Cardiovascular Disease Risk In Adults Research Articles

Cardiovascular disease risk factors and their associations with inflammation among US adolescents: NHANES, 2015 to March 2020

IntroductionThe prevalence of obesity and glycemic dysfunction in adolescents has increased over the past several decades but less is known on how these conditions are associated with systemic inflammation in...

Sex-specific associations between self-reported sleep characteristics and 10-year cardiovascular disease risk in men and women of African descent living in a low socioeconomic status environment

BackgroundRisk factors for cardiovascular disease (CVD) and sleep health are well-known to be sex- and race-specific. To build on the established relationship between sleep duration and CVD risk, this cross-sectional study aimed to describe sex-specific associations between CVD risk and other sleep characteristics (sleep quality, sleep timing and sleep onset latency) in low-income adults of African descent. MethodsSelf-reported sleep (Pittsburgh Sleep Quality Index [PSQI], Epworth Sleepiness Scale [ESS], Insomnia Severity Index [ISI]), demographic and lifestyle data were collected in 412 adults (56 % women, 35.0 ± 7.6y, 40 % employed) living in an informal settlement in South Africa. CVD risk was determined using the BMI-modified Framingham 10-year CVD risk formula. ResultsLogistic regression analyses, adjusted for employment, alcohol use and physical activity, indicated that men reporting poor sleep quality (OR: 1.95[95 %CI: 1.07–3.51], p=0.025) and earlier bedtimes (0.54[0.39–0.74], p<0.001) were more likely to belong to a higher 10-year CVD risk score quintile. Women reporting earlier bedtimes (0.72[0.55–0.95], p=0.020) and wake-up times (0.30[0.13–0.73], p=0.007), longer sleep-onset latency (1.47[1.43–1.88], p=0.003), shorter total sleep times (0.84[0.72–0.98], p=0.029), higher PSQI global scores (1.93[1.29–2.90], p=0.001) and more moderate to severe symptoms of insomnia (ISI≥15)(3.24[1.04–10.04], p=0.016) were more likely to belong to higher 10-year CVD risk score quintile. ConclusionIn addition to sleep duration, we found that sleep quality, sleep timing and sleep onset latency are additional risk factors for CVD in adults of African descent. Sex-specific differences in the sleep-CVD-risk relationship observed suggests that future studies and recommendations about sleep health in relation to CVD should take sex into account.

Sex-specific associations between self-reported sleep characteristics and 10-year cardiovascular disease risk in men and women of African descent living in a low socioeconomic status environment

BackgroundRisk factors for cardiovascular disease (CVD) and sleep health are well-known to be sex- and race-specific. To build on the established relationship between sleep duration and CVD risk, this cross-sectional study aimed to describe sex-specific associations between CVD risk and other sleep characteristics (sleep quality, sleep timing and sleep onset latency) in low-income adults of African descent. MethodsSelf-reported sleep (Pittsburgh Sleep Quality Index [PSQI], Epworth Sleepiness Scale [ESS], Insomnia Severity Index [ISI]), demographic and lifestyle data were collected in 412 adults (56% women, 35.0±7.6y, 40% employed) living in an informal settlement in South Africa. CVD risk was determined using the BMI-modified Framingham 10-year CVD risk formula. ResultsLogistic regression analyses, adjusted for employment, alcohol use and physical activity, indicated that men reporting poor sleep quality (OR: 1.9[95%CI: 1.1-3.5],p=0.025) and earlier bedtimes (0.54[0.39-0.74],p<0.001) were more likely to belong to a higher 10-year CVD risk score quintile. Women reporting earlier bedtimes (0.72[0.55-0.95],p=0.020) and wake-up times (0.30[0.1-0.7],p=0.007), longer sleep-onset latency (1.5[1.4-1.9],p=0.003), shorter total sleep times (0.84[0.7-0.9],p=0.029), higher PSQI global scores (1.9[1.3-2.9],p=0.001) and more moderate to severe symptoms of insomnia (ISI≥15)(3.24[1.04-10.04],p=0.016) were more likely to belong to higher 10-year CVD risk score quintile. ConclusionIn addition to sleep duration, we found that sleep quality, sleep timing and sleep onset latency are additional risk factors for CVD in adults of African descent. Sex-specific differences in the sleep-CVD-risk relationship observed suggests that future studies and recommendations about sleep health in relation to CVD should take sex into account.

