Increased Incidence Of Cardiovascular Disease Research Articles

Tuberculosis and increased incidence of cardiovascular disease: Cohort study using US and UK health records.

Limited evidence suggests elevated risks of cardiovascular disease (CVD) among people diagnosed with tuberculosis (TB) disease, though studies have not adjusted for pre-existing CVD risk. We carried out a cohort study using two separate datasets, estimating CVD incidence in people with TB versus those without. Using data from the United States (Veterans Health Administration) and the United Kingdom (Clinical Practice Research Datalink) for 2000-2020 we matched adults with incident TB disease and no CVD history 2-years before TB diagnosis (US n=2,121; UK n=15,820) with up to 10 people without TB on the basis of age, sex, race/ethnicity and healthcare practice. Participants were followed beginning 2-years before TB diagnosis and for 2-years subsequently. The acute period was defined as 3-months before/after TB diagnosis. TB, CVD and covariates were identified from electronic routinely collected data (primary and secondary care; mortality). Poisson models estimated incident rate ratios (IRR) for CVD events in people with TB compared to those without. CVD incidence was consistently higher in people with TB, including during the baseline period (pre-TB) and particularly in the acute period: IRRs were US 3.5 (95% Confidence Interval 2.7-4.4), UK 2.7 (2.2-3.3). Rate Ratios remained high after adjusting for differences in pre-existing CVD risk: US 3.2 (2.2-4.4), UK 1.6 (1.2-2.1). Increased CVD incidence was observed in people with TB versus those without, especially within months of TB diagnosis, persistent after adjustment for differences in pre-existing risk. Enhancing CVD screening and risk management may improve long-term outcomes in people with TB.

Exploring the pathogenesis linking primary aldosteronism and obstructive sleep apnea via bioinformatic analysis.

Primary aldosteronism (PA) and obstructive sleep apnea (OSA) are both considered independent risk factors for hypertension, which can lead to an increase in cardiovascular disease incidence and mortality. Clinical studies have found a bidirectional relationship between OSA and PA. However, the underlying mechanism between them is not yet clear. This study aims to investigate the shared genetic characteristics and potential molecular mechanisms of PA and OSA. We obtained microarray datasets of aldosterone-producing adenoma (APA) and OSA from the gene expression omnibus (GEO) database. Weighted gene co-expression network analysis (WGCNA) was used to select co-expression modules associated with APA and OSA, and common genes of the two diseases were obtained by intersection. Subsequently, hub genes for APA and OSA were identified through functional enrichment analysis, protein-protein interaction (PPI), datasets, and public database. Finally, we predicted the transcription factors (TFs) and mirRNAs of the hub genes. In total, 52 common genes were obtained by WGCNA. The Gene Ontology (GO) of common genes includes interleukin-1 response, cytokine activity, and chemokine receptor binding. Functional enrichment analysis highlighted the TNF, IL-17 signaling, and cytokine-cytokine receptor interactions related to APA and OSA. Through PPI, datasets, and public databases verification, we identified 5 hub genes between APA and OSA (IL6, ATF3, PTGS2, CCL2, and CXCL2). Our study identified shared 5 hub genes between APA and OSA (IL6, ATF3, PTGS2, CCL2, and CXCL2). Through bioinformatics analysis, we found that the 2 disorders showed relative similarity in terms of inflammation, stress, and impaired immune function. The identification of hub genes may offer potential biomarkers for the diagnosis and prognosis of PA and OSA.

GCLM Expression Drives Macrophage Efferocytosis

Atherosclerosis, a chronic inflammatory disease characterized by the accumulation of lipids, apoptotic cells (ACs), and fibrous elements within the arterial wall, can lead to plaque rupture, one of the most common causes of death in cardiovascular disease (CVD). Rupture prone plaques, characterized by large necrotic cores and thin fibrous caps, lead to acute luminal thrombosis resulting in myocardial infarctions (MI) and strokes. AC accumulation coupled with deficiency in their clearance, results in necrotic core formation. Macrophages are responsible for clearing ACs through efferocytosis; however, as atherosclerosis progresses efferocytosis is impaired. AC accumulation leads to chronic inflammation driven by reactive oxygen species production that disrupts cellular redox balance. Glutathione (GSH), the main antioxidant in the body, maintains redox balance; however, it fails to do so in atherosclerosis. Reports have shown a single nucleotide polymorphism (SNP) in the promoter region of the modifier subunit of GCL (GCLM), a rate limiting enzyme responsible for de novo synthesis of GSH, limits its transcription under oxidative stress and is associated with increased risk of MI. Moreover, deletion of GCLM shows an increase in atherosclerotic plaque area and necrotic core, however it remains unknown how GCLM contributes to necrotic core formation and increased CVD incidence. Methods: Bone marrow derived macrophages from WT, Het, and KO GCLM mutant mice and peripheral blood mononuclear cells (PBMCs) from blood donors were isolated and used for efferocytosis and protein assays. PBMCs and atherosclerosis plaque sections were used for SNP genotyping and in situ efferocytosis assays. Results: Efferocytosis impairment correlated with decreased GCLM expression in mice. The presence of a SNP in GCLM significantly decreases efferocytosis in vitro as well as in situ in stage 5 human plaques. Conclusion: These results suggest that loss of GCLM in macrophages impairs primary and secondary efferocytosis in mice. This is corroborated with the inhibition of GSH synthesis. We also observed an impairment in efferocytosis in human macrophages with the presence of the risk allele in GCLM. Malcolm Feist Pre-doctoral Fellowship, Center of Cardiovascular Diseases and Sciences. 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.

