Cardiovascular Disease Risk Research Articles

Comparison of lipid profile alterations in chronic hepatitis b patients receiving tenofovir alafenamide or tenofovir disoproxil fumarate

This study aimed to compare the serum lipid profiles between tenofovir disoproxil fumarate (TDF) and tenofovir alafenamide (TAF) in the long-term treatment of chronic hepatitis B (CHB). We analyzed data from treatment-naïve CHB patients administered with TDF or TAF, collected from electronic medical records between May 2017 and September 2022. Serum lipid indices, including total cholesterol (TC), triglycerides (TG), low-density (LDL) and high-density lipoprotein (HDL), and their ratios (TC/HDL, LDL/HDL), were assessed at baseline, and at 48 and 96 weeks. Propensity score matching (PSM) adjusted for baseline differences between groups. From 2344 patients initially screened, 418 were included for the 48-week analysis (265 on TDF, 153 on TAF) and 292 for the 96-week analysis (238 on TDF, 54 on TAF). At 48 weeks, comparing the serum lipid indicators between the pre- and post-treatment, TDF significantly reduced TC and TC/HDL, whereas TAF induced widespread dyslipidemia, characterized by elevated levels of TC, TG, LDL, LDL/HDL, and TC/HDL, and reduced HDL (P < 0.05). After PSM grouping, TAF remained significantly associated with higher TC, TG, LDL, LDL/HDL, and TC/HDL compared to TDF (P < 0.05). Over 48 weeks, TAF treatment was associated with significant increases in TC, TG, and LDL, whereas TDF treatment led to decreases (P < 0.05). TC/HDL and LDL/HDL increased in both groups, but more significant in TAF (P < 0.05). At 96 weeks, the TAF group continued to exhibit significantly higher levels of TC, LDL, and LDL/HDL compared to the TDF group (P < 0.05). Notably, LDL levels were 115.65 ± 28.07 mg/dL in TAF versus 96.07 ± 23.97 mg/dL in TDF. The increase in TC/HDL ratio in the TAF group was higher than in the TDF group, though not statistically significant. Furthermore, TAF treatment was associated with significant increases in LDL (18.58 ± 24.35 mg/dL) and LDL/HDL ratio (0.41 ± 0.95) over 96 weeks, while TDF treatment showed reductions in TC (-8.13 ± 30.86 mg/dL). Between 48 and 96 weeks, most lipid changes in the TDF group were not statistically significant, except for increases in LDL and LDL/HDL. In the TAF group, an increasing trend of LDL and TC/HDL was noted, although LDL showed a slight turnover after 48 weeks. This real-world study provides new evidence that TAF can induce dyslipidemia, while TDF exhibits a lipid-lowering effect in CHB. Patients at high risk for hepatic steatosis and cardiovascular diseases should consider these effects when choosing between TAF and TDF.

A service evaluation of the uptake and effectiveness of a digital delivery of the NHS health check service

ObjectivesTo compare the uptake, effectiveness and costs of a digital version of the National Health Service (NHS) Health Check (DHC) to the standard face-to-face NHS Health Check (F2F).Participants and settingA...

Correlation of Eight (8) Polymorphisms and Their Genotypes with the Risk Factors of Cardiovascular Disease in a Black Elderly Population

Single nucleotide polymorphisms (SNPs) have been associated with the development of cardiovascular diseases (CVDs). This study correlated eight SNPs with the risk factors of CVD in a black elderly population. Genotyping was used to detect eight polymorphisms; rs675 (ApoA-IV), rs699 (Angiotensinogen (AGT)), rs247616 and rs1968905 (Cholesteryl ester transfer protein (CETP)), rs1801278 (Insulin receptor substrate 1 (IRS-1)), rs1805087 (Methylenetetrahydrofolate reductase (MTHFR)) and rs28362286 and rs67608943 (Proprotein convertase subtilisin/kexin type 9 (PCSK9)), as well as their genotypes in deoxyribonucleic acid (DNA) extracted from peripheral blood. The cardiovascular risk (CVR) measurements were conducted on a Konelab 20i Thermo Scientific autoanalyzer and an enzyme-linked immunoassay (ELISA) assay. International Business Machines Corporation (IBM)® Statistical Package for the Social Sciences ® (SPSS) version 28 was used for statistical analysis. The heterozygous and homozygous genotypes of the eight polymorphisms were detected with the corresponding CVD risk factors. Subgroup analysis indicated that certain genotype carriers exhibited variations in their concentrations of CVR factors compared to others; however, these differences did not reach statistical significance. For example, carriers of the G genotype of the rs699 polymorphism showed marginally different blood pressure readings compared to the AG genotype carriers. The multiple linear regression analysis indicated that the only significant association was between PCSK9 and the rs28362286 (p = 0.029) polymorphism. The findings of our study show that single nucleotide polymorphisms are disseminated across the human genome. The heterozygous and homozygous genotypes of the SNPs require further investigation as they may have independent and possible collective roles in increasing the risk of CVDs.

