Increased Risk Of Cardiovascular Disease Research Articles

Age-specific in the relationship between diastolic blood pressure and the risk of cardiovascular disease: A cohort study of the UK Biobank.

To investigate the effect of optimal diastolic blood pressure (DBP) level on cardiovascular disease (CVD) events, considering different age groups. And the nonlinear relationship between DBP and CVD events by age were evaluated. 358,734 participants of the UK biobank were included. Multivariable Cox regressions were performed to evaluate the relation between DBP and cardiovascular risk, and the natural cubic spline was applied to estimate the nonlinear relationship between the DBP measures and the hazard. In the UK Biobank, a total of 358,734 participants (mean [SD] age, 55.3 [8.1] years; 205,215 [57.2 %] female) were included in this analysis. The rate of CVD cases was 6.05 per 1000 person-years. For each SD increase, DBP was associated with elevated CVD events for both <50 year (HR, 1.19; 95 % CI, 1.12 to 1.26) and 50-59 year-old group (HR, 1.04; 95 % CI, 1.01 to 1.08). However, for every SD increment, a marginal protective effect against CVD events was observed between DBP and the CVD events in elder people (≥60 years old) and lower DBP (<70 mm Hg) may confer an increased CVD risks (HR, 1.10; 95 % CI, 1.03 to 1.17). For adults younger than 60 years old, the study seems to support the ACC/AHA blood pressure guidelines lowering the DBP threshold to 80 mm Hg. Conversely, it may be reasonable to rule out large effects of high DBP on CVD events and DBP <70 mm Hg may be cause for caution in older people aged 60-69.

Relationship between liver and cardiometabolic health in type 1 diabetes

IntroductionType 1 diabetes (T1D) is a chronic condition marked by insulin deficiency and hyperglycemia, with an increasing global incidence, particularly among children. Despite improvements in diabetes management, individuals with T1D continue to experience higher rates of cardiovascular disease (CVD), the leading cause of mortality in this population. Traditional CVD risk factors such as dyslipidemia and poor glycemic control are insufficient to fully explain the elevated risk in T1D, prompting further investigation into additional factors. Emerging evidence suggests that metabolic dysfunction-associated steatotic liver disease (MASLD) plays a critical role in this heightened CVD risk.ObjectiveThis narrative review aims to explore the relationship between MASLD and CVD in individuals with T1D. The review focuses on the prevalence of MASLD, its contributing risk factors, and the potential impact of liver dysfunction on cardiovascular outcomes in this population.MethodsA review of existing literature was conducted, focusing on observational studies, cohort studies, and meta-analyses that investigate the prevalence of MASLD in T1D populations and its association with CVD. The review also examines the physiological mechanisms linking MASLD and CVD, including insulin resistance, systemic inflammation, and hepatic dyslipidemia. Key studies were evaluated to identify patterns in MASLD prevalence based on diagnostic modalities and to assess the independent contribution of MASLD to cardiovascular risk in T1D patients.ConclusionMASLD is increasingly recognized as a significant contributor to CVD in individuals with T1D, particularly in those with shared risk factors like obesity and insulin resistance. Evidence suggests that MASLD exacerbates hepatic and systemic metabolic dysfunction, increasing CVD risk through mechanisms such as chronic inflammation and atherogenic lipid profiles. Routine liver health assessments and tailored management strategies targeting MASLD should be incorporated into clinical care for individuals with T1D to mitigate long-term cardiovascular complications.

Linking Antibodies Against Apolipoprotein A-1 to Metabolic Dysfunction-Associated Steatohepatitis in Mice

Metabolic dysfunction-associated fatty liver disease (MASLD) is a common liver and health issue associated with heightened cardiovascular disease (CVD) risk, with Cytokeratin 18 (CK-18) as a marker of liver injury across the MASLD to cirrhosis spectrum. Autoantibodies against apolipoprotein A-1 (AAA-1s) predict increased CVD risk, promoting atherosclerosis and liver steatosis in apoE−/− mice, though their impact on liver inflammation and fibrosis remains unclear. This study examined AAA-1s’ impact on low-grade inflammation, liver steatosis, and fibrosis using a MASLD mouse model exposed to AAA-1s passive immunization (PI). Ten-week-old male C57BL/6J mice under a high-fat diet underwent PI with AAA-1s or control antibodies for ten days. Compared to controls, AAA-1-immunized mice showed higher plasma CK-18 (5.3 vs. 2.1 pg/mL, p = 0.031), IL-6 (13 vs. 6.9 pg/mL, p = 0.035), IL-10 (27.3 vs. 9.8 pg/mL, p = 0.007), TNF-α (32.1 vs. 24.2 pg/mL, p = 0.032), and liver steatosis (93.4% vs. 73.8%, p = 0.007). Transcriptomic analyses revealed hepatic upregulation of pro-fibrotic mRNAs in AAA-1-recipient mice, though histological changes were absent. In conclusion, short-term AAA-1 PI exacerbated liver steatosis, inflammation, and pro-fibrotic gene expression, suggesting that AAA-1s may play a role in MASLD progression. Further research with prolonged AAA-1 exposure is warranted to clarify their potential role in liver fibrosis and associated complications.

