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Background: To examine the association of ultrasensitive cTnI (cardiac troponin I) with incident cardiovascular disease events (CVDs) in the primary prevention setting. Methods: cTnI was analyzed in the baseline plasma (2008–2012) of CVD-free volunteers from the Paris Prospective Study III using a novel ultrasensitive immunoassay (Simoa Troponin-I 2.0 Kit, Quanterix, Lexington) with a limit of detection of 0.013 pg/mL. Incident CVD hospitalizations (coronary heart disease, stroke, cardiac arrhythmias, deep venous thrombosis or pulmonary embolism, heart failure, or arterial aneurysm) were validated by critical review of the hospital records. Hazard ratios were estimated per log-transformed SD increase of cTnI in Cox models using age as the time scale. Results: The study population includes 9503 participants (40% women) aged 59.6 (6.3) years. cTnI was detected in 99.6% of the participants (median value=0.63 pg/mL, interquartile range, 0.39–1.09). After a median follow-up of 8.34 years (interquartile range, 8.0–10.07), 516 participants suffered 612 events. In fully adjusted analysis, higher cTnI (per 1 SD increase of log cTnI) was significantly associated with CVD events combined (hazard ratio, 1.18 [1.08–1.30]). Among all single risk factors, cTnI had the highest discrimination capacity for incident CVD events (C index=0.6349). Adding log cTnI to the SCORE 2 (Systematic Coronary Risk Evaluation) risk improved moderately discriminatory capacity (C index 0.698 versus 0.685; bootstrapped C index difference: 0.0135 [95% CI, 0.0131–0.0138]), and reclassification of the participants (categorical net reclassification index, 0.0628 [95% CI, 0.023–0.102]). Findings were consistent using the US pooled cohort risk equation. Conclusions: Ultrasensitive cTnI is an independent marker of CVD events in the primary prevention setting.

Introduction: Evidence on the link between sleep habits and cardiovascular diseases (CVD) in the community predominantly relies on studies that have investigated only one sleep habit, measure at one timepoint. Therefore, this study examined the joint effect of five sleep habits at baseline and at follow-up with incident CVD events. Hypothesis: We assessed the hypothesis that change in sleep habits over time including improvement in sleep habits and maintenance of a high level of sleep habits are related to reduced CVD risk. Methods: We combined data from two large independent community-based cohorts, the Paris Prospective Study 3 (France) and the CoLaus/PsyCoLaus study (Switzerland), involving 11 347 participants in total, aged 53–64 and comprising 44.6% women, initially free from CVD at baseline (respectively 2008-2012 and 2003-2006). Information on participants’ sleep habits were collected twice (median time interval between the 2 time points=2.0; interquartile range [IQR]: 2.0-5.2) by validated questionnaires. A healthy sleep score (HSS) combining five sleep habits (early chronotype, sleep duration of 7-8 h/day, never/rarely insomnia, no sleep apnea, and no frequent excessive daytime sleepiness) was calculated at baseline and follow-up. Each sleep habit was scored 1 point if optimal, otherwise 0 point. The score ranged from 0 to 5, reflecting the number of optimal sleep habits. Associations of HSS at baseline and the change in the score over time with CVD events (coronary heart disease, CHD, or stroke) were examined using Cox proportional hazard models. Results: During a median follow-up of 8.9 years (IQR: 8.0-10.0), 499 first CVD events occurred (339 CHD and 175 stroke). In multivariate Cox analysis, the risk of CVD decreased by 18% per one-point increment in the HSS (hazard ratio, HR=0.82 [95% confidence interval, CI, 0.76-0.89]). At follow-up, 38% remained in stable high score (score≥3 at both time points, the median of the baseline HSS), 11% had a stable low HSS (score Conclusions: Higher HSS and increase in the HSS are associated with a lower risk of CHD and stroke in the community. This study supports the promotion of healthy sleep habits in the population and strong collaboration between sleep medicine and CVD medicine.