NOISE POLLUTION AND ITS EFFECTS ON HUMAN HEALTH: A REVIEW

Noise pollution is a pervasive environmental issue with significant adverse effects on human health. This abstract explores the impact of noise pollution on both physical and mental well-being, emphasizing its role in increasing risks for cardiovascular diseases, hearing loss, sleep disturbances, and cognitive impairments. Vulnerable populations, including children and the elderly, are particularly affected by high noise levels, which exacerbate stress, anxiety, and depression, and impair cognitive development in children. The economic implications of noise pollution are considerable, with substantial costs associated with healthcare and productivity losses, as well as negative effects on community cohesion and quality of life. Effective noise management is essential, requiring robust regulations, improved urban planning, and heightened public awareness. Further research is needed to understand the long-term health impacts, refine noise reduction technologies, and assess effects on specific populations. Interdisciplinary studies will be crucial in developing comprehensive strategies to mitigate the health impacts of noise pollution. KEYWORDS: Noise Pollution; Health Impacts; Noise Reduction Technologies; Economic Costs; Interdisciplinary Research

Metformin associates with higher myocardial perfusion reserve and survival in type 2 diabetes mellitus patients

Metformin is an antihyperglycemic used to treat type 2 diabetes mellitus (T2DM). Patients with T2DM are at increased risk of cardiovascular disease. We explored the association between metformin use and cardiovascular magnetic resonance (CMR) derived stress myocardial blood flow (MBF), myocardial perfusion reserve (MPR) and major adverse cardiovascular events (MACE; all cause death, MI, stroke, heart failure hospitalisation and coronary revascularisation) in patients with T2DM. Multi-centre study of patients with T2DM, and healthy controls, underwent quantitative myocardial perfusion CMR using an artificial intelligence supported process. Multivariable regression analysis, and cox proportional hazard models of propensity score weighted patients quantified associations between metformin use, MBF, MPR, all cause death and MACE. Analysis included 572 patients with T2DM (68% prescribed metformin) with median follow-up 851 days (IQR 935 − 765). Metformin use was associated with an increase of MPR of 0.12 [0.08–0.40], p = 0.004. There were 82 MACE events (14.3%) including 25 (4.4%) deaths of which 16 were in those not prescribed metformin (8.7%), compared to 9 in patients prescribed metformin (2.3%): adjusted hazard ratio 0.24 (95% CI 0.08–0.70, p = 0.009). MACE events were similar between groups. This multicentre, inverse probability weighting propensity score analysis study showed that in patients with T2DM, metformin use is associated with higher MPR and improved all cause survival.

Association Between Employment Factors and Prevalence of Cardiovascular Disease in US Law Enforcement Workers: The National Health Interview Survey, 2006–2018

ABSTRACTBackgroundLaw enforcement workers face a higher risk of cardiovascular disease (CVD), however, employment factors impacting CVD remain systematically understudied, particularly in a national US sample. We describe temporal trends in prevalent CVD including coronary heart disease (CHD), angina, myocardial infarction (MI) and other heart disease; and investigate associations of select employment factors with CVD among law enforcement workers using the National Health Interview Survey (NHIS) from 2006 to 2018.MethodsWe analyzed prevalent CVD in law enforcement workers employed in local, state, and federal establishments using the NHIS, a nationally representative sample of US workers. We estimated odds ratios (OR [95% confidence interval, CI]) of CVD in relation to employment factors using survey‐weighted multivariable logistic regression models adjusted for sociodemographic and traditional CVD risk factors.ResultsAmong 2177 law enforcement workers, mean age 46 years, 19% female, prevalence of CVD was higher among disabled (OR = 5.37; 95% CI: 2.53, 11.38 for aggregate CVD outcome) and retired (OR = 2.14; 95% CI: 1.18, 3.88 for aggregate CVD outcome) workers compared to currently employed workers. Workers employed in smaller (1–24 employees) or larger (≥ 500 employees) departments and those with tenure &gt; 20 years also demonstrated higher prevalence odds of select CVD outcomes. Although not statistically significant, higher prevalence odds across CVD outcomes were observed in local government employees, hourly paid workers, and workers with 10–19 years of tenure.ConclusionsOur study highlights that select employment factors, some previously underexplored, may be associated with prevalent CVD in law enforcement workers. Leveraging national surveys and worker cohorts to enhance surveillance of identified groups in this high‐risk population could help elucidate the role of employment on CVD development and inform workplace interventions.