Abstract P169: Cardiovascular Disease Incidence Among Male Veterans by Sexual Orientation and Race

Introduction: Studies of cardiovascular disease (CVD) in sexual minority (SM) men (i.e., gay, bisexual) vs. heterosexual men are limited by small sample sizes and lack of objective CVD ascertainment. Small samples also hinder study at the intersection of race and sexual orientation on CVD events. We used the Veterans Healthcare Administration Lesbian, Gay, Bisexual, Transgender Electronic Health Record cohort to fill these knowledge gaps. Methods: We studied 919,404 male cisgender veterans who were free of prevalent CVD and classified as SM or non-SM by a natural language processing tool. We defined incident CVD as first instance of AMI, ischemic stroke, cardiac revascularization, or CVD death between baseline and date of death or 8/31/22. We stratified sample statistics by SM status and race. We used Cox proportional hazards regression to assess the intersection of sexual orientation and race with incident CVD; we adjusted for Hispanic ethnicity and age. Based on the minority stress model, non-SM White men were the referent. Results: Within races, traditional CVD risk factors were similarly distributed by SM status but SM men had greater prevalence of stress-associated characteristics like substance use, depression, and anxiety. Heterosexual, gay, and bisexual Asian men had lower CVD risk than non-SM White men, while Black/African American and Multiracial men had persistently increased CVD risk ( Table ). White and American Native gay men had increased CVD risk vs. non-SM White men. With the exception of Asians, all unclassified SM men had increased CVD incidence vs. non-SM White men. Risk was highest in among Black or Multiracial SM men. Conclusion: This is one of the first studies to examine the intersection of sexual orientation and race on CVD risk in male veterans. CVD risk appears increased or decreased in certain racial groups regardless of sexual orientation but this is not always true and invites further study into the mechanisms by which stress results in inequitable CVD events across groups.

Abstract 14123: Cardiovascular Disease Incidence Among Female Veterans by Sexual Orientation and Race

Introduction: Studies of cardiovascular disease (CVD) in sexual minority (SM) women (i.e., lesbian, bisexual) vs. heterosexual women are limited by small sample sizes and lack of objective CVD ascertainment. Small samples also hinder study at the intersection of race and sexual orientation on CVD events. We used the Veterans Healthcare Administration Lesbian, Gay, Bisexual, Transgender Electronic Health Record cohort to fill these knowledge gaps. Methods: We studied 132,571 female cisgender veterans who were free of prevalent CVD and classified as SM or non-SM by a natural language processing tool. We defined incident CVD as first instance of AMI, ischemic stroke, cardiac revascularization, or CVD death between baseline and date of death or 8/31/22. We stratified sample statistics by SM status and race. We used Cox proportional hazards regression to assess the intersection of sexual orientation and race with incident CVD; we adjusted for Hispanic ethnicity and age. Based on the minority stress model, non-SM White women were the referent. Results: Within races, traditional CVD risk factors were similarly distributed by SM status but SM women had greater prevalence of stress-associated characteristics like substance use, depression, and anxiety. Regardless of sexual orientation, Asian women had lower CVD risk than non-SM White women, while Black/African American women had persistently increased CVD risk ( Table ). White lesbians had increased CVD risk vs. their non-SM counterparts. Unclassified SM women of American Native race or multiple races also had increased CVD incidence vs. non-SM White women. Conclusion: This is one of the first studies to examine the intersection of sexual orientation and race on CVD risk in female veterans. CVD risk appears increased or decreased in certain racial groups regardless of sexual orientation but this is not always true and invites further study into the mechanisms by which stress results in inequitable CVD events across groups.