Large artery stiffness is an index of vascular aging associated with cardiovascular mortality. Whereas traditional risk factors for arterial stiffness are known, the contribution of socioeconomic factors is less reported. We sought to determine the relationship between arterial stiffness and socioeconomic deprivation (at the individual and neighborhood levels) in healthy males and females. In 7803 adults, carotid stiffness was determined by high-precision carotid echo-tracking. Individual deprivation data included education, living alone, occupation, and Evaluation of the Deprivation and Inequalities of Health in Healthcare Centers score. Neighborhood deprivation was determined from commune level data (smallest administrative subdivision) available from French National Institute of Statistics and Economic Studies (2011) using principal component analysis. The separate and combined associations between individual and neighborhood deprivation (main exposures) and carotid stiffness (outcome) were quantified using linear and multilevel model adjusted for traditional risk factors. Analyses were conducted separately in males and females. Individual deprivation (lower education and occupation in males and living alone and higher Evaluation of the Deprivation and Inequalities of Health in Healthcare Centers in both populations) was adversely related to carotid stiffness, independently of potential confounders ( P0.05). Neighborhood deprivation was adversely related to carotid stiffness in males ( P0.05), but not in females. Socioeconomic deprivation, both at individual and, to a lesser extent, neighborhood level are associated with carotid stiffness in males. Only individual deprivation is associated with carotid stiffness in females.

Background— We assess the contribution of common and rare putatively functional genetic variants (most of them coding) present on the Illumina exome Beadchip to the variability of plasma lipids and stiffness of the common carotid artery. Methods and Results— Measurements were obtained from 2283 men and 1398 women, and after filtering and exclusion of monomorphic variants, 32 827 common (minor allele frequency >0.01) and 68 770 rare variants were analyzed. A large fraction of the heritability of plasma lipids is attributable to variants present on the array, especially for triglycerides (fraction of variance attributable to measured genotypes: V (G)/ V p =31.4%, P –11 ) and high-density lipoprotein cholesterol ( V (G)/ V p =26.4%, P –12 ). Plasma lipids were associated with common variants located in known candidate genes, but no implication of rare variants could be established. Gene sets for plasma lipids, blood pressure, and coronary artery disease were defined on the basis of recent meta-analyses of genome-wide association studies. We observed a strong association between the plasma lipids gene set and plasma lipid variables, but none of the 3 genome-wide association studies gene sets was associated with the carotid parameters. Significant V (G)/ V p ratios were observed for external (14.5%, P –5 ) and internal diameter (13.4%, P –4 ), stiffness (12.5%, P –4 ), intima-media thickness (10.6%, P –4 ), and wall cross-sectional area (13.2%, P –5 ). A significant association was observed between the common rs2903692 polymorphism of the CLEC16A gene and the internal diameter ( P –7 ). Conclusions— These results suggest an involvement of CLEC16A , a gene that has been reported to be associated with immune disorders, in the modulation of carotid vasodilatation.

Background: The hemodynamic and metabolic correlates of specific sodas have not been extensively studied. We used data from the IPC cohort, a large cohort of presumably healthy individuals having a general medical work-up reimbursed by the French National Health Insurance, to determine blood pressure, heart rate, BMI, waist circumference, glycemia, and LDL-cholesterol according to soda drinking habits. A self-administered questionnaire recorded daily habits for drinking colas or taurine sodas, with a 3-grade scale (no daily consumption, average daily consumption of 1-4 drinks, average daily consumption >= 4 drinks. Because consumption of taurine sodas and colas strongly declined after 50 years, only individuals aged 50 years or less (n=26,127) were included in the present analysis. Results: Daily consumption of colas and taurine drinks was reported in 8614 (33%) and 657 (2.5%) individuals, respectively. Compared with non-drinkers, cola and taurine soda consumers were younger (37 vs 34 vs 29 years, respectively, P After adjustment for age, sex, education, social status, and smoking status cola consumption was associated with slightly but significantly elevated BMI, waist circumference, blood pressure and heart rate, with no difference for fasting glucose or LDL-c. Taurine soda consumers had significantly higher BMI, and a trend to higher systolic blood pressure. Conclusion: Daily consumption of colas was associated with a modest increase in hemodynamic risk factors and body mass index, and the association with taurine sodas was essentially similar. Overall, very high consumers (5+ drinks per day) had hemodynamic nd metabolic effects similar to those of milder daily consumers.