Causal association between remnant cholesterol level and risk of cardiovascular diseases: a bidirectional two sample mendelian randomization study

Serum lipids have been associated with an increased risk of various cardiovascular diseases (CVDs) in several observational studies, but the causal inference between the remnant cholesterol (RC) levels and several CVDs risk has not been established. The purpose of this study was to investigate whether there is a causal relationship between RC levels and risk of developing CVDs by a bidirectional two-sample Mendelian randomization (TSMR) analysis. One TSMR analysis was performed using the publicly released large-scale genome-wide association study (GWAS) data. Inverse variance weighted (IVW) method was chosen as the main analysis method, and MR-Egger, weighted median, simple mode, and weighted mode were used as supplementary methods. We conducted a series of sensitivity analyses to assess the robustness of the main results, including the Cochran’s Q test, MR-Egger intercept test, leave-one-out sensitivity analysis, and funnel plot. The main IVW method revealed that genetically predicted serum level of RC is significantly associated with an increased risk of developing ischemic heart disease (OR = 1.409, 95%CI = 1.284–1.546, P value = 4.753E-13), unstable angina pectoris (OR = 1.621, 95%CI = 1.398–1.880, P value = 1.672E-10), myocardial infarction (OR = 1.526, 95%CI = 1.337–1.741, P value = 3.771E-10), cardiac arrest (OR = 1.595, 95%CI = 1.322–1.924, P value = 1.076E-06), heart failure (OR = 1.086, 95%CI = 1.009–1.169, P value = 0.028), hypertension (OR = 1.089, 95%CI = 1.043–1.136, P value = 9.458E-05), major coronary heart disease (CHD) events (OR = 1.515, 95%CI = 1.376–1.669, P value = 3.217E-17), coronary atherosclerosis (OR = 1.388, 95%CI = 1.231–1.564, P value = 7.739E-08), cardiac arrhythmias (OR = 1.067, 95%CI = 1.008–1.130, P value = 0.025), and atrial fibrillation and flutter (OR = 1.122, 95%CI = 1.039–1.211, P value = 0.003). Additionally, the causal associations between the RC levels and these CVDs remained significant after correcting for the false discovery rate (all P value < 0.05). However, this study did not find any significant association of RC with cardiomyopathy and pericarditis (both P value > 0.05). Heterogeneity existed in the IVs of RC and ischemic heart disease, unstable angina pectoris, myocardial infarction, heart failure, hypertension, major CHD events, cardiomyopathy, coronary atherosclerosis, cardiac arrhythmias and atrial fibrillation and flutter using the Cochran’s Q test (all P value < 0.05). Moreover, there was no horizontal pleiotropy in this study (all P value > 0.05). The leave-one-out sensitivity analyses showed that the causal effects between RC level and CVDs (except for heart failure, cardiomyopathy, pericarditis and cardiac arrhythmias) are not driven by a single SNP. The funnel plots showed that there is no obvious potential bias in our study. In the replication analysis, the genetically predicted RC levels were positively associated with a 43.12% higher risk of coronary artery disease. This present study supported the causal link between RC and heightened the risk of CVDs, indicating that RC-lowering treatment might be effective in preventing CVDs.