The impact of metabolic heterogeneity of obesity and transitions on cardiovascular disease incidence in Chinese middle-aged and elderly population: A nationwide prospective cohort study.

Previous studies indicated that metabolic heterogeneity of obesity would affect the risk of cardiovascular disease (CVD). However, the alterations in CVD risk associated with transitions between various metabolic health statuses influenced by obesity status remain unclear. We utilized data from the China Health and Retirement Longitudinal Study (CHARLS), a longitudinal cohort study involving Chinese residents aged 45 years and older. Baseline data were collected in 2011-2012, with follow-up surveys conducted up to 2020. Participants in the study were categorized into four body mass index-metabolic phenotypes: metabolically healthy normal weight (MHNW), metabolically healthy overweight/obesity (MHOO), metabolically unhealthy normal weight (MUNW) and metabolically unhealthy overweight/obesity (MUOO). Transitions in these phenotypes over 4 years were analysed. Cox regression models were used to assess the associations of these phenotypes and their transitions with CVD incidence. Among 7721 participants, 1353 (17.5%) developed CVD during the follow-up period. Both overweight/obese and metabolically unhealthy statuses were associated with increased CVD risk. The highest risk was observed in the MUOO group (hazard ratio [HR]: 1.74, 95% confidence interval [CI]: 1.50-2.09, p < 0.0001), followed by the MUNW (HR 1.35, 95% CI: 1.13-1.66, p < 0.001) and MHOO (HR: 1.29, 95% CI: 1.08-1.56, p = 0.002) groups compared to the MHNW group. The deteriorations of obesity and metabolic health status elevated the incidence of CVD, whereas improvements in these statuses reduced the risk of CVD. Additionally, alterations in metabolic health status conferred greater benefits in overweight/obese individuals compared to those with normal weight. The study highlights the importance of maintaining and promoting metabolic health, particularly in overweight/obese individuals, to reduce CVD risk. Metabolic health status plays a more crucial role than obesity status in predicting CVD incidence.

Beyond the change: exploring age of menopause, lifestyle, and cardiovascular risk in women

Abstract Background Premature/early menopause increases the risk of future cardiovascular disease (CVD); however, whether lifestyle can offset this risk is unknown. Purpose Investigate the association between premature/early menopause and incident CVD and whether a healthy lifestyle modifies this association. Methods The 45 and Up Study prospectively recruited participants aged ≥45 years (n=267,357) between 2005-2009. Our study included women without prior CVD and those reporting menopausal age at baseline. Primary outcome was incident CVD (self-reported heart disease/stroke) based on survey data1 at Wave 2 (2012-2015) and/or Wave 3 (2018-2020). Logistic regression models assessed associations of premature (age &amp;lt;40 years) and early (age 40-44 years) menopause with CVD, compared to standard menopause (age 50-52 years), adjusting for sociodemographic and clinical variables. Healthy lifestyle adherence was assessed using a score of five factors: smoking, physical activity, sitting, sleep, and diet. Interaction effects were analysed between menopause and healthy lifestyle adherence on CVD. Results We included 46,273 women (mean age 62.1±8.2 years), with 5,425(11.7%) incident CVD over 15-year follow-up. After adjustment, the CVD risk was higher in women with premature menopause (odds ratio (OR): 1.36, 95% confidence intervals (CI), 1.17-1.59; p&amp;lt;0.0001) and early menopause (OR: 1.15, 95% CI, 1.03-1.28; p=0.013) compared to standard menopause. Among all menopausal women, high versus low healthy-lifestyle adherence led to 20% lower CVD risk (OR: 0.80, 95% CI, 0.71-0.90; p=0.0003). In the subset of high-risk women with premature menopause, high versus low healthy lifestyle adherence led to 50% lower risk of CVD (OR: 0.50, 95% CI, 0.31-0.80, p=0.0040). The healthy lifestyle effect was not significantly different across menopause groups (p=0.71). Conclusion Early and premature menopause were independently associated with increased CVD risk. Healthy versus unhealthy lifestyle significantly attenuated the risk of CVD in all menopausal women, particularly in the highest risk group of women with premature menopause, reducing this risk by 50%. 1 Secure data access was provided through the Sax Institute’s Secure Unified Research Environment (SURE).