Long-Term Cardiovascular Outcomes in Children and Adolescents With Hypertension

Hypertension affects 6% of all children, and its prevalence is increasing. Childhood hypertension tracks into adulthood and is associated with subclinical cardiovascular disease; however, there is a lack of evidence linking childhood hypertension to cardiovascular outcomes, which may contribute to underdiagnosis and undertreatment. To determine the long-term associated risk of major adverse cardiac events (MACE) among children diagnosed with hypertension. This was a population-based, retrospective, matched cohort study conducted from 1996 to 2022. The study included all children (aged 3-18 years) alive in Ontario, Canada, from 1996 to 2021, who were identified using provincial administrative health databases. Children with prior kidney replacement therapy were excluded. Incident hypertension diagnosis, identified by validated case definitions using diagnostic and physician billing claims. Each case was matched with 5 controls without hypertension by age, sex, birth weight, maternal gestational hypertension, prior comorbidities (chronic kidney disease, diabetes, cardiovascular surgery), and a propensity score for hypertension. The primary outcome was MACE (a composite of cardiovascular death, stroke, hospitalization for myocardial infarction or unstable angina, or coronary intervention). Time to MACE was evaluated using the Kaplan-Meier method and Cox proportional hazards regression. A total of 25 605 children (median [IQR] age, 15 [11-17] years; 14 743 male [57.6%]) with hypertension were matched to 128 025 controls without hypertension. Baseline covariates were balanced after propensity score matching, and prior comorbidities were uncommon (hypertension vs control cohort: malignancy, 1451 [5.7%] vs 7908 [6.2%]; congenital heart disease, 1089 [4.3%] vs 5408 [4.2%]; diabetes, 482 [1.9%] vs 2410 [1.9%]). During a median (IQR) of 13.6 (7.8-19.5) years of follow-up, incidence of MACE was 4.6 per 1000 person-years in children with hypertension vs 2.2 per 1000 person-years in controls (hazard ratio, 2.1; 95% CI, 1.9-2.2). Children with hypertension were at higher associated risk of stroke, hospitalization for myocardial infarction or unstable angina, coronary intervention, and congestive heart failure, but not cardiovascular death, compared with nonhypertensive controls. Children diagnosed with hypertension had a higher associated long-term risk of MACE compared with controls without hypertension. Improved detection, follow-up, and control of pediatric hypertension may reduce the risk of adult cardiovascular disease.

Sex-Related Differences in Vascular Function Among Older Adults with Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) is a sleep disorder associated with hypertension and cardiovascular disease (CVD) risk. Endothelial dysfunction and altered shear stress are implicated in OSA-related CVD pathogenesis, however, their contributions to CVD risk in males vs females remains unclear. We obtained measures of resting blood pressure (BP), brachial artery flow-mediated dilation (FMD), brachial artery diameter, and shear stress in 71 older adults (F=30, M=41; age=66.9±7.7) diagnosed with mild, moderate, or severe OSA based on oxygen desaturation index (ODI) score. All were prospective participants in an ongoing clinical trial (NCT04932447). Group differences (mean ± SD) were assessed with two-way ANOVAs (sex X severity) and associations between ODI score, baseline diameter, relative FMD, shear stress, and BP were assessed with Pearson correlations. We hypothesized that a) regardless of sex, individuals with greater OSA severity exhibit lower relative FMD and mean shear stress, greater baseline diameter and higher BP, and b) for a given OSA severity, females have greater relative FMD and mean shear stress and lower baseline diameter and BP compared to males. In line with our hypotheses, we found greater mean shear stress in females compared to males (F=69.6±26.9 s−1, M=53.5±16.7 s−1, p=0.035) and among females, those with mild OSA had higher mean shear stress than those with severe OSA (mild=77.6±26.1 s−1, severe= 44.4±8.5 s−1, p=0.009). Contrary to expectations, mean shear stress did not differ as a function of OSA severity in male subjects, nor was there any difference in FMD or BP across OSA severity between males and females. In subjects with moderate OSA, FMD was greater in females than males (F=6.07±3.89%, M=3.07±2.39%, p=0.047). On average, baseline diameters were larger in adults with severe OSA compared to moderate OSA (moderate=3.66±0.59 mm, severe=4.33±0.61 mm, p=0.003), and females with mild (F=3.20±0.47 mm, M=4.73±0.50 mm, p&lt;0.001) and moderate (F=3.31±0.42 mm, M=3.91±0.57 mm, p=0.007) OSA had smaller baseline diameters than their male counterparts. There were no differences in baseline diameter between males and females with severe OSA. We report a negative correlation between mean shear stress and BP (systolic BP, r=-0.48, p=0.011; diastolic BP, r=-0.55, p=0.002) and a positive correlation between ODI score and baseline diameter (r=0.54, p=0.003) in females but not males. Conversely, ODI score and relative FMD were positively correlated in male subjects (r=0.45, p=0.009), but not females. Overall, our findings highlight sex-specific vascular differences in older adults with OSA. Relative to males, females with mild OSA exhibit greater mean shear stress and lower baseline diameters, which may confer a cardiovascular advantage. In contrast, males and females with severe OSA exhibit similar vascular characteristics. Our findings provide new insights into the impact of sex and OSA severity on vascular function and CVD risk in older adults. This work is supported by NIH/NIA grant number: 1R01AG065346. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Salivary biomarkers as assessment of metabolic function and inflammation in children with obesity

