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Although the association between sleep behavior and morbidity and mortality risk has been reported before, there is still uncertainty whether the observed associations are causal or confounding. Therefore, we investigated the causal relationships between sleep-behavioral traits and terminated healthspan risk using Mendelian randomization (MR). We conducted a one-sample MR analysis to evaluate causality between six sleep-behavioral traits (sleep duration, chronotype/morningness, napping, sleeplessness/insomnia, and getting up from bed) and risk of healthspan termination among 388, 909 UK Biobank (UKB) participants. Instrumental variables for sleep behaviors (N = 590) were obtained from recent genome-wide association studies (GWAS). We defined healthspan based on eight predominant health-terminating events associated with longevity (congestive heart failure, myocardial infarction, chronic obstructive pulmonary disease, stroke, dementia, diabetes, cancer, and death). We further constructed a sleep score and a weighted genetic risk score to increase the predictive ability of the sleep-behavioral traits. Cox regression models and Inverse Probability Treatment Weighting (IPTW) were implemented, followed by MR to assess causation. We used inverse-variance-weighted MR to estimate causal effects, and weighted-median and MR-egger for sensitivity analysis to test the pleiotropic effects. In IPTW, we observed a decreased risk of terminated healthspan for healthy sleep behaviors such as 'sleep duration 7-8h/d' (Hazard ratio, HR = 0.93; 95 % confidence interval, CI: 0.92–0.96; P < 0.001); 'morningness' (HR = 0.95; 95%CI: 0.93–0.98; P < 0.01); 'napping' (HR = 0.93; 95%CI: 0.91–0.94; P < 0.001); 'easy getting up from bed' (HR = 0.91; 95%CI: 0.88–0.93; P < 0.001); and, 'never/rarely experience sleeplessness/insomnia' (HR = 0.94; 95%CI: 0.92–0.96; P < 0.001). MR results further indicated causal associations between healthy sleep duration (OR = 0.98; 95%CI: 0.97–1.00; P = 0.036) and insomnia (OR = 1.02; 95%CI: 1.01–1.03; P < 0.001) with terminated healthspan. MR-egger did not suggest any potential pleiotropy. This study supports abnormal sleep duration and insomnia as potential causal risk factors for terminated healthspan. Thus, healthy sleep behavior is valuable for the extension of healthspan, and well-designed and tailored sleep health interventions are warranted. [ABSTRACT FROM AUTHOR]

Mendelian randomization confirmed multiple risk factors for primary events of coronary artery disease (CAD), but no such studies have been performed on recurrent major coronary events despite interesting insights derived from other designs. We examined the associations between genetically-influenced classical cardiovascular risk factors and the risk of recurrent major coronary events in a cohort of CAD patients. We included all first-time CAD cases (defined as angina pectoris, chronic ischemic heart disease or acute myocardial infarction) of European ancestry from the UK Biobank. Cases were followed till the end of follow-up, death or when they developed a recurrent major coronary event (chronic ischemic heart disease or acute myocardial infarction). Standardized weighted genetic risk scores were calculated for body mass index (BMI), systolic blood pressure, LDL cholesterol and triglycerides. From a total of 22,949 CAD patients (mean age at first diagnosis 59.8 (SD 7.3) years, 71.1% men), 12,539 (54.6%) reported a recurrent major coronary event within a period of maximum 17.8 years. One standard deviation higher genetically-determined LDL cholesterol was associated with a higher risk of a recurrent major coronary event (odds ratio: 1.08 [95% confidence interval: 1.05, 1.11]). No associations were observed for genetically-influenced BMI (1.00 [0.98, 1.03]), systolic blood pressure (1.01 [0.98, 1.03]) and triglycerides (1.02 [0.995, 1.05]). Despite the use risk-reducing medications following a first coronary event, this study provided genetic evidence that, of the classical risk factors, mainly high LDL cholesterol was associated with a higher risk of developing recurrent major coronary events. [Display omitted] • Most Mendelian randomization studies were performed on primary disease. • In atherosclerosis patients, LDL cholesterol associated with secondary disease. • Other classical cardiovascular disease did not associate with secondary disease. • LDL cholesterol should be mainly targeted to reduce secondary disease risk. [ABSTRACT FROM AUTHOR]

• A stochastic post COVID-19 was developed. • An eradication of Omicron variant as well as post COVID-19 with heart attack. • Persistence of the disease was presented. • The numerical simulation was obtained by utilizing real data. In this study, a latest version of COVID-19 pandemic is hand overed. A Stochastic post COVID-19 delayed model is developed to explore the spread of COVID-19 as well as omicron variant with the correlation of heart attack. This article provides an eradication of the COVID-19 and omicron variant as well as the population who have heart attack after post COVID-19 of these epidemic diseases. Then the existence and uniqueness of global positive solution are studied. Ensuing, In this article, we classify COVID-19 virus and omicron variant which go to extinction and become persistent in mean. By using Lyapunov function, the existence of ergodic stationary distribution are established. Later from the persistent disease as well as extinction, heart disease are ready to develop in the human body. By Eventually, an optimal control strategies are introduced in the form of stochastic post COVID-19 delayed model to control two different types of virus. Finally, the numerical simulation are presented to determine the behavior of dynamical system by utilizing the real data of United Kingdom. [ABSTRACT FROM AUTHOR]