Association of high-density lipoprotein cholesterol with all-cause and cause-specific mortality in a Chinese population of 3.3 million adults: a prospective cohort study

High-density lipoprotein cholesterol (HDL-C) has been inversely associated with cardiovascular disease (CVD) risk, but recent evidence suggests that extremely high levels of HDL-C are paradoxically related to increased CVD incidence and mortality. This study aimed to comprehensively examine the associations of HDL-C with all-cause and cause-specific mortality in a Chinese population. The China Health Evaluation And risk Reduction through nationwide Teamwork (ChinaHEART) project included 3,397,547 participants aged 35-75 years with a median follow-up of 3.9 years. Baseline HDL-C levels were measured, and mortality data was ascertained from the National Mortality Surveillance System and Vital Registration of Chinese Center for Disease Control and Prevention. This study found U-shaped associations of HDL-C with all-cause, cardiovascular and cancer mortality. When compared with the groups with the lowest risk, the adjusted hazard ratios (95% CIs) for HDL-C<30mg/dL was 1.23 (1.17-1.29), 1.33 (1.23-1.45) and 1.18 (1.09-1.28) for all-cause, CVD and cancer mortality, respectively. For HDL-C >90mg/dL, the corresponding HR (95% CIs) was 1.10 (1.05-1.15), 1.09 (1.01-1.18) and 1.11 (1.03-1.19). Similar U-shaped patterns were also found in associations of HDL-C with ischemic heart disease, ischemic stroke, and liver cancer. About 3.25% of all-cause mortality could be attributed to abnormal levels of HDL-C. The major contributor to mortality was ischemic heart disease (16.06 deaths per 100,000 persons, 95% UI: 10.30-22.67) for HDL-C<40mg/dL and esophageal cancer (2.29 deaths per 100,000 persons, 95% UI: 0.57-4.77) for HDL-C >70mg/dL. Both low and high HDL-C were associated with increased mortality risk. We recommended 50-79mg/dL as the optimal range of HDL-C among Chinese adults. Individuals with dyslipidemia might benefit from proper management of both low and high HDL-C. The CAMS Innovation Fund for Medical Science (2021-1-I2M-011), the National High Level Hospital Clinical Research Funding (2022-GSP-GG-4), the Ministry of Finance of China and National Health Commission of China, and the 111 Project from the Ministry of Education of China (B16005), the Program for Guangdong Introducing Innovative and Enterpreneurial Teams (2019ZT08Y481), Sanming Project of Medicine in Shenzhen (SZSM201811096), the Young Talent Program of the Academician Fund, Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen (YS-2022-006) and Guangdong Basic and Applied Basic Research Foundation (2023A1515010076 & 2021A1515220173).

Cardiovascular Disease Risk Screening for Commercial Drivers Examined in Occupational Practice: Implementing Evidence-Based Practice to Champion the Health of Essential Workers.

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality in the United States, with 20% of deaths in adults under age 65. Commercial drivers have an increased CVD incidence rate of 50% compared to 30% for the general population, yet one third of drivers will not be screened for risk factors due to a lack of insurance or primary care. With approximately 3.5 million commercial drivers nationally and correlation of CVD to increased motor vehicle accidents, fatalities, and excessive healthcare costs, addressing the care gap for this high-risk population is imperative. An evidence-based practice (EBP) project synthesized the literature and implemented CVD risk screening for commercial drivers examined in an occupational practice setting. Using the non-laboratory Framingham CVD risk score calculator, over 90% of drivers were screened during mandated medical examinations and provided education regarding modifiable risk factors during a 2-month period. Over 40% of commercial drivers were at high risk for CVD with 25% uninsured and 32% without primary care. The average CVD risk score was twice the general population's risk score, with obesity, hypertension, and smoking being the most common risk factors discussed. Incorporating CVD risk screening and education during opportune encounters is logical, efficient, and financially prudent. The EBP change supports occupational professionals' standards, and ongoing review of CVD screening guidelines with integration into practice provides health promotion and promotes public safety for these essential workers.

Abstract 327: Gclm-dependent Gsh Synthesis Regulates Efferocytosis During Atherosclerosis

