression, FGF-23 was associated with an increased prevalence of concentric hypertrophy (odds ratio 1.66, CI 1.00 to 2.76, per 1 SD increase in ln FGF-23) but not eccentric hypertrophy (odds ratio 1.14, CI 0.96 to 1.36). The association between FGF-23 and concentric hypertrophy was stronger among individuals with an estimated GFR < 60 mL/min per 1.73 m 2 , and was not statistically significant among individuals with normal to mildly reduced kidney function (Figure, p interaction 0.11). Conclusion: In conclusion, FGF-23 was associated with greater left ventricular mass and concentric hypertrophy, particularly among individuals with diminished kidney function. Additional studies are necessary to determine the pathways that mediate this association.

Background: Fibroblast growth factor-23 (FGF23) increases renal phosphorus excretion and inhibits calcitriol synthesis. In advanced chronic kidney disease (CKD), high FGF23 levels are associated with increased mortality. The relationship of FGF23 with all-cause mortality, incident heart failure (HF), and incident cardiovascular disease (CVD) in community-living populations is uncertain Methods: Among 3,107 community-living individuals aged > 65 years, we measured plasma FGF23 concentrations in 1996-97. Follow-up for death and adjudicated HF and CVD events continued through 2008. Cox proportional hazards models evaluated associations of FGF23 with each outcome. We tested interactions by CKD status (eGFR < 60ml/min/1.73m 2 or ACR ≥ 30mg/g). Results: During 10.5 years median follow-up, there were 1,730 deaths, 697 adjudicated incident HF events, and 797 adjudicated incident CVD events. FGF23 was elevated in persons with eGFR < 80ml/min/1.73m 2 or with urine ACR > 30mg/g. Although higher FGF23 concentrations were associated with death and HF o in combined analyses when adjusted for traditional CVD risk factors and kidney function (HR 1.25 [1.14, 1.36] for death, 1.41 [1.23, 1.61] for HF, and 1.12 [0.98, 1.29] for CVD), the associations were consistently stronger for those with CKD (all P interactions < 0.006; Table ). Conclusions: FGF23, a hormone involved in phosphorous and vitamin D homeostasis, is independently associated with all-cause death and incident HF in community-living older persons. These relationships appear stronger in persons with CKD. Association of FGF23 with Incident Heart Failure, Cardiovascular Disease, and All-Cause Death Stratified by CKD. The Cardiovascular Health Study FGF23 Quartiles Linear model 1 2 3 4 Per Doubling of FGF23 P-value FGF23 Range (RU/mL) < 51 51-70 71-100 > 100 Chronic Kidney Disease (N=1,128) All-Cause Mortality Annual event rate (# events / # at risk) 7.7 (90/141) 7.6 (150/235) 8.7 (191/285) 14.3 (404/467) Adjusted * HR (95% CI) 1.00 (ref) 0.97 (0.75, 1.26) 1.09 (0.84, 1.41) 1.87 (1.47, 2.38) 1.41 (1.30, 1.52) Incident Heart Failure † Annual event rate (# events / # at risk) 3.7 (38/136) 3.8 (63/213) 4.6 (81/256) 7.7 (145/350) Adjusted * HR (95% CI) 1.00 (ref) 0.97 (0.64, 1.46) 1.16 (0.78, 1.73) 1.94 (1.32, 2.83) 1.52 (1.33, 1.72) Incident Cardiovascular Disease ‡ Annual event rate (# events / # at risk) 5.1 (39/104) 6.2 (71/156) 6.2 (76/184) 9.5 (126/257) Adjusted * HR (95% CI) 1.00 (ref) 1.09 (0.74, 1.63) 1.09 (0.73, 1.62) 1.49 (1.02, 2.18) 1.24 (1.09, 1.43) 0.002 No Chronic Kidney Disease (N=1,979) All-Cause Mortality Annual event rate (# events / # at risk) 4.3 (270/651) 4.8 (247/550) 5.0 (228/489) 5.9 (150/289) Adjusted * HR (95% CI) 1.00 (ref) 1.10 (0.93, 1.32) 1.15 (0.96, 1.38) 1.29 (1.05, 1.59) 1.07 (0.98, 1.17) 0.15 Incident Heart Failure † Annual event rate (# events / # at risk) 1.9 (109/631) 2.3 (106/531) 2.3 (91/463) 3.1 (64/256) Adjusted * HR (95% CI) 1.00 (ref) 1.19 (0.90, 1.56) 1.11 (0.84, 1.48) 1.37 (0.99, 1.89) 1.17 (1.02, 1.33) 0.023 Incident Cardiovascular Disease ‡ Annual event rate (# events / # at risk) 3.5 (149/496) 4.0 (142/431) 4.2 (129/374) 4.0 (65/204) Adjusted * HR (95% CI) 1.00 (ref) 1.12 (0.89, 1.42) 1.16 (0.91, 1.42) 1.07 (0.79, 1.45) 0.99 (0.87, 1.13) 0.899 P-values for interaction in the adjusted model were < 0.001 for all cause mortality, 0.008 for incident HF, and 0.006 for incident CVD † Excludes 271 participants with prevalent HF at baseline. ‡ Excludes 901 participants with prevalent CVD at baseline * Adjusted for age, sex, race, health status (fair or poor vs. better), current smoking, prior stroke, prior MI, prior HF, prior claudication, hypertension, diabetes (nl, ifg, dm), bmi, estrogen use (women), total chol, lipid med use, natural log (CRP). Funding(This research has received full or partial funding support from the American Heart Association, National Center)