Impact of addressing modifiable risk factors on the 10-year risk of cardiovascular disease in individuals with familial hypercholesterolemia: a causal analysis utilising UK biobank

Abstract Background Familial hypercholesterolemia (FH) is a prevalent autosomal dominant disorder characterised by elevated low-density lipoprotein cholesterol (LDL-C) levels from birth. These elevated LDL-C levels significantly amplify the lifetime risk of cardiovascular disease (CVD). While the impact of early and effective initiation of lipid-lowering medication (LLM) on CVD risk is well documented in genetically confirmed FH, the additional impact of addressing modifiable lifestyle risk factors (MLRF) in that patient population remains largely unquantified. Methods This study quantified the potential effects of successfully managing 4 MLRF (smoking, obesity, alcohol consumption, and low physical activity) on the 10-year incidence of a first CVD diagnosis in adults with genetically confirmed FH treated with LLM within the UK Biobank. The synthesised causal estimates of these 4 MLF were obtained using two recent causal analysis frameworks, namely the doWhy causal calculus framework and the Causal Forest Double Machine Learning Method. Results In 660 FH individuals (mean age 56±8 years; 60.15% women), smoking cessation and reducing body mass index below 30 kg/m2 delivered the most substantial risk reductions (pooled estimates, adjusted for the 3 other MLRF: -6.5% and -3.2%, respectively; both p&amp;lt;0.001), followed by initiating moderate or high physical activity (-1.7%; p&amp;lt;0.001; Figure). Notably, cessation of alcohol consumption significantly increased CVD risk (+2.5%; p&amp;lt;0.001), aligning with existing literature. Conclusion In over 10 years, reductions in CVD risk ranging from 1.7% to 6.5% were achievable through smoking cessation, BMI reduction, and enhanced physical activity in FH individuals. Leveraging causal inference methodologies facilitates the discernment of which risk factors offer the most pronounced additional benefits beyond lipid-lowering interventions in this high-risk population.Forest Plot of Causal Effect Estimates

Cardiovascular events risk in office-masked nocturnal hypertension defined by home blood pressure monitoring: the J-HOP nocturnal blood pressure study

Abstract Background Elevated nocturnal home blood pressure (BP) has been reported to be associated with increased risk for cardiovascular disease (CVD). Masked hypertension defined by home BP monitoring is also a strong risk factor for adverse CVD outcomes. However, no study has investigated the association between office-masked nocturnal hypertension defined by home BP monitoring and CVD events risk. Purpose This study aimed to examine the association between office-masked nocturnal hypertension defined by home BP monitoring and CVD events risk in a clinical practice-based population. Methods This was a prospective observational study including Japanese participants with CVD or high risk of CVD. Three office BPs were taken on two different occasions. Nocturnal home BP was measured three times per night for two weeks. The association between office-masked nocturnal hypertension and incident total CVD events (including fatal and non-fatal stroke and coronary heart disease) was examined using Cox regression. Results 2,545 participants were followed for the mean of 7.1 years (18,116 person-years), during which 152 (6.0%) CVD events occurred. Mean age (standard deviation) was 63.3 (10.3) years; 49.0% were male; 82.6% took antihypertensive medications. The proportions of participants with normotension (office BP &amp;lt;140/90 mmHg and nocturnal home BP &amp;lt;120/70 mmHg), white-coat hypertension (office BP ≥140/90 mmHg and nocturnal home BP &amp;lt;120/70 mmHg), office-masked nocturnal hypertension (office BP &amp;lt;140/90 mmHg and nocturnal home BP ≥120/70 mmHg), and sustained hypertension (office BP ≥140/90 mmHg and nocturnal home BP ≥120/70 mmHg) were 25.3%, 14.4%, 23.2%, and 37.1%, respectively. The office-masked nocturnal hypertensive group and sustained hypertensive group had higher incidence rates of total CVD events compared with the normotensive group. Relative to normotension, those with both office-masked nocturnal hypertension (adjusted hazard ratio [aHR] 1.72, 95% confidence interval [CI] 1.01–2.92) and sustained hypertension (aHR 1.75, 95%CI 1.03–2.96) had similarly increased CVD risk, even after adjustment for daytime home BP values. Conclusions Screening for office-masked nocturnal hypertension with home BP monitoring identifies a potentially important group of patients with increased risk for incident CVD events for whom additional preventative measures may be appropriate.

Load-Dependent Mechanisms Contribute to Increased Aortic Stiffness Among Women with a History of Preeclampsia: Relation with Cardiovagal Baroreflex Sensitivity.