Atherosclerosis, a chronic inflammatory disease characterized by the accumulation of lipids, apoptotic cells, and fibrous elements within the arterial wall, can lead to plaque rupture, one of the most common causes of death in cardiovascular disease (CVD). Rupture prone plaques, characterized by large necrotic cores and thin fibrous caps, lead to acute luminal thrombosis resulting in myocardial infarctions (MI) and strokes. Apoptotic cell (AC) accumulation coupled with deficiency in their clearance, results in necrotic core formation. Macrophages are responsible for clearing ACs through efferocytosis; however, as atherosclerosis progresses efferocytosis is impaired. AC accumulation contributes to the chronic inflammatory response in CVD. Within this response, reactive oxygen species production increases disrupting cellular redox balance. Glutathione (GSH), the main antioxidant in the body, maintains redox balance; however, it fails to do so in atherosclerosis. Reports have shown that a single nucleotide polymorphism (SNP) in the promoter region of the modifier subunit of GCL (GCLM), a rate limiting enzyme responsible for de novo synthesis of GSH, limits its transcription under oxidative stress and is associated with increased risk of MI. Moreover, deletion of GCLM shows an increase in atherosclerotic plaque area and necrotic core, however it remains unknown how GCLM contributes to necrotic core formation and increased CVD incidence. Methods: Bone marrow derived macrophages from WT, Het, and KO GCLM mutant mice and peripheral blood mononuclear cells (PBMCs) from blood donors were isolated and used for efferocytosis and protein assays. PBMCs and atherosclerosis plaque sections were used for SNP genotyping and in situ efferocytosis assays. Results: Efferocytosis impairment correlated with decreased GCLM expression in mice. The presence of a SNP in GCLM significantly decreases efferocytosis in vitro as well as in situ in stage 5 human plaques. Conclusion: These results suggest that loss of GCLM in macrophages impairs primary and secondary efferocytosis in mice. This is corroborated with the inhibition of GSH synthesis. We also observed an impairment in efferocytosis in human macrophages with and without the presence of the risk allele in GCLM.

Impact of COVID-19 on Cardiovascular Disease.

Coronavirus disease 2019 (COVID-19) is a viral infection with the novel severe acute respiratory distress syndrome corona virus 2 (SARS-CoV-2). Until now, more than 670 million people have suffered from COVID-19 worldwide, and roughly 7 million death cases were attributed to COVID-19. Recent evidence suggests an interplay between COVID-19 and cardiovascular disease (CVD). COVID-19 may serve as a yet underappreciated CVD risk modifier, including risk factors such as diabetes mellitus or arterial hypertension. In addition, recent data suggest that previous COVID-19 may increase the risk for many entities of CVD to an extent similarly observed for traditional cardiovascular (CV) risk factors. Furthermore, increased CVD incidence and worse clinical outcomes in individuals with preexisting CVD have been observed for myocarditis, acute coronary syndrome, heart failure (HF), thromboembolic complications, and arrhythmias. Direct and indirect mechanisms have been proposed by which COVID-19 may impact CVD and CV risk, including viral entry into CV tissue or by the induction of a massive systemic inflammatory response. In the current review, we provide an overview of the literature reporting an interaction between COVID-19 and CVD, review potential mechanisms underlying this interaction, and discuss preventive and treatment strategies and their interference with CVD that were evaluated since the onset of the COVID-19 pandemic.

Cardiometabolic outcomes up to 12 months after COVID-19 infection. A matched cohort study in the UK.

Acute Coronavirus Disease 2019 (COVID-19) has been associated with new-onset cardiovascular disease (CVD) and diabetes mellitus (DM), but it is not known whether COVID-19 has long-term impacts on cardiometabolic outcomes. This study aimed to determine whether the incidence of new DM and CVDs are increased over 12 months after COVID-19 compared with matched controls. We conducted a cohort study from 2020 to 2021 analysing electronic records for 1,356 United Kingdom family practices with a population of 13.4 million. Participants were 428,650 COVID-19 patients without DM or CVD who were individually matched with 428,650 control patients on age, sex, and family practice and followed up to January 2022. Outcomes were incidence of DM and CVD. A difference-in-difference analysis estimated the net effect of COVID-19 allowing for baseline differences, age, ethnicity, smoking, body mass index (BMI), systolic blood pressure, Charlson score, index month, and matched set. Follow-up time was divided into 4 weeks from index date ("acute COVID-19"), 5 to 12 weeks from index date ("post-acute COVID-19"), and 13 to 52 weeks from index date ("long COVID-19"). Net incidence of DM increased in the first 4 weeks after COVID-19 (adjusted rate ratio, RR 1.81, 95% confidence interval (CI) 1.51 to 2.19) and remained elevated from 5 to 12 weeks (RR 1.27, 1.11 to 1.46) but not from 13 to 52 weeks overall (1.07, 0.99 to 1.16). Acute COVID-19 was associated with net increased CVD incidence (5.82, 4.82 to 7.03) including pulmonary embolism (RR 11.51, 7.07 to 18.73), atrial arrythmias (6.44, 4.17 to 9.96), and venous thromboses (5.43, 3.27 to 9.01). CVD incidence declined from 5 to 12 weeks (RR 1.49, 1.28 to 1.73) and showed a net decrease from 13 to 52 weeks (0.80, 0.73 to 0.88). The analyses were based on health records data and participants' exposure and outcome status might have been misclassified. In this study, we found that CVD was increased early after COVID-19 mainly from pulmonary embolism, atrial arrhythmias, and venous thromboses. DM incidence remained elevated for at least 12 weeks following COVID-19 before declining. People without preexisting CVD or DM who suffer from COVID-19 do not appear to have a long-term increase in incidence of these conditions.