Associations of physiologic subtypes based on HOMA2 indices of β-cell function and insulin sensitivity with the risk of kidney function decline, cardiovascular disease, and all-cause mortality from the 4C study

BackgroundPrevious studies have been limited by their inability to differentiate between the effects of insulin sensitivity and β-cell function on the risk of kidney function decline, cardiovascular disease (CVD), and all-cause mortality. To address this knowledge gap, we aimed to investigate whether the physiological subtypes based on homeostasis model assessment-2 (HOMA2) indices of β-cell function (HOMA2-B) and insulin sensitivity (HOMA2-S) could be used to identify individuals with subsequently high or low of clinical outcome risk.MethodsThis retrospective cohort study included 7,317 participants with a follow-up of up to 5 years. Based on HOMA2 indices, participants were categorized into four physiologic subtypes: the normal phenotype (high insulin sensitivity and high β-cell function), the insulinopenic phenotype (high insulin sensitivity and low β-cell function), the hyperinsulinaemic phenotype (low insulin sensitivity and high β-cell function), and the classical phenotype (low insulin sensitivity and low β-cell function). The outcomes included kidney function decline, CVD events (fatal and nonfatal), and all-cause mortality. Cox regression models were used to calculate hazard ratios (HRs) for outcomes, and spline models were used to examine the dose-dependent associations of HOMA2-B and HOMA2-S with outcomes.ResultsA total of 1,488 (20.3%) were classified as normal, 2,179 (29.8%) as insulinopenic, 2,173 (29.7%) as hyperinsulinemic, and 1,477 (20.2%) as classical subtypes. Compared with other physiological subtypes, the classical subtype presented the highest risk of kidney function decline (classical vs. normal HR 11.50, 95% CI 4.31–30.67). The hyperinsulinemic subtype had the highest risk of CVD and all-cause mortality (hyperinsulinemic vs. normal: fatal CVD, HR 6.56, 95% CI 3.09–13.92; all-cause mortality, HR 4.56, 95% CI 2.97–7.00). Spline analyses indicated the dose-dependent associations of HOMA2-B and HOMA2-S with outcomes.ConclusionsThe classical subtype had the strongest correlation with the risk of kidney function decline, and the hyperinsulinemic subtype had the highest risk of CVD and all-cause mortality, which should be considered for interventions with precision medicine.Graphical abstract

Changes in the estimated glucose disposal rate and incident cardiovascular disease: two large prospective cohorts in Europe and Asia

Background and aimsPrevious study found that estimated glucose disposal rate (eGDR) was significantly associated with cardiovascular disease (CVD). However, little is known about the change in eGDR over time and its association with the development of CVD. The aim of this study was to investigate the association of change in eGDR with CVD risk.MethodsThis study used data of two prospective cohorts: UK Biobank and China Health and Retirement Longitudinal Study (CHARLS) with two measurements of eGDR. Changes in the eGDR were classified using K‑means clustering analysis, and the cumulative eGDR was also calculated. Cox proportional hazard models were used to calculate the hazard ratio (HR) and 95% confidence interval (95% CI) after adjusting for potential confounders.ResultsA total of 11,682 individuals from the UK Biobank, and 4,974 individuals from the CHARLS were included. The median follow-up periods were 9.7 years in the UK Biobank and 3.0 years in the CHARLS. Compared with persistently high level of eGDR (class 1), individuals with low level increasing (class 3) and persistently low level of eGDR (class 4) showed elevated risks of incident CVD in both UK Biobank (HR = 2.79, 95% 2.15–3.62 for class 3; HR = 3.19, 95% 2.50–4.08 for class 4) and CHARLS (HR = 1.66, 95% 1.29–2.13 for class 3; HR = 1.69, 95% 1.34–2.14 for class 4). In addition, lower level of cumulative eGDR were associated with elevated risks of incident CVD. The dose-response curve between cumulative eGDR and CVD risk showed a negative linear relationship.ConclusionDifferent changes in eGDR level are associated with different risks of incident CVD. Dynamic monitoring of eGDR level is of significant importance for the CVD prevention and treatment.

Investigating the correlation of hip circumference to cardiovascular disease and type-2 diabetes using Mendelian randomization.