Introduction: Preeclampsia, a hypertensive disorder of pregnancy, results in increased lifetime cardiovascular disease (CVD) risk. Total aortic stiffness, a robust risk factor for CVD, is composed of load-dependent (blood pressure load on arterial wall) and structural (intrinsic changes in arterial wall) mechanisms. Total aortic stiffness is also associated with reduced cardiovagal baroreflex sensitivity (BRS). We sought to determine 1) whether elevated total aortic stiffness among women with a history of preeclampsia (hxPE) is attributed to load-dependent or structural stiffness, and 2) whether either mechanism is associated with lower BRS. Methods: Total aortic stiffness (carotid-femoral pulse wave velocity) and spontaneous cardiovagal BRS (sequence technique) were measured among women 1-5 years postpartum (n=115; age 34 ±4yrs; hxPE n=51; controls n=64). Structural aortic stiffness was calculated from participant-specific exponential models, standardizing aortic stiffness to a 'reference' blood pressure. Load-dependent stiffness was calculated as total minus structural stiffness. Results: Total (+0.8 m/sec, 95% CI (-0.99, -0.23), p=0.002) and load-dependent (+0.4 m/sec, 95% CI (-0.56, -0.22), P<0.001), but not structural (95% CI (-0.52, 0.08), p=0.16), aortic stiffness were higher among women with hxPE compared with controls. Women with a hxPE had lower BRS (p=0.042) that was negatively associated with total (B =-3.24 ms/mmHg, 95% CI (-6.35, -0.13), p=0.042) and load-dependent (B =-5.91ms/mmHg, 95% CI (-11.31, -0.51), p=0.033) aortic stiffness. Conclusion: Load-dependent, not structural, aortic stiffness mechanisms contribute to higher total aortic stiffness among women with hxPE and was associated with lower cardiovagal BRS. Postpartum BP monitoring is critical to reduce increased CVD risk in preeclampsia.

Assessing the relative importance of vitamin D deficiency in cardiovascular health.

Previous research has suggested a potential link between vitamin D (VD) deficiency and adverse cardiovascular health outcomes, although the findings have been inconsistent. This study investigates the association between VD deficiency and cardiovascular disease (CVD) within the context of established CVD risk factors. We utilized a Random Forest model to predict both CVD and VD deficiency risks, using a dataset of 1,078 observations from a rural Chinese population. Feature importance was evaluated using SHapley Additive exPlanations (SHAP) to discern the impact of various risk factors on the model's output. The results showed that the model for CVD prediction achieved a high accuracy of 87%, demonstrating robust performance across precision, recall, and F1 score metrics. Conversely, the VD deficiency prediction model exhibited suboptimal performance, with an accuracy of 52% and lower precision, recall, and F1 scores. Feature importance analysis indicated that traditional risk factors such as systolic blood pressure, diastolic blood pressure, age, body mass index, and waist-to-hip ratio significantly influenced CVD risk, collectively contributing to 70% of the model's predictive power. Although VD deficiency was associated with an increased risk of CVD, its importance in predicting CVD risk was notably low. Similarly, for VD deficiency prediction, CVD risk factors such as systolic blood pressure, glucose levels, diastolic blood pressure, and body mass index emerged as influential features. However, the overall predictive performance of the VD deficiency prediction model was weak (52%), indicating the absence of VD deficiency-related risk factors. Ablation experiments confirmed the relatively lower importance of VD deficiency in predicting CVD risk. Furthermore, the SHAP partial dependence plot revealed a nonlinear relationship between VD levels and CVD risk. In conclusion, while VD deficiency appears directly or indirectly associated with increased CVD risk, its relative importance within predictive models is considerably lower when compared to other risk factors. These findings suggest that VD deficiency may not warrant primary focus in CVD risk assessment and prevention strategies, however, further research is needed to explore the causal relationship between VD deficiency and CVD risk.

6870 Cardiac Imaging And Metabolomics Studies Suggest Differential Risk And Protective Biomarkers For Cardiovascular Disease In Renoprotected, Long-Duration Type 1 Diabetes