Childhood obesity increases adult metabolic and cardiovascular disease risk. Using blood for long-term biomarker analysis in children is problematic because of the discomfort, pain, and anxiety associated with frequent blood draws. Noninvasive methods are vital for predicting childhood obesity complications. This study examined body mass index-for-age percentile scores (zBMI) as a predictor of salivary biomarkers of metabolism and inflammation, including insulin and C-Reactive Protein (CRP), over time. A school sample of 288 adolescents (Mage = 12.1 at study initiation; 46% female; 48% Black, 37% non-Hispanic White, 15% Hispanic or other minorities) were enrolled from greater Birmingham, Alabama. Participants provided salivary samples across four days once per year from 2019–2021. In year 1 of the study, 19% of adolescents were overweight, 18% had obesity, 6.6% had severe obesity, and 7.3% had very severe obesity based on the 2022 CDC Extended BMI-for-Age Growth Charts. Multivariable models showed that lower parental income was associated with an increased risk of obesity (OR = 0.91; 95% CI = 0.85, 0.97; p = 0.009). Greater concentrated poverty, a measure of spatial distribution of socioeconomic deprivation, was associated with an increased risk of severe or very severe obesity (OR = 1.58; 95% CI = 1.01, 2.46; p = 0.043). However, race/ethnicity was not associated with obesity risk. Longitudinal analyses showed that greater zBMI in year 1 was associated with greater salivary CRP ( β = 0.188, SE = 0.058, p = 0.001) and insulin ( β = 0.263, SE = 0.076, p&lt;0.001) in years 2 and 3 of the study after adjusting for year 1 biomarker levels, sex, race/ethnicity, and concentrated poverty. Multivariable models indicated that an accelerated increase in zBMI/year was associated with an accelerated increase in CRP/year ( β = 0.119, SE = 0.048, p = 0.014), but there was no association between the rates of change in zBMI and insulin. Future analyses will incorporate additional hormones, such as adiponectin, and inflammatory cytokines measured in saliva. In conclusion, these results indicate that salivary biomarkers can capture physiological differences associated with zBMI in school-age children. Saliva may constitute a useful non-invasive tool for evaluating markers of inflammation and/or metabolism related to zBMI in children outside clinical settings. This research was supported by an Institute of Education Sciences, U.S. Department of Education Grant (R305A180074) to SM and RE and a National Heart, Lung, and Blood Institute K99R00 Grant (1K99HL165091-01A1) to KMK. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Non–High-Density Lipoprotein Cholesterol Levels From Childhood to Adulthood and Cardiovascular Disease Events

Elevated non-high-density lipoprotein cholesterol (non-HDL-C; a recommended measure of lipid-related cardiovascular risk) is common in children and increases risk of adult cardiovascular disease (CVD). Whether resolution of elevated childhood non-HDL-C levels by adulthood is associated with reduced risk of clinical CVD events is unknown. To examine the associations of non-HDL-C status between childhood and adulthood with incident CVD events. Individual participant data from 6 prospective cohorts of children (mean age at baseline, 10.7 years) in the US and Finland. Recruitment took place between 1970 and 1996, with a final follow-up in 2019. Child (age 3-19 years) and adult (age 20-40 years) non-HDL-C age- and sex-specific z scores and categories according to clinical guideline-recommended cutoffs for dyslipidemia. Incident fatal and nonfatal CVD events adjudicated by medical records. Over a mean length of follow-up of 8.9 years after age 40 years, 147 CVD events occurred among 5121 participants (60% women; 15% Black). Both childhood and adult non-HDL-C levels were associated with increased risk of CVD events (hazard ratio [HR], 1.42 [95% CI, 1.18-1.70] and HR, 1.50 [95% CI, 1.26-1.78] for a 1-unit increase in z score, respectively), but the association for childhood non-HDL-C was reduced when adjusted for adult levels (HR, 1.12 [95% CI, 0.89-1.41]). A complementary analysis showed that both childhood non-HDL-C levels and the change between childhood and adulthood were independently associated with the outcome, suggesting that from a preventive perspective, both childhood non-HDL-C levels and the change into adulthood are informative. Compared with those whose non-HDL-C levels remained within the guideline-recommended range in childhood and adulthood, participants who had incident non-HDL-C dyslipidemia from childhood to adulthood and those with persistent dyslipidemia had increased risks of CVD events (HR, 2.17 [95% CI, 1.00-4.69] and HR, 5.17 [95% CI, 2.80-9.56], respectively). Individuals who had dyslipidemic non-HDL-C in childhood but whose non-HDL-C levels were within the guideline-recommended range in adulthood did not have a significantly increased risk (HR, 1.13 [95% CI, 0.50-2.56]). Individuals with persistent non-HDL-C dyslipidemia from childhood to adulthood had an increased risk of CVD events, but those in whom dyslipidemic non-HDL-C levels resolve by adulthood have similar risk to individuals who were never dyslipidemic. These findings suggest that interventions to prevent and reduce elevated childhood non-HDL-C levels may help prevent premature CVD.

The Significant Impact of High-Fat, Low-Carbohydrate Ketogenic Diet on Serum Lipid Profile and Atherosclerotic Cardiovascular Disease Risk in Overweight and Obese Adults.