This study aimed to assess the correlation between hip circumference (HC) and the risk of cardiovascular disease (CVD) and type 2 diabetes mellitus using Mendelian randomization (MR) to overcome observational study limitations. MR analysis utilized genetic variation from the MR Base in a two-sample analysis. Three methods were employed: MR-Egger regression, weighted median estimator, and inverse variance weighting (IVW). Data was acquired from MR Base, a platform summarizing genome-wide association study (GWAS) data for MR research. Publicly available summary statistics datasets from GWAS meta-analyses were used, with HC and HC adjusted for body mass index (BMI) as exposures. Data for CVD and type 2 diabetes mellitus were obtained as outcomes. Results indicated a positive causal relationship between HC and CVD (IVW: P = 1.84e-07, OR: 1.37, 95% CI: 1.22-1.54) as well as type 2 diabetes mellitus (IVW: P = 0.04, OR: 1.62, 95% CI: 1.02-2.56), independent of BMI. However, HC after BMI adjustment showed no significant causal relationship with CVD (IVW: P = 0.05, OR: 1.09, 95% CI: 1.00-1.19) and exhibited a negative association with type 2 diabetes mellitus (IVW: P = 0.00, OR: 0.76, 95% CI: 0.66-0.88), suggesting a protective effect against type 2 diabetes mellitus. After adjusting for BMI, adipose tissue concentrated in the hip region showed a protective effect against type 2 diabetes mellitus but not against CVD. These findings offer insights into diabetes prevention and treatment strategies, and may inform plastic surgery procedures. Further research is needed to validate these findings and explore underlying mechanisms.

Comparing five-year and ten-year predicted cardiovascular disease risk in Aotearoa New Zealand: national data linkage study of 1.7 million adults.

There is no consensus on the optimal time horizon for predicting cardiovascular disease (CVD) risk to inform treatment decisions. New Zealand and Australia recommend 5 years, whereas most countries recommend 10 years. We compared predicted risk and treatment-eligible groups using 5-year and 10-year equations. Individual-level linked administrative datasets identified 1,746,665 New Zealanders without CVD, aged 30-74 years in 2006, with follow-up to 2018. Participants were randomly allocated to derivation and validation cohorts. Sex-specific 5-year and 10-year risk prediction models were developed in the derivation cohort and applied in the validation cohort. 28,116 (3.2%) and 62,027 (7.1%) first CVD events occurred during 5-years and 10-years follow-up respectively (cumulative risk, derivation cohort). Median predicted 10-year CVD risk (3.8%) was approximately 2.5 times 5-year risk (1.6%) and 95% of individuals in the top quintile of 5-year risk were also in the top quintile of 10-year risk, across age/gender groups (validation cohort). Using common guideline-recommended treatment thresholds (5% 5-year, 10% 10-year risk), approximately 14% and 28% of women and men respectively were identified as treatment-eligible applying 5-year equations compared to 17% and 32% of women and men applying 10-year equations. Older age was the major contributor to treatment eligibility in both sexes. Predicted 10-year CVD risk was approximately 2.5 times 5-year risk. Both equations identified mostly the same individuals in the highest risk quintile. Conversely, commonly used treatment thresholds identified more treatment-eligible individuals using 10-year equations and both equations identified approximately twice as many treatment-eligible men as women. The treatment threshold, rather than the risk horizon, is the main determinant of treatment eligibility.

Maternal under-nutrition during pregnancy alters the molecular response to over-nutrition in multiple organs and tissues in nonhuman primate juvenile offspring.

Previous studies in rodents suggest that mismatch between fetal and postnatal nutrition predisposes individuals to metabolic diseases. We hypothesized that in nonhuman primates (NHP), fetal programming of maternal undernutrition (MUN) persists postnatally with a dietary mismatch altering metabolic molecular systems that precede standard clinical measures. We used unbiased molecular approaches to examine response to a high fat, high-carbohydrate diet plus sugar drink (HFCS) challenge in NHP juvenile offspring of MUN pregnancies compared with controls (CON). Pregnant baboons were fed ad libitum (CON) or 30% calorie reduction from 0.16 gestation through lactation; weaned offspring were fed chow ad libitum. MUN offspring were growth restricted at birth. Liver, omental fat, and skeletal muscle gene expression, and liver glycogen, muscle mitochondria, and fat cell size were quantified. Before challenge, MUN offspring had lower body mass index (BMI) and liver glycogen, and consumed more sugar drink than CON. After HFCS challenge, MUN and CON BMIs were similar. Molecular analyses showed HFCS response differences between CON and MUN for muscle and liver, including hepatic splicing and unfolded protein response. Altered liver signaling pathways and glycogen content between MUN and CON at baseline indicate in utero programming persists in MUN juveniles. MUN catchup growth during consumption of HFCS suggests increased risk of obesity, diabetes, and cardiovascular disease. Greater sugar drink consumption in MUN demonstrates altered appetitive drive due to programming. Differences in blood leptin, liver glycogen, and tissue-specific molecular response to HFCS suggest MUN significantly impacts juvenile offspring ability to manage an energy rich diet.

Burden of liver steatosis and liver fibrosis in a large cohort of people living with HIV.