Abstract Disclosure: M. Yu: None. S. Jangolla: None. N. Ziemniak: None. E. Viebranz: None. T. Chokshi: None. K. Park: None. I. Wu: None. H. Shah: None. G.L. King: None. Cardiovascular disease (CVD) is a major cause of mortality in people with Type 1 diabetes (T1D), especially in those with nephropathy (DN). However, in long-duration T1D, a substantial proportion of individuals without DN still exhibit excessive CVD risks. The Joslin 50-Year “Medalist” Study (n=1043), composed of people with T1D≥50 years, are ideal for studying CVD in a renoprotected T1D cohort, as only 13% have DN, and yet 40% have CVD, despite excellent control of lipids and blood pressure. Stratifying the Medalists by DN revealed that exercise was cardioprotective in the group with DN (OR 0.60, p=0.04); while age at T1D diagnosis (OR 1.03, p=0.01), HbA1c (OR 1.25, p=0.01), C-reactive protein (OR 1.14, p=0.01), and interleukin-6 (OR 1.13, p=0.01) all increased CVD risk in Medalists without DN. A subset of Medalists also underwent coronary artery calcification scans (CAC; n=153) and cardiac magnetic resonance imaging of left ventricular (LV) structure and function (CMR; n=111). The majority of these Medalists (97.8%) had detectable CAC&amp;gt;0; furthermore, the median CAC score of 1000 was higher at any cutoff compared to similar age-matched T1D and Type 2 diabetes (T2D) populations with higher DN prevalence. In contrast, mean CMR values in this Medalist subset were comparable to other cohorts. Continuous glucose monitoring (CGM) metrics for hyperglycemia (mean glucose, β=0.002, p=0.03; glucose management indicator, β=0.09, p=0.03; and time above range&amp;gt;180 mg/dL, β=0.003, p=0.02), but not glucose variability or hypoglycemia, were associated with LV remodeling in the Medalists, even after adjusting for eGFR. Likewise, plasma levels of advanced glycation end-products (AGEs) N-carboxyethyl-lysine (CEL), N-carboxymethyl-lysine (CML), and methylglyoxal-derived hydroimidazolone (MGH1) were associated with CAC (β=16.22, p=0.05; β=15.21, p=0.01; and β=10.18, p=0.01, respectively) and LV remodeling (β=0.001, p=0.09; β=0.001, p=0.05; and β=0.001, p=0.04, respectively) in the Medalists. The association of CEL with CVD replicated in a separate Medalist subset (n=311) with self-reported CVD data (OR 1.26, p=0.01). Plasma global metabolomics studies (n=140) revealed that amino acid activation pathways, with lower levels of branched chain amino acids, were associated with CAC (FDR=0.002); while amino acid metabolism pathways were associated with less favorable LV volumes (FDR=0.03). In this comprehensive study of aging T1D people with no substantial DN, hyperlipidemia, or hypertension, cardiac imaging and metabolomics studies suggest disproportionate advanced CAC, as compared to subclinical LV remodeling or dysfunction, and highlight the importance of targeting hyperglycemia for CVD risk reduction. Plasma metabolites associated with CVD in T1D are different from those in T2D, and may provide novel information on potential therapeutic targets for CVD in T1D. Presentation: 6/1/2024

Death of a Parent, Racial Inequities, and Cardiovascular Disease Risk in Early to Mid-adulthood.

Black Americans experience the death of a parent much earlier in the life course than White Americans on average. However, studies have not considered whether the cardiovascular health consequences of early parental death vary by race. Using data from the National Longitudinal Study of Adolescent to Adult Health, we explore associations between early parental death and cardiovascular disease (CVD) risk in early to mid-adulthood (N = 4,193). We find that the death of a parent during childhood or adolescence (ages 0-17) or the transition to adulthood (ages 18-27) is associated with increased CVD risk for Black Americans, whereas parental death following the transition to adulthood (ages 28+) undermines cardiovascular health for both Black Americans and White Americans. These findings illustrate how a stress and life course perspective can help inform strategies aimed at addressing both the unequal burden of bereavement and high cardiovascular risk faced by Black Americans.

Differences in Emotion Expression, Suppression, and Cardiovascular Consequences Between Black and White Americans in the Midlife in the United States (MIDUS) Study.

Recent theoretical work suggests the expression of emotions may differ among Black and White Americans, such that Black Americans engage more frequently in expressive suppression to regulate emotions and avoid conflict. Prior work has linked expressive suppression usage with increases in cardiovascular disease risk, suggesting that racialized differences in expressive suppression usage may be one mechanism by which racism "gets under the skin" and creates heath disparities. To examine racialized differences in expressive suppression and blood pressure (a measure of cardiovascular disease risk), we used self-report and facial electromyography (fEMG) data from two cohorts of Black and White Americans from the Midlife in the United States (MIDUS) longitudinal study (MIDUS 2, n = 271, 34.7% Black, collected from 2004-2009; MIDUS Refresher 1, n = 114, 31.6% Black, collected from 2012-2016; total N = 385, 33.9% Black). Black Americans reported engaging in expressive suppression more frequently than White Americans (t(260.95) = 2.18, p = .002) and showed less corrugator fEMG activity during negative images(t(969) = 2.38, pFDR = .026). Less corrugator activity during negative images was associated with higher systolic blood pressure only for Black Americans (b = -4.63, t(375) = 2.67, p = .008). Overall, results are consistent with theoretical accounts that Black Americans engage more frequently in expressive suppression, which in turn is related to higher cardiovascular risk. Additional research is needed to further test this claim, particularly in real-world contexts and self-reports of in-the-moment usage of expressive suppression.