Background and objectives Overweight and obesity are becoming more commonplace globally. The ketogenic diet (KD), also known as the high-fat, low-carbohydrate diet, has become increasingly popular in recent years as a means to lose weight quickly. This present study aims to examine the clinical effects of ketogenic diets in individuals who are obese or overweight by evaluating or assessing variations in metabolic parameters associated with lipid control, the risk of atherosclerotic cardiovascular disease, and other kidney risk indicators. Methods and subjects This observational case-control research involved 250 individuals in total and was conducted from May 2023 to January 2024. Of these, 158 were on a ketogenic diet, and 92 adults not following any type of diet were chosen to serve as controls. The biochemistry parameters of the kidney function test and lipid profile were measured for the two comparing groups. Data were analyzed for statistical significance using the Student t-test, Mann-Whitney U test, and one-way analysis of variance (ANOVA), followed by a post hoc test (least significant difference (LSD)). Chi-square tests were employed in the analysis to compare proportions. Results Out of 250 participants, there was a 20-80 age range, with their median age being 40 years old. The two comparing groups' lipid profiles were very different from one another; the cardiovascular risk (triglyceride (TG)/high-density lipoprotein (HDL)), total cholesterol, low-density lipoprotein (LDL), and triglyceride levels were all greater in the KD group when compared to the non-KD group. The mean LDL cholesterol (LDL-C) of the normal-weight participants was 56 mg/dL (p=0.079). Thereafter, it experienced a significant rise to 97.58 mg/dL and 108.2 mg/dL in thoseindividuals who were overweight and obese, respectively (p<0.020). Conclusions As obesity rates in the populace keep rising, dietary fads such as the ketogenic diet are gaining traction. Although they could help with weight loss, this study had a notable observation of severe hypercholesterolemia and increased risk of atherosclerotic cardiovascular disease among the ketogenic diet participants. Additional research is necessary to ascertain if a ketogenic diet can be sustained over the long term and how it affects endpoints that are more clinically significant, such as morbidity and mortality due to obesity.

Long-term ambient ozone exposure and incident cardiovascular diseases: National cohort evidence in China

BackgroundLong-term ozone (O3) exposure has been associated with cardiovascular disease (CVD) mortality in mounting cohort evidence, yet its relationship with incident CVD was poorly understood, especially in low- and middle-income countries (LMICs) experiencing high ambient air pollution. MethodsWe carried out a nationwide perspective cohort study from 2010 through 2018 by dynamically enrolling 36948 participants across Chinese mainland. Warm-season (April–September) O3 concentrations were estimated using satellite-based machine-learning models with national coverage. Cox proportional hazards model with time-varying exposures was employed to evaluate the association of long-term O3 exposure with incident CVD (overall CVD, hypertension, stroke, and coronary heart disease [CHD]). Assuming causality, a counterfactual framework was employed to estimate O3-attributable CVD burden based on the exposure-response (E-R) relationship obtained from this study. Decomposition analysis was utilized to quantify the contributions of four key direct driving factors (O3 exposure, population size, age structure, and incidence rate) to the net change of O3-related CVD cases between 2010 and 2018. ResultsA total of 4428 CVD, 2600 hypertension, 1174 stroke, and 337 CHD events were reported during 9-year follow-up. Each 10-μg/m³ increase in warm-season O3 was associated with an incident risk of 1.078 (95% confidence interval [CI]: 1.050–1.106) for overall CVD, 1.098 (95% CI: 1.062–1.135) for hypertension, 1.073 (95% CI: 1.019–1.131) for stroke, and 1.150 (95% CI: 1.038–1.274) for CHD, respectively. We observed no departure from linear E-R relationships of O3 exposure with overall CVD (Pnonlinear= 0.22), hypertension (Pnonlinear= 0.19), stroke (Pnonlinear= 0.70), and CHD (Pnonlinear= 0.44) at a broad concentration range of 60–160 µg/m3. Compared with rural dwellers, those residing in urban areas were at significantly greater O3-associated incident risks of overall CVD, hypertension, and stroke. We estimated 1.22 million (10.6% of overall CVD in 2018) incident CVD cases could be attributable to ambient O3 pollution in 2018, representing an overall 40.9% growth (0.36 million) compared to 2010 (0.87 million, 9.7% of overall CVD in 2010). This remarkable rise in O3-attributable CVD cases was primary driven by population aging (+24.0%), followed by increase in O3 concentration (+10.5%) and population size (+6.7%). ConclusionsLong-term O3 exposure was associated with an elevated risk and burden of incident CVD in Chinese adults, especially among urban dwellers. Our findings underscored policy priorities of implementing joint control measures for fine particulate matter and O3 in the context of accelerated urbanization and population aging in China.