Liver steatosis (LS) and liver fibrosis (LF) can increase the risk of cardiovascular disease in people with HIV, but their prevalence and associated factors are poorly understood. This study aimed to assess the prevalence of and factors associated with LS and LF in a large cohort of people with HIV. We conducted a cross-sectional study of consecutive people with HIV attending the Clinic of Barcelona from September 2022 to September 2023, excluding those with chronic B or/and C hepatitis virus coinfection. LS was assessed using the Hepatic Steatosis Index (HSI) and Fatty Liver Index (FLI), and LF was assessed using the Non-Alcoholic Fatty Liver Disease Fibrosis Score (NFS), Fibrosis-4 score (FIB-4), and the European AIDS Clinical Society (EACS) algorithm in both the whole cohort (cohort 1) and in a specific cohort more susceptible to liver disease (cohort 2). We identified independent variables associated with LS and LF using logistic regression. Cohort 1 included 4664 people with HIV; 76% and 37% of them had available HSI and FLI data, LS was present in 28% and 19%, respectively. LF risk was present in 1%, 2%, and 1% of people with HIV according to NFS, FIB-4, and EACS algorithm scores, respectively. Cohort 2 included 1345 people with HIV; 60% and 30% of them had available HSI and FLI data, LS affected 55% and 43% and LF 2%, 5%, or 3%, respectively. Factors associated with LS included current CD4 cell count, diabetes, and hypertension, whereas LF was associated with previous exposure to dideoxynucleoside drugs and current CD4 to LF. Current integrase strand transfer inhibitor (INSTI) therapy appeared protective for LF in cohort 1. In this study, one in four people with HIV had LS, and the prevalence rose to one in two in those with cardiovascular risk factors. The prevalence of LF was low, but it should be considered in older people with HIV with low CD4 counts or high aspartate transaminase levels. A possible protective effect from INSTIs deserves further investigation.

Sex Differences in Cardiovascular Risk Profiles of Patients with Rheumatoid Arthritis: Results from an Italian Multicentre Cohort

Objective: The effect of sex and gender-related variables on the evaluation of cardiovascular (CV) risk in rheumatoid arthritis patients has been poorly explored. We investigated the differences in CV risk features and scores according to sex in a wide rheumatoid arthritis (RA) cohort. Methods: This is a cross-sectional analysis of a consecutive RA cohort. Disease-specific clinical and serologic variables, traditional CV risk factors and the 10-year CV risk calculated by the SCORE-2, Progetto CUORE and Expanded Risk Score-RA algorithms were compared in males and females. Results: A total of 820 patients (193 men, 627 women) were included. Disease activity was similar between the two sexes. A significantly higher prevalence of traditional CV risk factors and higher mean CV risk scores were detected in male compared to female patients. In the multiple linear regression analysis, a higher HAQ, csDMARD use and ACPA positivity were significantly associated with an increased CV risk in females, while b/tsDMARDs was associated with a lower CV risk in males according to different algorithms. Conclusions: The distribution of traditional CV risk factors and the 10-year risk of CV disease significantly differed in female and male patients despite similar disease activity. Disease-specific variables may contribute differently to CV risk according to sex. The CV screening in RA should also take into account the different distribution of CV risk factors between sexes.

Developing a question prompt tool to prevent and manage early cardiovascular disease after hypertensive pregnancy: qualitative interviews with women and clinicians

BackgroundPersons (henceforth, women) who have hypertensive disorders of pregnancy (HDP) are at risk of premature cardiovascular disease (CVD). While largely preventable through lifestyle management, many women and clinicians are unaware of the risk. Based on prior research, we developed a question prompt tool (QPT) on preventing and managing CVD after HDP. The purpose of this study was to refine QPT design.MethodsWe recruited Canadian women who had HDP and clinicians who might care for them using multiple strategies, conducted telephone interviews with consenting participants, and used qualitative description and inductive content analysis to derive themes.ResultsWe interviewed 21 women who varied in HDP type, CVD status, years since HDP pregnancy, age, geography and ethno-cultural group; and 21 clinicians who varied in specialty (midwife, nurse practitioner, family physician, internist, obstetrician, cardiologist), geography and years in practice. Participating women and clinicians agreed on needed improvements: more instructions, lay and gender-neutral language, links to additional information, more space for answers, graphic appeal, and both print and electronic format. Both groups identified similar barriers: clinicians lack time/willingness, and low language/health literacy and access to technology among women; enablers: translated, credible source/endorser, culturally relevant, organized by health trajectory stages; and likely benefits: raise awareness, empower women, encourage them to adopt healthy lifestyle. Women desired exposure to the QPT before or during pregnancy, while clinicians recommended waiting until postpartum to avoid overwhelming women. Similarly, most women said the QPT should be available through multiple avenues to empower them for health self-advocacy, while clinicians thought they should introduce the QPT to women, and decide when and which questions to address. To mitigate reluctance, clinicians recommended self-directed educational materials accompany the QPT.ConclusionsWe will use this information to refine QPT design and plan for future evaluation. If found to be effective and widely disseminated, the QPT could improve awareness and communication about this issue, and may reduce CVD risk in many women who have hypertensive pregnancies. Ongoing research is needed to more fully understand how QPTs support patient-clinician communication, and how to alert and prime both patients and clinicians to use QPTs.