Synergy Between NK Cells and Monocytes in Potentiating Cardiovascular Disease Risk in Severe COVID-19.

Evidence suggests that COVID-19 predisposes to cardiovascular diseases (CVDs). While monocytes/macrophages play a central role in the immunopathogenesis of atherosclerosis, less is known about their immunopathogenic mechanisms that lead to CVDs during COVID-19. Natural killer (NK) cells, which play an intermediary role during pathologies like atherosclerosis, are dysregulated during COVID-19. Here, we sought to investigate altered immune cells and their associations with CVD risk during severe COVID-19. We measured plasma biomarkers of CVDs and determined phenotypes of circulating immune subsets using spectral flow cytometry. We compared these between patients with severe COVID-19 (severe, n=31), those who recovered from severe COVID-19 (recovered, n=29), and SARS-CoV-2-uninfected controls (controls, n=17). In vivo observations were supported using in vitro assays to highlight possible mechanistic links between dysregulated immune subsets and biomarkers during and after COVID-19. We performed multidimensional analyses of published single-cell transcriptome data of monocytes and NK cells during severe COVID-19 to substantiate in vivo findings. During severe COVID-19, we observed alterations in cardiometabolic biomarkers including oxidized-low-density lipoprotein, which showed decreased levels in severe and recovered groups. Severe patients exhibited dysregulated monocyte subsets, including increased frequencies of proinflammatory intermediate monocytes (also observed in the recovered) and decreased nonclassical monocytes. All identified NK-cell subsets in the severe COVID-19 group displayed increased expression of activation and tissue-resident markers, such as CD69 (cluster of differentiation 69). We observed significant correlations between altered immune subsets and plasma oxidized-low-density lipoprotein levels. In vitro assays revealed increased uptake of oxidized-low-density lipoprotein into monocyte-derived macrophages in the presence of NK cells activated by plasma of patients with severe COVID-19. Transcriptome analyses confirmed enriched proinflammatory responses and lipid dysregulation associated with epigenetic modifications in monocytes and NK cells during severe COVID-19. Our study provides new insights into the involvement of monocytes and NK cells in the increased CVD risk observed during and after COVID-19.

Hormones, Stress, and Heart Disease in Transgender Women with HIV in LITE Plus

Cardiovascular disease (CVD) is a leading cause of death among transgender women and people with HIV. Exogenous estrogen and psychosocial stressors are known risk factors for CVD. Yet, few studies have used biomarkers to examine the role of stress in CVD risk among transgender women with HIV (TWHIV). This analysis examined whether stress moderates relationships between gender-affirming hormone therapy (GAHT) duration and CVD risk among TWHIV. This cross-sectional analysis of baseline data from an observational cohort of 108 Black and Latina TWHIV in Boston, New York, and Washington, DC, enrolled December 2020 to June 2022, measured sociodemographics, medical diagnoses, medications, smoking history, and perceived stress via interviewer-administered surveys. Physiological stress was measured with 14 biomarkers to calculate allostatic load indices (ALI). Forty participants provided saliva samples used to calculate cortisol awakening response and cortisol daily decline. The 2018 American College of Cardiology Revised Pooled Cohort Equation estimated 10-year CVD risk. Data were analyzed in 2024. GAHT duration was positively associated with CVD risk scores in bivariate regression. In multivariable linear regression models (adjusting for age, income, education), only age and ALI remained significantly associated with CVD risk scores (β 1.13, CI: 1.05, 1.21). No stress measure significantly interacted with GAHT duration to affect CVD risk scores. In visual plots, GAHT duration increased CVD risk scores only for TWHIV experiencing the highest ALI. Stress plays an important role in CVD in TWHIV. More research is needed on non-GAHT factors, which influence CVD health among transgender women.

Risk of cardiovascular disease among head and neck cancer survivors: A population-based matched cohort study

BackgroundIn the United States, approximately 63,000 Americans develop head and neck cancer (HNC) annually. Our study aims were to investigate cardiovascular complications and risk factors for development of CVD among HNC survivors. MethodsUtilizing the Utah Populations Database, a total of 1,901 HNC patients diagnosed and 7,796 birth year, sex, and birth state matched individuals from the general population were identified. Multivariate Cox proportional hazard models were used. ResultsWithin the first two years after cancer diagnosis, HNC survivors had a higher likelihood of developing cardiovascular disease (CVD). High Charleston Comorbidity Index (CCI) score at baseline (Hazard Ratio (HR) 1.67, 95 % 1.28–2.17), stage II and IV disease (HR 1.80, 95 % 1.29–2.51), age >=65 years old (HR 2.31, 95 % 1.85–2.88), chemotherapy (HR 1.47, 95 % 1.15–1.88) were associated with increased CVD risk. ConclusionsCompared to the general population, HNC survivors were more likely to develop cardiovascular diseases, particularly if they had the following risk factors: older age, stage II or IV cancer, high baseline CCI score, and chemotherapy were risk factors for development of CVD.