Triglyceride-glucose index variability and incident cardiovascular disease: a prospective cohort study

BackgroundRecent studies have suggested that triglyceride-glucose (TyG) index is an independent predictor of cardiovascular disease (CVD). However, the impact of long-term visit-to-visit variability in TyG index on the risk of CVD is not known. We aimed to investigate the longitudinal association between baseline and mean TyG index as well as TyG index variability and incident CVD in a Chinese population.MethodsWe included 49,579 participants without previous history of CVD in the Kailuan study who underwent three health examinations (2006, 2008, and 2010) and were followed up for clinical events until 2019. TyG index was calculated as Ln [fasting triglyceride (mg/dL) × fasting glucose (mg/dL)/2]. We measured TyG index variability as the SD of the residuals obtained from a linear regression on the three TyG index measurements for each individual. Multivariate-adjusted Cox models were used to estimate the adjusted hazard ratio (aHR) and 95% confidence interval (CI) with incident CVD.ResultsDuring a median follow-up time of 9.0 years, 2404 developed CVD. The highest tertile (T3) of baseline and mean TyG index were each associated with higher CVD incidence as compared with the lowest tertile (T1): aHR, 1.25; 95% CI 1.11–1.42; and aHR 1.40; 95% CI 1.24–1.58, respectively. Tertile 3 of TyG index variability was associated with increased CVD incidence compared to T1 group (aHR, 1.12; 95% CI 1.01–1.24). Similar findings were observed in a series of sensitivity analyses.ConclusionHigher TyG index level and greater TyGindex variability were each independently associated with a higher incidence of CVD.

0717 Obstructive Sleep Apnea Symptom Subtype Transitions over Five Years are Associated with Increased Cardiovascular Disease Incidence Risk

Abstract Introduction Efforts to characterize clinical heterogeneity of obstructive sleep apnea (OSA) resulted in the identification and replication of symptom-based subtypes. Individuals with moderate-severe OSA that are excessively sleepy are at increased risk of cardiovascular disease (CVD). There is limited evidence about whether OSA patients that worsen their symptom presentation over time are at increased cardiovascular burden. This study aimed to assess the association between five-year transitions among OSA symptom subtypes and incidence of CVD in a community-based cohort. Methods Participants of the Sleep Heart Health Study with complete baseline and 5-year follow-up data on symptom presentation, polysomnographic data and CVD outcomes were included (N=2,643). We used latent transition analysis on 14 symptom items to determine symptom subtype transitions in participants diagnosed with OSA (apnea-hypopnea index [AHI]≥5) across both visits. The primary outcome was incidence of CVD, defined as first occurrence of a composite of coronary heart disease, heart failure or stroke after the follow-up visit (median CV follow-up: 6.7 years). Cox proportional hazards models were used to assess the association between symptom subtype transitions and CVD incidence, adjusted by relevant demographic and cardiovascular risk factors. Results Four OSA symptom subtypes were identified at baseline and follow-up visits: minimally symptomatic, disturbed sleep, moderately sleepy and excessively sleepy. When compared to participants without OSA at baseline and follow-up visits, those with OSA that transitioned from moderately sleepy to excessively sleepy had increased CVD incidence risk (HR=2.09; 95%CI=1.27-3.45; p=0.004), independent of other CV risk factors. Increased CVD incidence risk was also observed in participants who transitioned from moderately sleepy to excessively sleepy when compared to those that remained moderately sleepy (HR=2.02; 95%CI=1.20-3.40; p=0.008) and in participants who transitioned from disturbed sleep to excessively sleepy when compared to those that remained with disturbed sleep (HR=3.25; 95%CI=1.03-10.23; p=0.044). Conclusion Five-year transitions across OSA symptom subtypes are associated with increased CVD incidence risk when adjusted by other relevant cardiovascular risk factors. Participants that transitioned from moderately sleepy or from disturbed sleep to excessively sleepy were at higher CVD risk. Results of this study might inform the role of symptom progression on CVD risk in OSA. Support (If Any) American Heart Association (20CDA35310360), National Institutes of Health (U01HL53916, U01HL53931, U01HL53934, U01HL53937, U01HL53938, U01HL53940, U01HL53941, U01HL64360 R24 HL114473, 75N92019R002).