Implications of elevated troponin on time-to-surgery in non-ST elevation myocardial infarction(NIHR Health Informatics Collaborative:TROP-CABG study). Benedetto et al. The optimal timing of coronary artery bypass grafting (CABG) in patients with non-ST elevation myocardial infarction (NSTEMI) and the utility of pre-operative troponin levels in decision-making remains unclear. We investigated (a) the association between peak pre-operative troponin and survival post-CABG in a large cohort of NSTEMI patients and (b) the interaction between troponin and time-to-surgery. Our cohort consisted of 1746 patients (1684 NSTEMI; 62 unstable angina) (mean age 69 ± 11 years,21% female) with recorded troponins that had CABG at five United Kingdom centers between 2010 and 2017. Time-segmented Cox regression was used to investigate the interaction of peak troponin and time-to-surgery on early (within 30 days) and late (beyond 30 days) survival. Average interval from peak troponin to surgery was 9 ± 15 days, with 1466 (84.0%) patients having CABG during the same admission. Sixty patients died within 30-days and another 211 died after a mean follow-up of 4 ± 2 years (30-day survival 0.97 ± 0.004 and 5-year survival 0.83 ± 0.01). Peak troponin was a strong predictor of early survival (adjusted P = 0.002) with a significant interaction with time-to-surgery (P interaction = 0.007). For peak troponin levels <100 times the upper limit of normal, there was no improvement in early survival with longer time-to-surgery. However, in patients with higher troponins, early survival increased progressively with a longer time-to-surgery, till day 10. Peak troponin did not influence survival beyond 30 days (adjusted P = 0.64). Peak troponin in NSTEMI patients undergoing CABG was a significant predictor of early mortality, strongly influenced the time-to-surgery and may prove to be a clinically useful biomarker in the management of these patients. • In patients with NSTEMI undergoing CABG, pre-operative peak troponin level was a significant predictor of early mortality. • The relationship between troponin level and mortality was influenced by timing of CABG. • In patients with a pre-operative peak troponin >100 xULN, CABG within 10 days was associated with lower survival. • The interaction between troponin, timing of surgery and mortality should be discussed with NSTEMI patients undergoing CABG. [ABSTRACT FROM AUTHOR]

Lack of physical activity (PA) and sarcopenia is a known risk factors for ischemic heart disease (IHD). However, considering their coexistence in the middle-aged and elderly population, the interaction of these two factors remains uncertain. Here, we investigated the interactive effects of PA and sarcopenia on IHD. We extracted 344,688 participants free of IHD at baseline from the UK Biobank. PA was classified into low, moderate, and high according to the International Physical Activity Questionnaire. Sarcopenia was identified in accordance with the European Working Group on Sarcopenia in Older People 2. Cox proportional hazard models were applied to estimate the effect of PA and sarcopenia on incident IHD and its subtypes. We also used objective PA data measured by wrist-worn devices to repeat these analyses. Over a median follow-up of 11.7 years, 24,809 (7.2%) participants developed incident IHD. Lack of PA was associated with a higher risk of IHD after adjusting for potential confounders. The hazard ratio (HR) was 1.09 (95% CI: 1.05–1.13) for individuals without sarcopenia and 1.29 (95% CI: 1.17–1.42) for those with sarcopenia. Regarding the joint effect, the combination of low PA and sarcopenia was associated with the highest risk of IHD, with an HR of 1.54 (95% CI: 1.44–1.66), and both additive and multiplicative interactions were significant (RERI 0.27, 95% CI: 0.14–0.39, p -interaction <0.01). For subtypes of IHD, the interaction was pronounced in acute myocardial infarction and chronic ischemic heart disease. These results suggest a synergistic interaction between lack of PA and sarcopenia on the risk of IHD. Findings from this study may help facilitate more effective primary prevention of IHD. [Display omitted] • Lack of physical activity (PA) and sarcopenia have synergistic interaction on ischemic heart disease (IHD). • The synergistic interaction is also found in subtypes of IHD. • Moderate volume of PA can provide beneficial protective effects. • Protective effects may only be achieved with moderate to high-intensity PA. [ABSTRACT FROM AUTHOR]

Objective: We aimed to investigate the individual and combined associations of depression and low socioeconomic status (SES) with risk of major cardiovascular events (MCVE), defined as first-ever fatal or non-fatal stroke or myocardial infarction, in a large prospective cohort study.Methods: We used data from 466,238 UK Biobank participants, aged 40-69 years without cardiovascular disease, bipolar disorder or schizophrenia at baseline. We performed Cox proportional hazard models to estimate adjusted hazard ratios (HR) and 95% confidence intervals (CI) for the individual and combined associations of depression and each of educational attainment, area-based deprivation and income with risk of MCVE. We assessed effect modification and explored interaction on the additive and multiplicative scale.Results: Depression, low education, high area-based deprivation and low income were individually associated with increased risks of MCVE (adjusted HR, 95% CI: 1.28, 1.19-1.38; 1.20, 1.14-1.27; 1.17, 1.11-1.23; and 1.22, 1.16-1.29, respectively). Depression was associated with increased risks of MCVE among individuals with high and low SES. Individuals with depression and each of low education, high area-based deprivation and low income were at particularly high risk of MCVE (HR, 95% CI: 1.50, 1.38-1.63; 1.63, 1.46-1.82; 1.31, 1.23-1.40, respectively). There was interaction between depression and area-based deprivation on multiplicative and additive scales but no interaction with education or income.Conclusion: Depression was associated with increased risks of MCVE among individuals with high and low SES, with particularly high risks among those living in areas of high deprivation. [ABSTRACT FROM AUTHOR]