Exposure to green spaces, cardiovascular risk biomarkers and incident cardiovascular disease in older adults: The Seniors-Enrica II cohort

IntroductionThe impact of residential green spaces on cardiovascular health in older adults remains uncertain. MethodsCohort study involving 2114 adults aged ≥ 65 years without cardiovascular disease (CVD), residing in five dense municipalities (Prince et al., 2015) of the Madrid region and with detailed characterization of their socioeconomic background, health behaviors, CVD biological risk factors, and mental, physical, and cognitive health. Greenness exposure was measured using the Normalized Difference Vegetation Index (NDVI) at varying distances from participants' homes. Traffic exposure, neighborhood environment, neighborhood walkability, and socioeconomic deprivation at the census level were also assessed. Serum N-terminal pro-B-type natriuretic peptide (NT-ProBNP), high-sensitivity troponin T (hs-TnT), interleukin 6 (IL-6), and Growth Differentiation Factor 15 (GDF‐15) were measured at baseline, and incident CVD events identified through electronic medical records (International Classification of Primary Care-2 codes K74, K75, K77, K90, and K92). ResultsAfter adjusting for sex, age, educational attainment, financial hardship and socioeconomic deprivation at the census level, an interquartile range (IQR) increase in NDVI at 250, 500, 750, and 1000 m around participants' homes was associated with mean differences in ProBNP of −5.56 % (95 %CI: −9.77; −1.35), −5.05 % (-9.58; −0.53), −4.24 % (-8.19, −0.19), and −4.16 % (-7.59; −0.74), respectively; and mean differences in hs-TnT among diabetic participants of −8.03 % (95 %CI: −13.30; −2.77), −9.52 % (-16.08; −2.96), −8.05 % (-13.94, −2.16) and −5.56 % (-10.75; −0.54), respectively. Of similar magnitude, although only statistically significant at 250 and 500 m, were the observed lower IL-6 levels with increasing greenness. GDF-15 levels were independent of NDVI. In prospective analyses (median follow-up 6.29 years), an IQR increase in residential greenness at 500, 750, and 1000 m was associated with a lower risk of incident CVD. The variables that contributed most to the apparent beneficial effects of greenness on CVD were lower exposure to traffic, improved cardiovascular risk factors, and enhanced physical performance. Additionally, neighborhood walkability and increased physical activity were notable contributors among individuals with diabetes. ConclusionIncreased exposure to residential green space was associated with a moderate reduction in CVD risk in older adults residing in densely populated areas.

Food Environments and Cardiovascular Disease: Evidence From the Health and Retirement Study

IntroductionResidential food environments are one of the important determinants of cardiovascular health. However, past literature has been limited by short-term follow-ups, time-invariant environmental measurements at baseline, and/or not investigating both healthy and unhealthy aspects of the food environment. This study examines the effects of time-varying healthy and unhealthy food environments on incident cardiovascular disease (CVD) over ten years, extracting data from the Health and Retirement Study (2006-2016; N=10,413). MethodsCox proportional hazards modeling was performed with inverse probability weighting to assess the association between time-varying food environmental measures (i.e., densities of grocery stores, supercenters/club stores, full-service restaurants, and fast-food restaurants) and incident CVD over 10 years. Education level and race/ethnicity were tested as potential moderators. Analyses were conducted in 2022-2023. ResultsRace/ethnicity had a significant interaction effect with supercenters/club stores and indicated that a 1-standard-deviation increase in the density of supercenters/club stores was associated with a 6-8% lower risk of incident CVD in non-Hispanic Black (HR=0.78, 95% CI=0.70-0.87) and Hispanic older adults (HR=0.69, 95% CI=0.50-0.96), but not non-Hispanic White older adults. Additionally, education had a significant interaction effect with full-service restaurants, indicating that a 1-standard-deviation increase in the density of full-service restaurants was associated with a 10% lower risk of incident CVD in individuals with 13+ years of schooling, but not those with zero to 12 years of schooling. ConclusionsFindings suggest that public policymakers should be aware of the benefits and nuances of varying food environment components as they can contribute to positive or negative cardiovascular health.

Associations between birth weight and adult apolipoproteins: The LifeGene cohort.

Early life factors may predict cardiovascular disease (CVD), but the pathways are still unclear. There is emerging evidence of an association of early life factors with apolipoproteins, which are linked to CVD. The study objective was to assess the associations between birth variables and adult apolipoproteins (apoA1 and apoB, and their ratio) in a population-based cohort. The LifeGene Study is a prospective cohort comprising index participants randomly sampled from the general population. Blood samples were collected between 2009 and 2016. In this sub-study, we used birth variables, obtained from a national registry for all participants born 1973 or later, including birth weight and gestational age, while adult CVD risk factors included age, sex, body mass index (BMI), lipids, and smoking history. We employed univariate and multivariate general linear regression to explore associations between birth variables, lipid levels and other adult CVD risk factors. The outcomes included non-fasting apoA1 and apoB and their ratio, as well as total cholesterol and triglycerides. A total of 10,093 participants with both birth information and lipoprotein levels at screening were included. Of these, nearly 42.5% were men (n = 4292) and 57.5% were women (n = 5801). The mean (standard deviation) age of men was 30.2 (5.7) years, and for women 28.9 (5.8) years. There was an increase of 0.022 g/L in apoA1 levels per 1 kg increase in birth weight (p = 0.005) after adjusting for age, sex, BMI, gestational age, and smoking history. Similarly, there was a decrease of 0.023 g/L in apoB levels per 1 kg increase in birth weight (p<0.001) after adjusting for the same variables. There were inverse associations of birth weight with the apoB/apoA1 ratio. No independent association was found with total cholesterol, but with triglyceride levels (ẞ-coefficient (95% Confidence Interval); -0.067 (-0.114, -0.021); p-value 0.005). Lower birth weight was associated with an adverse adult apolipoprotein pattern, i.e., a higher apoB/apoA1 ratio, indicating increased risk of future CVD manifestations. The study highlights the need of preconception care and pregnancy interventions that aim at improving maternal and child outcomes with long-term impacts for prevention of cardiovascular disease by influencing lipid levels.