The mediating effect of TyG-related indicators between long-term exposure to particulate matter and cardiovascular disease: evidence from a national longitudinal cohort study

BackgroundAmbient particulate matter (PM) exposure is recognized as a risk factor for cardiovascular disease (CVD). However, the extent to which PM exposure is associated with CVD via triglyceride glucose (TyG)-related indicators remains unknown. This study examines the relationship between long-term PM exposure and CVD events, further assessing whether TyG-related indicators mediate this association.MethodsThis cohort study involved 7,532 individuals aged at least 45 years who were not diagnosed with CVD in 2011 from the China Longitudinal Study of Health and Retirement (CHARLS) and were followed up for the occurrence of CVD until 2020. The annual PM concentration data at the city level, with aerodynamic diameters ≤ 1 μm (PM1), ≤ 2.5 μm (PM2.5), and ≤ 10 μm (PM10), were obtained from the ChinaHighAirPollutants (CHAP). The average concentration of PM in the 3 years before the baseline survey in 2011 was defined as the long-term exposure level of the individual. The relationship between PM exposure and CVD incidence was examined via Cox proportional hazards models, with a focus on probing the role of TyG-related indicators through mediation analysis.ResultsA total of 1,865 individuals with CVD were diagnosed over the span of a 7.4-year follow-up period. The 3-year average concentrations before baseline were 31.29 µg/m³ for PM1, 56.03 µg/m³ for PM2.5, and 95.73 µg/m³ for PM10. In fully adjusted model, the Cox proportional hazards models revealed that an increase of 10 µg/m³ in the PM1, PM2.5, and PM10 exposure concentrations corresponded to elevated CVD risk, with HRs (95% CI) of 1.135 (1.078–1.195), 1.092 (1.062–1.123), and 1.075 (1.059–1.090), respectively. Mediation analyses further suggested that the correlation between PM exposure and CVD could be partly mediated via TyG-BMI, TyG-WC, and TyG-WHtR, with mediation proportions varying from 5.54 to 15.30%.ConclusionA significant correlation was observed between long-term PM exposure and increased CVD risk, with TyG-related indicators, such as TyG-BMI, TyG-WC, and TyG-WHtR, partially mediating this relationship.

Changes in 10-Year Predicted Cardiovascular Disease Risk for a Multiethnic Semirural Population in South East Asia: Prospective Study.

Cardiovascular disease (CVD) risk factors tend to cluster and interact multiplicatively and have been incorporated into risk equations such as the Framingham risk score, which can reasonably predict CVD over short- and long-term periods. Beyond risk factor levels at a single time point, recent evidence demonstrated that risk trajectories are differentially related to CVD risk. However, factors associated with suboptimal control or unstable CVD risk trajectories are not yet established. This study aims to examine factors associated with CVD risk trajectories in a semirural, multiethnic community-dwelling population. Data on demographic, socioeconomic, lifestyle, mental health, and cardiovascular factors were measured at baseline (2013) and during follow-up (2018) of the South East Asia Community Observatory cohort. The 10-year CVD risk change transition was computed. The trajectory patterns identified were improved; remained unchanged in low, moderate, or high CVD risk clusters; and worsened CVD risk trajectories. Multivariable regression analyses were used to examine the association between risk factors and changes in Framingham risk score and predicted CVD risk trajectory patterns with adjustments for concurrent risk factors. Of the 6599 multiethnic community-dwelling individuals (n=3954, 59.92% female participants and n=2645, 40.08% male participants; mean age 55.3, SD 10.6 years), CVD risk increased over time in 33.37% (n=2202) of the sample population, while 24.38% (n=1609 remained in the high-risk trajectory pattern, which was reflected by the increased prevalence of all major CVD risk factors over the 5-year follow-up. Meanwhile, sex-specific prevalence data indicate that 21.44% (n=567) of male and 41.35% (n=1635) of female participants experienced an increase in CVD risk. However, a stark sex difference was observed in those remaining in the high CVD risk cluster, with 45.1% (n=1193) male participants and 10.52% (n=416) female participants. Regarding specific CVD risk factors, male participants exhibited a higher percentage increase in the prevalence of hypertension, antihypertensive medication use, smoking, and obesity, while female participants showed a higher prevalence of diabetes. Further regression analyses identified that Malay compared to Chinese (P<.001) and Indian (P=.04) ethnicity, nonmarried status (P<.001), full-time employment (P<.001), and depressive symptoms (P=.04) were all significantly associated with increased CVD risk scores. In addition, lower educational levels and frequently having meals from outside were significantly associated to higher odds of both worsening and remaining in high CVD risk trajectories. Sociodemographics and mental health were found to be differently associated with CVD risk trajectories, warranting future research to disentangle the role of psychosocial disparities in CVD. Our findings carry public health implications, suggesting that the rise in major risk factors along with psychosocial disparities could potentially elevate CVD risk among individuals in underserved settings. More prevention efforts that continuously monitor CVD risk and consider changes in risk factors among vulnerable populations should be emphasized.