439 Continuous Positive Airway Pressure and Cardiovascular Risk in a Large Clinical Sample of Obstructive Sleep Apnea Patients

Abstract Introduction While studies support the beneficial short-term role of continuous positive airway pressure (CPAP) therapy on cardiometabolic risk in adults with obstructive sleep apnea (OSA), its sustained effect on cardiovascular disease (CVD) risk is unknown. CPAP use data linked to electronic health records (EHR) offer opportunities to understand the role of OSA treatment for preventing CVD. We evaluated the association between CPAP use and CVD incidence in patients referred to a sleep study at a large health system. Methods We included adult patients with available apnea-hypopnea index (AHI) between 01/2018-02/2020 in Kaiser Permanente Southern California. At baseline, eligible participants had &amp;gt;1 year of continuous insurance coverage allowing gaps &amp;lt;90 days and were free of CVD 1 year prior to OSA diagnosis. Participants were distributed into three groups: no OSA (AHI&amp;lt;5), OSA (AHI≥5) with any CPAP use (median[IQR] 2.5[0.7–5.0] h/day) and OSA without evidence of CPAP use. CVD incidence was defined as first occurrence of myocardial infarction, stroke, unstable angina, heart failure or CVD death, based on validated EHR algorithms. We used Cox proportional hazards models to assess the association between OSA with or without CPAP use and CVD incidence, adjusted for baseline age, sex, body mass index, race/ethnicity, Charlson comorbidity index, and use of anti-hypertensives and lipid-lowering medications. Stratified analyses were conducted based on OSA severity. Results We included 11,145 patients without OSA, 13,898 with OSA and CPAP use, and 20,884 patients without CPAP use. Median follow-up was 262 days (IQR=129–409). CVD incidence rates were, respectively, 0.26%, 0.45% and 0.56%. In adjusted models, moderate-severe OSA (AHI≥15) without CPAP use was associated with increased CVD incidence when compared to no OSA (HR=1.71; 95%CI=1.11–2.64; p=0.016). OSA with any CPAP use was associated with lower CVD incidence (HR=0.68; 95%CI=0.50–0.93; p=0.016) when compared to OSA patients with no CPAP use. Stronger effects were observed when restricting the sample to moderate-severe OSA (HR=0.56; 95%CI=0.39–0.81; p=0.002). Conclusion Our analysis in a large observational clinical sample suggests that moderate-severe OSA with no CPAP use is associated with increased CVD incidence. Moreover, OSA with CPAP use was associated with decreased CVD incidence relative to no CPAP use. Support (if any) AASM Foundation (194-SR-18;205-SR-19); AHA (20CDA35310360).

Pain Characteristics, Cardiovascular Risk Factors, and Cardiovascular Disease.

There is unclear evidence that chronic pain may increase the risk of cardiovascular disease (CVD) incidence and mortality. This work evaluated the association between chronic pain, incidence of CVD, and changes in CVD risk factors. Cohort of 1091 community-dwelling individuals of at least 60 years, free from CVD at baseline, followed up for 6 years. Data on psychosocial factors and CVD risk factors were obtained through validated questionnaires and laboratory measurements. A pain scale ranging from 0 (no pain) to 6 (worst pain) was created according to pain frequency, location, and intensity. The cumulative incidence of CVD was 4.2% at 3 years and 7.7% at 5 years of follow-up. Compared to individuals without pain in the first 3 years (2012-2015), those with maintained scores of at least 2 showed a mean reduction of 3.57 (-5.77 to -1.37) METs-h/week in recreational physical activity, a 0.38-point (0.04-0.73) increase in psychological distress, and a 1.79 (1.03-3.11) higher odds of poor sleep. These associations held in the second follow-up period, when individuals with maintained pain also worsened their diet quality. A 1-point increase in the pain scale in 2012 was associated with a 1.21 (1.03-1.42) and 1.18 (0.97-1.44) increased CVD incidence in 2015 and 2017, respectively; none of the studied factors mediated this relationship. Older adults with chronic pain show important reductions in recreational physical activity and deterioration in mental health, sleep, and diet quality, which may well aggravate pain. Future studies should evaluate whether these factors mediate the increased risk of CVD observed in older adults with chronic pain.