Relationship between metabolic status, physical activity and cardiovascular disease in participants with obesity.

We aimed to investigate the independent and joint associations between metabolic status, PA (physical activity) and risk of CVD (cardiovascular disease) in participants with obesity. We included 109,301 adults with obesity free of baseline CVD enrolled from 2006 to 2010 in the UK Biobank cohort (aged 56 ± 7.9 years). Based on metabolic status, obesity was grouped into metabolically healthy obesity (MHO; free of hypertension, hypercholesterolemia and diabetes; n = 26,989; BMI 33 ± 3.3 kg/m2) and metabolically unhealthy obesity (MUO; n = 82,312; BMI 34 ± 4.0 kg/m2). PA was categorized into four groups according to moderate-to-vigorous PA (MVPA): none, low, medium, and high. Multivariable Cox regression models were used for the main analyses adjusting for sociodemographic factors, lifestyles and comorbidities. There were 8,059 CVD events during a median follow-up of 8.1 years. MHO was associated with a 42% reduced risk of CVD compared with MUO (HR = 0.58, 95% CI: 0.53-0.63). A significant interaction effect between PA and metabolic status on CVD risk was found. Among MUO participants, individuals with PA had significantly decreased CVD risk when compared with no MVPA (HR = 0.87, 95% CI: 0.81-0.94 for low PA; HR = 0.85, 95% CI: 0.78-0.93 for medium PA; and HR = 0.86, 95% CI: 0.80-0.92 for high PA). The lowest CVD risk was observed in MHO & medium PA group when compared with MUO & no MVPA (HR = 0.45, 95% CI: 0.37-0.56). Both MHO and any MVPA were associated with reduced risk of CVD in adults with obesity, while PA could modify the relationship between metabolic status and CVD risk.

Non-alcoholic fatty liver disease increases the risk of cardiovascular disease in young adults and children: a systematic review and meta-analysis of cohort studies.

It is uncertain if there is a link between non-alcoholic fatty liver disease (NAFLD) and cardiovascular diseases (CVD) in young adults and children. To evaluate the potential link between these two conditions, we conducted a systematic review and meta-analysis of cohort studies. A comprehensive search was conducted in PubMed, Web of Science and Embase in order to locate all relevant cohort studies published until August 2023. Random effects meta-analyses were conducted using the generic inverse variance method, with additional subgroup and sensitivity analyses. The Newcastle-Ottawa Scale was employed to evaluate the methodological quality. Four cohort studies (eleven datasets) involving 10,668,189 participants were included in this meta-analysis. This meta-analysis demonstrated that NAFLD increases the risk of CVD in young adults and children (HR = 1.63, 95% CI: 1.46-1.82, P < 0.00001). Further subgroup analyses showed that individuals with NAFLD were at a heightened risk of coronary heart disease (CHD) (HR = 3.10, 95% CI: 2.01-4.77, P < 0.00001), myocardial infarction (MI) (HR = 1.69, 95% CI: 1.61-1.78, P < 0.00001), atrial fibrillation (AF) (HR = 2.00, 95% CI: 1.12-3.57, P = 0.02), congestive heart failure (CHF) (HR = 3.89, 95% CI: 1.20-12.61, P = 0.02), and stroke (HR = 1.47, 95% CI: 1.39-1.55, P < 0.00001). The results of subgroup analyses based on the study location, NAFLD definition, and follow-up time also showed consistency with the overall results. Sensitivity analyses showed that our results were robust. All of the included studies were judged to be of medium to high quality. Current evidence reveals that NAFLD is linked to an increased risk of major CVD (including CHD, MI, AF, CHF and stroke) in young adults and children. Further research is needed to strengthen this association and provide stronger evidence for primary prevention of CVD in young adults and children with NAFLD. https://www.crd.york.ac.uk/PROSPERO/, PROSPERO registration number: CRD42023457817.

Impact of Hypomethylating Agents on Cardiovascular Disease Risk Among Patients with Myelodysplastic Syndromes

