Risultati per: Come stress e attacchi di cuore sono collegati

Circulation, Volume 150, Issue Suppl_1, Page A4142430-A4142430, November 12, 2024. Background:Cardiac allograft vasculopathy (CAV) is a major cause of morbidity and mortality following heart transplantation (OHT). Noninvasive methods to detect CAV and risk stratify OHT patients are needed. The value of fully quantitative stress cardiac magnetic resonance imaging has been recently validated and may be a promising technique for OHT surveillance. We aimed to evaluate the feasibility of quantitative stress CMR after OHT.Methods:We enrolled asymptomatic OHT recipients without coronary artery disease to undergo regadenoson stress CMR (1.5T GE HealthCare) with cine imaging, tissue mapping, and late gadolinium enhancement (LGE) imaging for routine CAV surveillance. Using the dual sequence technique, quantitative perfusion values were determined using Fermi deconvolution. Myocardial perfusion reserve (MPR) was calculated as the ratio of stress to rest myocardial blood flow (MBF).Results:Fifty-three subjects (mean age 47.06 ± 17.14 years) were included. OHT recipients (n=11, mean 6.77 ± 4.34 years post-transplant) were compared with healthy controls (n=43). No life-threatening adverse events, brief or prolonged atrioventricular block or other arrhythmias occurred with regadenoson. Coronary angiography was performed in 9 OHT patients before CMR, with an average of 1.99 ± 2.05 years between studies. No visual inducible ischemia was reported. Post OHT, rest MBF was significantly higher (1.69 ± 0.52 mL/g/min vs 1.01 ± 0.24 mL/g/min, p=0.004) and stress MBF was lower (2.33 ± 0.69 mL/g/min vs 2.95 ± 0.88 mL/g/min, p=0.02) compared to controls. MPR was significantly lower in OHT recipients compared to controls (1.46 ± 0.51 vs 3.11 ± 1.12, p

Circulation, Volume 150, Issue Suppl_1, Page A4147100-A4147100, November 12, 2024. Introduction:Perceived stress is known as the feeling of uncontrollability in one’s life and the inability to cope with the amount of stress one is experiencing due to one’s circumstances. There is evidence indicating that perceived stress may be a risk factor for cardiovascular disease (CVD). However, it is unclear whether perceived stress is associated with higher left ventricular mass index (LVMI), a measure of target organ damage and strong predictor of CVD.Aim:We examined the association between perceived stress and LVMI.Methods:The Masked Hypertension Study is a multi-site study that assessed the prevalence and predictors of masked hypertension in working adults from the New York Metropolitan area. A total of 1011 participants were recruited for the study; 826 participants completed the Perceived Stress Scale questionnaire and an echocardiogram. The perceived stress scale is a 14-item likert scale that assesses different situations that affects our perceived stress or our feelings in certain situations. It has a scale of 1 to 5 with 1 being never to 5 being very often. LVMI was determined according to the 2D method based on the American Society of Echocardiography (ASE) recommendations.Linear regression models were specified predicting LVMI from perceived stress. Covariates were sex, race/ethnicity, age, BMI, systolic bp, diastolic bp, and caregiving status.Results:Of the 826 participants, 40.7% were male, 6.9% were Black, 11.9% were Hispanic/Latinx , and 48.79% were caregivers. Mean (SD) age was 45.3 (10.3) years, mean body mass index was 27.6 (5.3) kg/m2, and mean SBP and DBP were 114.7 (12.0) and 74.8 (8.5). Mean perceived stress score was 21.8 (7.6) and mean LVMI was 63.3 (15.7) gm/m2.Contrary to our hypothesis, perceived stress was not significantly associated with LVMI, B = -0.00, 95% CI: -0.13, 0.13, p= 0.98.Conclusion:There was not an association between perceived stress and LVMI. Future research should examine whether other types of stresses/stressors are related to LVMI and the implications of this for patients and their health.

Circulation, Volume 150, Issue Suppl_1, Page A4144217-A4144217, November 12, 2024. Background:The ISCHEMIA trial questioned revascularization in chronic coronary syndrome (CCS) patients, but excluding subjects with left main (LM) coronary artery disease (CAD). A widely available diagnostic method excluding LMCAD would expand the implementation of an initial noninvasive strategy.Objective:Assessing the ability of excluding LMCAD through clinical and ECG stress testing (EST) variables in patients undergoing coronary angiography (CAG) for CCS.Methods:In a multicenter retrospective case-control study we evaluated CCS subjects undergoing CAG after a maximal EST.Caseswere patients with angiographic ≥50% LM stenosis or ≥70% stenoses of both proximal left anterior descending and proximal circumflex arteries; we matched them with similar patients without LMCAD (Controls)in a 1:3 ratio. Models were internally validated through logistic regressions.Results:219Caseswere matched with 554Controls. The c-statistic was 0.80 (optimism-adjusted: 0.73). Assuming LMCAD prevalence of 5% and a misclassification cost ratio of 1:100 (ratio of the cost of performing CAG in a subject without LMCAD to the cost of not performing CAG in a patient with LMCAD), the negative predictive value was 98.6%, correctly classifying 84.5% ofCases. CAG could be spared in 57.0% of subjects, missing one LMCAD diagnosis every 70 CAGs spared in patients without LMCAD (Figure).Conclusions:Among patients with CCS, LMCAD can be predicted withacceptablediagnostic accuracy anda very highnegative predictive value through a model based on clinical and EST parameters, allowing an initial noninvasive management of most patients able to perform an EST, reducing the costs of routine coronary imaging. Such results should enlarge the applicability of the ISCHEMIA results when coronary computed tomography angiography, used in ISCHEMIA, is not available, limiting the referral to invasive CAG.