Use of biomarkers of metals to improve prediction performance of cardiovascular disease mortality

BackgroundWhether including additional environmental risk factors improves cardiovascular disease (CVD) prediction is unclear. We attempted to improve CVD mortality prediction performance beyond traditional CVD risk factors by additionally using metals measured in the urine and blood and with statistical machine learning methods.MethodsOur sample included 7,085 U.S. adults aged 40 years or older from the National Health and Nutrition Examination Survey 2003–2004 through 2015–2016, linked with the National Death Index through December 31, 2019. Data were randomly split into a 50/50 training dataset used to construct CVD mortality prediction models (n = 3542) and testing dataset used as validation to assess prediction performance (n = 3543). Relative to the traditional risk factors (age, sex, race/ethnicity, smoking status, systolic blood pressure, total and high-density lipoprotein cholesterol, hypertension, and diabetes), we compared models with an additional 17 blood and urinary metal concentrations. To build the prediction models, we used Cox proportional hazards, elastic-net (ENET) penalized Cox, and random survival forest methods.Results420 participants died from CVD with 8.8 mean years of follow-up. Blood lead, cadmium, and mercury were associated (p < 0.005) with CVD mortality. Including these blood metals in a Cox model, initially containing only traditional risk factors, raised the C-index from 0.845 to 0.847. Additionally, the Net Reclassification Index showed that 23% of participants received a more accurate risk prediction. Further inclusion of urinary metals improved risk reclassification but not risk discrimination.ConclusionsIncorporating blood metals slightly improved CVD mortality risk discrimination, while blood and urinary metals enhanced risk reclassification, highlighting their potential utility in improving cardiovascular risk assessments.

Risk of Cardiovascular Disease in Patients With Classical Hodgkin Lymphoma: A Danish Nationwide Register-Based Cohort Study.

Risk of cardiovascular disease (CVD) in patients with classical Hodgkin lymphoma (cHL) undergoing contemporary treatment is unclear. cHL patients ≥ 18 years at diagnosis treated with doxorubicin-containing chemotherapy between 2000 and 2022 were matched 1:5 with comparators on birth year, sex, and Charlson Comorbidity Index at time of matching (score of 0 or ≥ 1). Cause-specific cumulative incidence of a composite of CVDs with corresponding 95% confidence intervals (CIs) were computed with death and lymphoma relapse as competing events (i.e., by censoring individuals at such occurrences) using the Aalen-Johansen estimator. A total of 1905 patients and 9525 comparators with a median follow-up of 10 years (interquartile range, [IQR]: 5.9-17.4). Median age was 39 years (IQR: 27-56), median cumulative doxorubicin dose was 250 mg/m2 (IQR: 200-300). The CVD cumulative incidences were 4.7% (95% CI: 3.6-5.7) for patients versus 2.6% (95% CI: 2.3-2.9) for comparators at 5 years, 8.9% (95% CI: 7.2-10.5) versus 5.5% (95% CI: 4.9-6.0) at 10 years, and 17.0% (95% CI: 14.1-19.9) versus 8.2% (95% CI: 7.4-9.0) at 15 years. CVD remains a substantial effect after contemporary treatment for cHL, suggesting that awareness of symptoms and a low threshold for referral to diagnostic examination are still important measures during survivorship.

Shared genetic factors between osteoarthritis and cardiovascular disease may underlie common etiology.