Introduction: The association between clonal hematopoiesis (CH) and cardiovascular disease (CVD) risk has drawn attention to cardiovascular outcomes in myelodysplastic syndromes (MDS). CVD accounts for 25% of deaths in MDS, potentially via CH-mediated accelerated atherosclerosis from inflammatory vascular responses. We previously demonstrated that MDS was independently associated with increased risk of CVD in older adults from SEER-Medicare. We subsequently hypothesized that treatment with hypomethylating agents (HMA) could reduce CVD risk by ameliorating CH clones and reducing the inflammation. In this study, we aimed to define the impact of HMA on incident cardiovascular events among older adults with MDS. Methods: We identified subjects ≥66 years diagnosed with MDS from 2007 to 2017 in SEER-Medicare. Exclusion criteria including lacking continuous Medicare parts A, B, and D, enrolled in HMO, or incomplete follow-up. Demographics included age, sex, race, rurality, socioeconomic quintile, marital status, and geographic region. Baseline CVD risk factors, defined from ICD-9/10 codes, included hypertension, hyperlipidemia, diabetes, atrial fibrillation, pre-existing cardiac disease, obesity, and smoking. MDS factors, defined using HCPCS codes, ICD-O-3 codes and prescription records, included MDS subtype and histologic risk stratification, transfusion dependence and treatment with hypomethylating agents (HMA), lenalidomide, or erythropoietin-stimulating agents (ESA) as time-varying variables. Incident CVD was defined as new myocardial infarction (MI) and/or ischemic stroke occurring after MDS diagnosis, using published ICD-9/10 algorithms. We controlled for confounding using 2 complementary analytic approaches. First, we assessed the association between HMA use and CVD using propensity score adjusted cause-specific competing risk Cox hazard models with death as competing risk, Second, we used a case-crossover design with conditional logistic regression, in which subjects with CVD served as their own controls, using a 3-month HMA treatment window and a control period 6 months prior to the incident event. Results: We identified a cohort of 15,227 eligible patients with MDS. Of these, 1,125 patients had an MI and/or ischemic stroke within 1 year before MDS diagnoses and were excluded. We analyzed 14,102 MDS patients, with median age 82 years (IQR 77 - 86), who were predominantly male (53.8%), non-Hispanic white (88.6%), and from urban/suburban areas (86.2%). MDS was of low, intermediate, and high histologic risk in 14.7%, 72.8%, and 12.5%, respectively, and 28.6% were transfusion dependent. Pre-existing CVD risk factors at time of MDS diagnosis were present in 12,538 patients, with baseline cardiovascular risk defined as low, intermediate, and high in 11.1%, 32.3%, and 56.6% of the cohort. The cumulative incidences of MI, ischemic stroke and composite CVD events were 11.3%, 10.6% and 20.4%, respectively. The propensity score (PS) conditional probability for being treated with HMA included demographic variables, CVD risk factors, MDS histology and transfusion dependence. Our PS model adequately predicted HMA treatment propensity (AUC 0.76). Cause-specific regression with death as competing risk, adjusted for PS and other MDS-specific treatments (ESA and lenalidomide), showed no significant effect of HMA on the risk of composite CVD events, MI, or ischemic stroke (Table 1). Conditional logistic regression in the case-crossover analysis of 1,907 patients with composite CVD events showed no significant effect of HMA. Results were similar for analysis of patients with MI and ischemic stroke (Table 2). Conclusions: No study has previously investigated the effect of HMA therapy on cardiovascular outcomes in patients with MDS. We demonstrate that HMA therapy is not associated with a significant risk reduction in cardiovascular events among patients with MDS patients from the SEER-Medicare database. These results show that HMA therapy is unlikely to reduce cardiovascular mortality and underscore the need for alternative therapeutic strategies targeting cardiovascular health patients with MDS.

Examining Relationships between Cognitive Flexibility, Exercise Perceptions, and Cardiovascular Disease Risk Factors.

Adults do not engage in enough physical activity. Investigating cognitive and physiological factors related to improving this behavior-and reducing health risks-remains a public health priority. Our objective was to assess whether cognitive flexibility influenced perceptions and choice of exercise programs and whether flexibility was associated with cardiovascular disease (CVD) risk factors. Independent sample groups of college-aged adults (18-24 yrs) participated in two studies. Data were collected on individuals' degree of cognitive flexibility (both self-reported and objectively measured), perceptions and choice of exercise programs, and health status markers known to be associated with CVD (vascular function, muscular strength, and body composition). Vascular function was assessed with a near-infrared spectroscopy device, strength was defined as handgrip, and body composition was estimated via digital circumferences. Self-reported flexibility reliably predicted individuals' choice of exercise program and perceptions of effort required for success on an exercise program. The relationships among CVD risk factors and objectively measured cognitive flexibility were not significant, demonstrating that identifying a healthy individual's degree of performance-based cognitive flexibility does not predict health status. Furthermore, although greater self-reported trait flexibility (rigidity) is known to predict higher (lower) likelihood of physical activity, this finding should not be extrapolated to also assume that flexibility (rigidity), as measured by objective cognitive tests, is associated with reduced CVD risk in healthy adults. We posit a rationale for how understanding cognitive flexibility and rigidity can play an impactful role in improving adherence to exercise prescriptions targeted to reducing risks.

Assessing the effect of regular swimming exercise on the micro- and macrovascular physiology of older adults (ACELA II study).