The Relationship Between Asthma and Cardiovascular Disease: An Examination of the Framingham Offspring Study

Although asthma has been suggested as a risk factor for cardiovascular disease (CVD), robust longitudinal evidence of this relationship is limited. Using Framingham Offspring Cohort data, the goal of this study was to longitudinally examine the association between asthma and lifetime risk of CVD while controlling for cardiovascular risk factors included in the Framingham Risk Score. Data were analyzed from a prospective population-based cohort of 3,612 individuals, ages 17 to 77 years, who participated in Framingham Offspring Study examinations from 1979 to 2014. Asthma was defined based on physician diagnosis during study interviews. Incident CVD included myocardial infarction, angina, coronary insufficiency, stroke, transient ischemic attack, and heart failure. Time-dependent Cox regression models were used to evaluate the relationship between asthma and CVD incidence. Overall, 533 (15%) participants had a diagnosis of asthma and 897 (25%) developed CVD during the course of the study. Unadjusted analyses revealed that asthma was associated with increased CVD incidence (hazard ratio, 1.40; 95%CI, 1.17-1.68). Cox regression also showed an adjusted association between asthma and CVD incidence (hazard ratio, 1.28; 95%CI, 1.07-1.54) after controlling for established cardiovascular risk factors. This prospective analysis with > 35 years of follow-up shows that asthma is a risk factor for CVD after adjusting for potential confounders. When assessing risk of cardiovascular disease, asthma should be evaluated and managed as a risk factor contributing to morbidity and mortality.

Chronic Periodontitis Could Increase Cardiovascular Events: A Ten Years Follow-Up Study

Background: Chronic periodontitis (CP) could be considered to have the causal relationship with cardiovascular disease (CVD). The aim of this study is to investigate the causal association between CP and CVD using representative health insurance cohort in Korea. Methods: A retrospective cohort study was performed to test the hypothesis that CP increased CVD incidence among Koreans who had no history of AMI (acute myocardial infarction) or ST (stroke) from 2002 to 2013, using the National Health Insurance Service-National Health Screening Cohort (NHIS-HEALS). A total of 298,128 participants were selected and followed up for ten years from this cohort. Multivariable cox regression analysis was applied to estimate adjusted hazard ratio (aHR). Findings: Our data showed that CP was significantly associated with higher incidence of AMI and ST. Compared with healthy participants, those with severe CP had higher incidence by 11% for AMI (aHR, 1.11 [95% CI 1.02-1.20]), by 4% for ST (aHR, 1.04 [95% confidence interval (CI) 1.01-1.07]), and by 4% for CVD (aHR, 1.04 [95% CI, 1.01-1.07]). The association for AMI and CVD was positively modified in females and participants aged 40-59 years, while the association for ST was modified in females but not in participants aged 40-59 years only in ST. CP increased total CVD events by 1.6% among Korean. Interpretation: Our data confirmed that CP could increase the event of CVD such as AMI and ST. The prevention and management of CP could be worth in clinical practice to prevent CVD. Funding Statement: This research was supported by the Bio & Medical Technology Development Program of the National Research Foundation (NRF) funded by the Ministry of Science and ICT, Korea (NRF2017M3A9B6062986). Declaration of Interests: The authors state: None exist. Ethics Approval Statement: The Institutional Review Board (IRB) at the Seoul National University Hospital, which is in compliance with the Declaration of Helsinki, approved this study (IRB number E-1801-019- 912). This study used the Korean National Health Insurance Service database (NHIS-2017-2-459).

Prognostic value of exercise tolerance test for predicting cardiovascular disease in asymptomatic individuals with heterozygous familiar hypercholesterolemia.

Heterozygous familiar hypercholesterolemia (hFH) is an autosomal dominant inherited dyslipidemia, associated with premature cardiovascular disease (CVD). Aim of the study was to define prognostic factors for cardiovascular events (CVE) in asymptomatic individuals with hFH. All participants with recent diagnosis of hFH were recruited from the outpatient lipid clinic from 1987 to 2016, without any previous clinical evidence of CVD. A detailed clinical evaluation and laboratory investigation was obtained. Exercise tolerance test (ETT) was performed until maximum exercise capacity was achieved, without evidence of ischemia. Primary endpoint of the study was the first CVE. Four hundred fifty one participants were followed up for 10 ± 8years, with 68 recorded cases of CVD (15%). Cumulative incidence of CVD was 15%, 24% and 32% for the 3 decades, respectively. In univariate analysis, male gender (p = 0.016), progression of age (p < 0.001), menopause (p = 0.030), waist-hip ratio (p = 0.043) and increased levels of Lp(α) (p = 0.014) were significantly associated with increased CVD incidence; whereas, exercise capacity (p = 0.025), low variation of heart rate (HR) during all stages of ETT compared to resting state (p = 0.020), maximum systolic (p = 0.014) and diastolic (p < 0.001) blood pressure were inversely associated with CVD. In multi-adjusted analysis, male gender (p < 0.001), duration of ETT (p = 0.023), estimated HR (p = 0.029), variation of HR during ETT compared to resting state (p < 0.05) and maximum diastolic pressure (p = 0.044) were significantly associated with CVD. Parameters of ETT in asymptomatic individuals with hFH, without any evidence of ischemia, may predict CVD in these high-risk patients after decades of observation.