Osteoarthritis is one of the most common musculoskeletal diseases and increases the risk of severe cardiovascular disease, like heart attack and stroke. In some individuals, osteoarthritis and cardiovascular disease will co-occur. This co-occurrence might be due to shared risk factors, for example high age, lifestyle factors and/or a shared genetic liability for the two diseases. Here, we show that the correlation between osteoarthritis and cardiovascular disease can be explained by shared genetic factors, independent of high age and body weight, and also likely independent of lifestyle factors, like smoking and physical activity level. Findings suggest that genetic factors that are shared for osteoarthritis and cardiovascular disease may contribute to both diseases. Thus, the prevailing idea that osteoarthritis is predominantly a risk factor for cardiovascular disease is challenged. Our findings imply that the current diagnostic boundaries between these diseases may need to be re-evaluated.

Influence of air pollution on the nonaccidental death before and after the outbreak of COVID-19

BackgroundDuring the COVID-19 pandemic, non-therapeutic interventions (NPIs), such as traffic restrictions, work stoppages, and school suspensions, have led to a sharp decline in the concentration of air pollutants in the epidemic sites. However, few studies focused on the impact of air pollutant changes on the risk of nonaccidental death.MethodWe selected Yancheng City, China, as the study site and applied a Generalized Additive Model (GAM) based on the quasi-Poisson distribution to evaluate the impact of atmospheric pollutants exposure on the nonaccidental death of local residents. The time span of this study was set from January 1, 2013, to December 21, 2022, that is, before and after the outbreak of COVID-19.ResultsThe concentration of some air pollutants has greatly varied after the outbreak of COVID-19, with a significant decline for PM2.5 (− 43.4%), PM10 (− 38.5%), SO2 (− 62.9%), and NO2 (− 22.6%), but an increase for O3 (+ 4.3%). Comparative analysis showed that PM2.5 contributed to an increased risk of nonaccidental death after the outbreak of COVID-19. With an increase in PM2.5 by 10 µg/m³, the excess relative risks (ER) of nonaccidental death of residents increased by 1.01% (95%CI: 0.19%,1.84%). The stratified analysis revealed that air pollutants impacted nonaccidental deaths in both men and women before the outbreak of COVID-19. After the outbreak of COVID-19, PM10 had a significant effect on male nonaccidental deaths. The concentrations of PM2.5, PM10, and SO2 increased by 10 µg/m³, the ER of PM2.5, PM10, and SO2 on female nonaccidental death increased by 1.52% (0.38%,2.67%), 0.58% (0.02%,1.13%), and 15.09% (5.73%,25.28%), respectively. Before the outbreak of COVID-19, five air pollutants had an impact on the death of residents from cardiovascular disease (CVD). After the outbreak of COVID-19, only PM10 significantly affected the death risk of CVD. In addition, we discovered that PM2.5, PM10, and SO2 significantly impacted the risk of death due to respiratory diseases before and after the outbreak of COVID-19.ConclusionsAir pollutants have different effects on nonaccidental deaths before and after the COVID-19 outbreak. A decrease in air pollutant concentration due to the NPIs for COVID-19 had a significant effect on the reduction of the risk of nonaccidental death.

Exploring COX-Independent Pathways: A Novel Approach for Meloxicam and Other NSAIDs in Cancer and Cardiovascular Disease Treatment

As a fundamental process of innate immunity, inflammation is associated with the pathologic process of various diseases and constitutes a prevalent risk factor for both cancer and cardiovascular disease (CVD). Studies have indicated that several non-steroidal anti-inflammatory drugs (NSAIDs), including Meloxicam, may prevent tumorigenesis, reduce the risk of carcinogenesis, improve the efficacy of anticancer therapies, and reduce the risk of CVD, in addition to controlling the body’s inflammatory imbalances. Traditionally, most NSAIDs work by inhibiting cyclooxygenase (COX) activity, thereby blocking the synthesis of prostaglandins (PGs), which play a role in inflammation, cancer, and various cardiovascular conditions. However, long-term COX inhibition and reduced PGs synthesis can result in serious side effects. Recent studies have increasingly shown that some selective COX-2 inhibitors and NSAIDs, such as Meloxicam, may exert effects beyond COX inhibition. This emerging understanding prompts a re-evaluation of the mechanisms by which NSAIDs operate, suggesting that their benefits in cancer and CVD treatment may not solely depend on COX targeting. In this review, we will explore the potential COX-independent mechanisms of Meloxicam and other NSAIDs in addressing oncology and cardiovascular health.