Introduction: Cardiovascular disease (CVD) remains the main cause of death in the Western world. Our recent findings demonstrate potential CVD risk reduction in older adults who undertake regular swimming exercise. Nevertheless, it remains unknown whether an exercise intervention based on swimming is feasible and effective prior to a wider implementation of a CVD risk prevention strategy. Methods: This was a pragmatic, two-group, randomised controlled trial. A total of 40 older adults were randomly split into two groups (n = 20 per group). The swimming exercise group consisted of participants who engaged in swimming exercise (2-3days/week, for 8weeks). The control group did not perform any exercise. Flow-mediated dilation (%FMD) was the primary outcome. Secondary outcomes included raw cutaneous vascular conductance. Feasibility outcomes (e.g., recruitment, adherence, and attrition rates) were also assessed. Results: Statistically significant macrovascular (%FMD; swimming group: 9.8% ± 4.2%, p <0.001; control group: 4.6% ± 2.5%) and microvascular function (raw cutaneous vascular conductance; swimming group: 4.1 ± 0.9, p <0.01; control group: 3.2 ± 1.1) improvements were observed in the swimming group compared to the control group. Compliance to twice and thrice weekly in an 8-week swimming exercise was 92.6% and 88.4%, respectively, with no dropouts. Conclusion: Our 8-week, community-based, pragmatic swimming exercise intervention is a feasible and effective exercise programme that could be implemented in older adults for the prevention of age-related CVD. These findings suggest that swimming exercise could significantly reduce CVD risk in older adults, and a large research clinical trial is warranted to establish these findings.

Relationship of trihalomethane in drinking water with hypertension and arrhythmia among young and middle-aged adults in Petropavlovsk, Kazakhstan

ABSTRACT There are no studies investigating the association of chlorinated drinking water with the risk of cardiovascular diseases (CVDs) among young and middle-aged adults. This study was aimed to assess the associations between trihalomethanes (THMs) in drinking water and the risk of CVDs in in the target group in Petropavlovsk, Kazakhstan. 448 dwellers of Petropavlovsk were asked about their demographic, socioeconomic, lifestyle, behavioural characteristics, and drinking water preferences. THMs exposure was assessed to each participant based on their residence address. We used multivariable logistic regression analysis to assess the risk of CVDs in young and middle-aged adults. The results showed that the risk of hypertension in the adjusted logistic regression model was increased by 68% and a 2.7-fold in the second and third THM tertiles, respectively. Participants in the second and third THM exposure tertiles had a 2.3-fold and a 4.8-fold increase in the risk of arrhythmia.

Adherence to a modified nordic diet and the risk of cardiovascular events in a non-nordic population: a prospective cohort study.

Even though studies have demonstrated that the Nordic diet is beneficial for cardiovascular disease (CVD) risk factors, it is unknown if this diet is associated with actual CVD cases. So, the aim of this study was to investigate the association between a modified Nordic diet and the risk of CVD in non-Nordic adults. In this cohort study, 2918 people who participated in the third phase of the Tehran Lipid and Glucose Study (TLGS) were examined. All participants had no CVD at the beginning of the study, which was monitored until 2018. The Nordic score was calculated using a validated food frequency questionnaire (FFQ). Patients' medical records were examined for cardiovascular events such as coronary heart disease (CHD), stroke, and mortality from CVD. The Cox proportional hazards model was used to assess the relationship between the Nordic score and the risk of CVD. During a median follow-up of 10.6 years, 203 subjects experienced cardiovascular events. The third and fourth quartiles of the Nordic score were associated with a 35% (HR: 0.65; 95% CI: 0.45, 0.95) and 60% (HR: 0.40; 95% CI: 0.27 to 0.65) reduced risk of CVD compared to the lowest quartile. Subgroup analyses revealed that a high Nordic score was inversely associated with a lower risk of CVD in adults older than 45 years of age, both sexes, and all BMI categories. Each 1-score increase in cereal consumption was associated with a 24% (HR: 0.76; 95% CI: 0.67 to 0.87) lower risk of CVD; low-fat milk with a 23% (HR: 0.77; 95% CI: 0.68 to 0.87); and fish with a 22% (HR: 0.78; 95% CI: 0.69 to 0.89) lower risk of CVD. We found that high Nordic score adherence may prevent cardiovascular events in non-Nordic populations. Cereals, fish, and low-fat milk were the primary components of the Nordic diet that indicated an inverse relationship with CVD.

Algorithms for Treating Dyslipidemia in Youth.

The goal of this article is to review algorithms for treating dyslipidemia in youth, discuss pitfalls, propose enhanced algorithms to address pitfalls, and consider future directions. The presence of modifiable and non-modifiable cardiovascular disease (CVD) risk factors during childhood is associated with CVD-related events in adulthood. Recent data has shown that childhood initiation of statin therapy in youth < 18years of age with familial hypercholesterolemia reduces the risk of adult CVD. However, pediatric dyslipidemia remains undertreated in part due to a lack of primary health care providers with adequate understanding of screening guidelines and pediatric lipidologists with experience in treatment and follow-up of this unique population. Management algorithms have been published by the National Heart, Lung, and Blood Institute and American Heart Association as tools to empower clinicians to manage dyslipidemia. We propose enhanced algorithms, which incorporate recently approved pharmacotherapy to address the management gaps. Future algorithms based upon clinical risk scores may enhance treatment and improve outcomes. Algorithms for dyslipidemia management which target youth < 18years of age are tools which empower clinicians to manage dyslipidemia in this unique population. Enhanced algorithms may help address pitfalls. We acknowledge the need for further risk assessment tools in pediatrics for tailored dyslipidemia management.