Circulation, Volume 150, Issue Suppl_1, Page A4138303-A4138303, November 12, 2024. Background:A higher stress hyperglycemic ratio (SHR) has been reported to be associated with adverse cardiac outcomes. However, the role of SHR in predicting clinical outcomes by comparing patients with and without diabetes mellitus is yet to be explored.Objective:To evaluate the prognostic value of the SHR for predicting major adverse cardiovascular (MACE) and all-cause mortality in ACS patients with and without diabetes mellitus.Methods:Per PRISMA guidelines, we comprehensively reviewed PubMed, Google Scholar, and SCOPUS for eligible studies reporting on SHR and its association with MACE (8 studies) and all-cause mortality (7 studies) in ACS patients. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using a binary random-effects model, with results displayed as forest plots. Heterogeneity was assessed using I2 statistics, and a leave-one-out sensitivity analysis was performed. P

Circulation, Volume 150, Issue Suppl_1, Page A4146032-A4146032, November 12, 2024. Background:Stress testing is a well-established non-invasive method commonly used in clinical practice for patients with angina. However, its benefit in diabetic patients after coronary intervention remains unclear. This systematic review aims to address this knowledge gap by evaluating the impact of routine stress testing in this specific patient population.Research Question:Does routine stress testing improve outcomes in diabetic patients with prior revascularization?Goals:We aimed to perform a systematic review and meta-analysis of studies that evaluated death, MACE and repeated revascularization episodes in diabetic patients who have prior coronary intervention.Methods:We searched PubMed, Embase and Cochrane databases for randomized controlled trials (RCT) and cohort studies evaluating diabetic patients who underwent cardiac revascularization and reporting the following outcomes: (1) Myocardial Infarction (MI) and Cardiovascular Death; (2) Ischemia; and (3) Repeat Revascularization. Statistical analysis was performed using Open Meta and heterogeneity was assessed with I2statistical.Results:We included 16924 patients from 16 studies, of which 15 were observational cohort studies and 1 was a RCT. All patients were diabetics and had a history of revascularization. Follow-up ranged from 1 to 5.2 years. The mean patient age was 60.8±9.5 years and 75% were male. MI and cardiovascular death was found in 9.8% (95% CI; range 6.8-12.8%; p

Circulation, Volume 150, Issue Suppl_1, Page A4140852-A4140852, November 12, 2024. Introduction:Posttraumatic stress disorder (PTSD) is an independent cardiovascular disease (CVD) risk factor with high prevalence in women, particularly women veterans (WV). While the impact of PTSD on ischemic heart disease (IHD) and stroke has been well established, its impact on a comprehensive set of CVD outcomes has not been studied in WV, a growing population at high risk for CVD in the U.S. The goal of this project was to investigate the impact of PTSD on a comprehensive set of CVD conditions in WV.Methods:National Veterans Health Affairs (VHA) electronic health records were used to identify all women who visited any VAs from 1/1/2000 to 12/31/2019. PTSD and CVD were identified based on International Classification of Disease versions 9 and 10 diagnoses ( 1 inpatient or 2 outpatient encounter documentations). Incident CVD outcomes included first onset of IHD, stroke, cardiomyopathy/heart failure (HF), pulmonary arterial hypertension/pulmonary hypertension (PH), atrial flutter/fibrillation (AF), peripheral arterial disease (PAD), venous thromboembolism (VTE), and aortic stenosis (AS). Propensity score matching and Cox survival analyses were performed to assess associations of PTSD with incident CVD outcomes.Results:We identified 622,312 WV, with 140,210 (22.53%) with PTSD. After 1:1 matching, 202,896 patients were included in the final analysis. WV had a mean age of 39.1 years, and the mean [MOU1] follow-up was 5.72 years. Table 1 reveals the association of PTSD with an incident CVD composite and the different component outcomes individually.Conclusion:In a large sample of WV, we demonstrate significant and clinically relevant associations of PTSD with a comprehensive set of incident CVD outcomes. The potential association with some of the specific outcomes warrant further investigation. Maybe more of a call to action for PTSD screening and treatment to potentially offset CVD risk instead?