Adipose Tissue Distribution and Cardiovascular Disease Risk Among Breast Cancer Survivors.

Cardiovascular disease (CVD) is a major source of morbidity and mortality among breast cancer survivors. Although body mass index (BMI) is associated with CVD risk, adipose tissue distribution may better identify patients with a high risk of CVD after breast cancer. Among 2,943 patients with nonmetastatic breast cancer without prior CVD, we used International Classification of Diseases (9th and 10th revisions) codes to identify incidence of nonfatal stroke, myocardial infarction, heart failure, or CVD death. From clinically acquired computed tomography scans obtained near diagnosis, we measured visceral adiposity (centimeters squared), subcutaneous adiposity (centimeters squared), and intramuscular adiposity (fatty infiltration into muscle [Hounsfield Units, scored inversely]). We estimated hazard ratios (HRs) and 95% CIs per SD increase in adiposity accounting for competing risks and adjusting for demographics, smoking, cancer treatment, and pre-existing CVD risk factors. Mean (SD) age was 56 (12) years. Over a median follow-up of 6 years, 328 CVD events occurred. Each SD increase in visceral or intramuscular adiposity was associated with an increase in CVD risk (HR, 1.15 [95% CI, 1.03 to 1.29] and HR, 1.21 [95% CI, 1.06 to 1.37]), respectively). Excess visceral and intramuscular adiposity occurred across all BMI categories. Among normal-weight patients, each SD greater visceral adiposity increased CVD risk by 70% (HR, 1.70 [95% CI, 1.10 to 2.62]). Visceral and intramuscular adiposity were associated with increased CVD incidence after breast cancer diagnosis, independent of pre-existing CVD risk factors and cancer treatments. The increased CVD incidence among normal-weight patients with greater visceral adiposity would go undetected with BMI alone. Measures of adipose tissue distribution may help identify high-risk patients and tailor CVD prevention strategies.

Noise and Cardiovascular Disease in a Nationwide Cohort Study

Background: Observational and experimental studies indicate that nighttime noise can cause disruption of sleep, increase blood pressure and heart rate, and increase stress hormone levels and oxidative stress, which in turn may result in endothelial dysfunction and arterial hypertension. Few prospective cohorts have examined the association between nighttime environmental noise and cardiovascular disease (CVD) in the United States. Methods: A total of 95,450 women (mean age 70.4 years) were followed from 2000-2010 in a nationwide prospective cohort study. Exposure to nighttime noise was based on the geocoded addresses of participants over followup, linked to a geospatial model of outdoor environmental sound levels. The geospatial sound model predicted expected noise exposure using empirical acoustical data and geospatial features such as topography, climate, hydrology, and anthropogenic activity. The acoustical data included 1.5 million hours of measurements from 492 urban and rural sites located across the contiguous United States during 2000-2014. We specifically examined nighttime median noise levels (A-weighted L50). CVD was defined as the first incidence of fatal coronary heart disease, nonfatal myocardial infarction, or stroke confirmed by medical record review. We conducted a survival analysis and incorporated multiple traditional CVD risk factors, PM2.5, region, and individual- and area-socioeconomic status. Results: Over 897,606 person years, we identified 3,639 CVD events. In multivariable models, a one standard deviation (3.55) increase in nighttime median noise levels (A-weighted L50) was associated with a 4% (95% CI 1%, 9%) increase in CVD incidence. Conclusions: Higher levels of nighttime environmental noise were linked to increased incidence of CVD in this cohort of adult women. This suggests that nighttime noise from anthropogenic sources, such as traffic, may contribute to CVD incidence independent of air pollution.

Bimanual elbow exoskeleton: Force based protocol and rehabilitation quantification.

An aging population, along with the increase in cardiovascular disease incidence that accompanies this demographic shift, is likely to increase both the economic and medical burden associated with stroke in western societies. Rehabilitation, the standard treatment for stroke, can be expanded and augmented with state of the art technologies, such as robotic therapy. This paper expands upon a recent work involving a force-feedback master-slave bimanual exoskeleton for elbow rehabilitation, named a Bimanual Wearable Robotic Device (BWRD). Elbow force data acquired during the execution of custom tasks is analyzed to demonstrate the feasibility of tracking patient progress. Two training tasks that focus on applied forces are examined. The first is called "slave arm follow", which uses the absolute angular impulse as a metric; the second is called "conditional arm static", which uses the rise time to target as a metric, both presented here. The outcomes of these metrics are observed over three days.