Cardiovascular Disease in Women and the Role of Hormone Replacement Therapy.

Cardiovascular disease (CVD) is the leading cause of death in women and manifests more severely and at a later stage in life compared to men. The low estrogen levels during menopause are linked to an increased CVD risk. This association has promoted research regarding the role of hormone replacement therapy (HRT) in reducing the symptoms and diseases related to menopause, including CVD. This review article aims to discuss the biological changes associated with menopause and their impact on CVD. It also examines the effects of HRT in women with comorbidities related to CVD,its indications, risks, and contraindications.

Use of Censored Data Methods to Estimate Blood Pressure Percentiles in US Adults

Abstract Blood pressure (BP) levels are important modifiable risk factors for incident cardiovascular disease (CVD). However, many adults are on anti-hypertensive medication (MEDS) which lowers their BP but is a marker for increased CVD risk. To capture the association of BP and its treatment with risk, it is important to estimate BP levels in the absence of medication, i.e., Underlying BP. One proposed ad-hoc solution is to add a fixed increment e.g., 10/5 mm Hg to systolic (SBP)/diastolic (DBP) for people on MEDS to approximate their Underlying BP. However, what this increment should be, and whether it applies to all MEDS users is unclear. In this manuscript, we propose a novel time-to-event approach to estimate Underlying BP, treating BPs on MEDS as censored observations. The results indicate that the median Treatment Effect (i.e., Underlying BP – Observed BP) for SBP/DBP is 12.0/7.7 for men and 16.9/6.5 for women and is significantly modified by age, BMI and black race. The Underlying BP for MEDS users is then combined with the observed BP for non-MEDS users to derive age-sex-specific BP percentiles for Underlying BP based on a representative sample of normal weight U.S. adults aged 18-79 using NHANES data from 1999-2018.

Association of Urinary Metals With Cardiovascular Disease Incidence and All-Cause Mortality in the Multi-Ethnic Study of Atherosclerosis (MESA).

Exposure to metals has been associated with cardiovascular disease (CVD) end points and mortality, yet prospective evidence is limited beyond arsenic, cadmium, and lead. In this study, we assessed the prospective association of urinary metals with incident CVD and all-cause mortality in a racially diverse population of US adults from MESA (the Multi-Ethnic Study of Atherosclerosis). We included 6599 participants (mean [SD] age, 62.1 [10.2] years; 53% female) with urinary metals available at baseline (2000 to 2001) and followed through December 2019. We used Cox proportional hazards models to estimate the adjusted hazard ratio and 95% CI of CVD and all-cause mortality by baseline urinary levels of cadmium, tungsten, and uranium (nonessential metals), and cobalt, copper, and zinc (essential metals). The joint association of the 6 metals as a mixture and the corresponding 10-year survival probability was calculated using Cox Elastic-Net. During follow-up, 1162 participants developed CVD, and 1844 participants died. In models adjusted by behavioral and clinical indicators, the hazard ratios (95% CI) for incident CVD and all-cause mortality comparing the highest with the lowest quartile were, respectively: 1.25 (1.03, 1.53) and 1.68 (1.43, 1.96) for cadmium; 1.20 (1.01, 1.42) and 1.16 (1.01, 1.33) for tungsten; 1.32 (1.08, 1.62) and 1.32 (1.12, 1.56) for uranium; 1.24 (1.03, 1.48) and 1.37 (1.19, 1.58) for cobalt; 1.42 (1.18, 1.70) and 1.50 (1.29, 1.74) for copper; and 1.21 (1.01, 1.45) and 1.38 (1.20, 1.59) for zinc. A positive linear dose-response was identified for cadmium and copper with both end points. The adjusted hazard ratios (95% CI) for an interquartile range (IQR) increase in the mixture of these 6 urinary metals and the corresponding 10-year survival probability difference (95% CI) were 1.29 (1.11, 1.56) and -1.1% (-2.0, -0.05) for incident CVD and 1.66 (1.47, 1.91) and -2.0% (-2.6, -1.5) for all-cause mortality. This epidemiological study in US adults indicates that urinary metal levels are associated with increased CVD risk and mortality. These findings can inform the development of novel preventive strategies to improve cardiovascular health.