Circulation, Volume 150, Issue Suppl_1, Page A4143092-A4143092, November 12, 2024. Background:Very high level, lifelong aerobic exercise results in lower ventricular stiffness and left ventricular wall stress (LVWS) LVWS is an important predictor of future heart failure risk. To what degree LVWS changes with various doses of lifelong aerobic exercise is unknown.Objective:The purpose of this study was to determine the impact of lifelong exercise on LVWS.Methods:Seniors (n = 58) who consistently participated in lifelong patterns of exercise training were recruited and categorized into 3 groups: “sedentary” (

Circulation, Volume 150, Issue Suppl_1, Page A4143599-A4143599, November 12, 2024. Background:The Steroids to Reduce Systemic Inflammation after Infant Heart Surgery (STRESS) trial randomized 1200 infants undergoing cardiac surgery with cardiopulmonary bypass to prophylactic intraoperative methylprednisolone (MP) versus placebo.Aims:Evaluate benefits and harms associated with MP in subset populations.Methods:STRESS participants were categorized based on STAT Mortality Category (1-3 and 4-5), age (neonate ≤ 30 days< non-neonate), prematurity (< 37 weeks gestation) and any chromosomal or syndromic diagnoses (CSD). Key postoperative outcomes included any steroid administration (< 72 hours after surgery), peak blood glucose (7 days), thrombosis, and infections.Results:The cohort consisted of 30% (364/1200) neonates, 16% (193/1197) premature, and 81% (969/1197) STAT 1-3 operations. Stratified analyses demonstrated notable beneficial effects with MP including reduced use of postoperative hydrocortisone in neonates (OR 0.39 [0.25-0.60]), those following STAT 1-3 (OR 0.65 [0.47-0.91]) and STAT 4-5 operations (OR 0.57 [0.34-0.97]), term infants (OR 0.62 [0.47-0.83]), and those without CSD (OR 0.63 [0.46-0.86]). MP associated with lower thrombosis occurrence among neonates (OR 0.37 [0.16-0.87]) and term infants (OR 0.38 [0.19-0.75]). Notable adverse associations with MP included increased postoperative peak blood glucose levels and insulin use (all subgroups, P

Circulation, Volume 150, Issue Suppl_1, Page A4140462-A4140462, November 12, 2024. Background:Right ventricular pacing (RVP) can have adverse cardiac effects and cause pacing induced cardiomyopathy (PiCM). His bundle pacing (HBP)&Left Bundle Branch area pacing (LBBAP) mimic physiologic conduction (PhysioP) and maintain biventricular synchrony.Hypothesis and Aims:Reduced left ventricular (LV) systolic function reserve in the presence of normal baseline LV ejection fraction (EF) could precede development of RV PiCM. Our aim was to compare the effects of RVP vs. PhysioP on bicycle exercise cardiopulmonary performance in patients with normal LVEF who required pacing for bradyarrhythmias.Methods:Patients with sinus rhythm and RVP or PhysioP&ventricular pacing burden of >70% who completed cardiopulmonary exercise test and simultaneous stress echocardiography (SE) were included. Pulmonary gas exchange was calculated using Ventilation/CO2 production at rest and during exercise. Changes in LV size, EF, longitudinal strain and diastolic function and gas exchange parameters were compared post and pre exercise in the 2 groups.Results:25 of 29 patients completed the study [68 ± 23 yrs, 48% M; LVEF 56±5%, 11 RVP, 14 PhysioP]. There was no difference in baseline demographic&clinical variables, exercise duration, rest and peak heart rate and blood pressure between 2 groups. Pacing duration was 2.61±1.48 yrs in RVP vs. 0.84±0.67 yrs (p=0.003) in the Physio group. Resting echocardiographic parameters (Table 1A)were comparable. Compared to RVP, reduction in LV end-diastolic volume (EDV) 3.4±14.1 ml vs. -23.1±18.1ml, p=0.006)&LV end-systolic volume (ESV -5.7±11.6 ml vs. -18.0±9.5ml, p=0.01) was more pronounced in the PhysioP group. Changes in LVEF, LV strain&diastolic function were not different between the 2 groups (Table 1B). There were no significant differences in changes in pulmonary gas exchange parameters in the 2 groups.Conclusions:In patients with normal LVEF and pacemaker dependent, RVP is associated with impaired but PhysioP with preserved LV systolic function reserve, which can be detected by exercise SE. SE may help identify patients at risk for RV PiCM. Benefit of PhysioP needs to be determined by larger studies with longer follow-up.

Circulation, Volume 150, Issue Suppl_1, Page A4137735-A4137735, November 12, 2024. Background:Aortic aneurysms account for ~10,000 deaths annually in the USA. Oxidative stress is implicated in both abdominal (AAA) and thoracic (TAA) aneurysm formation, but the mechanisms are incompletely understood. We used a chemogenetic approach to modulate oxidative stress in the vascular wall by creating a transgenic mouse (DAAO-TGTie2) that expresses yeast D-amino acid oxidase (DAAO) driven by the endothelial Tie2 promoter. DAAO generates the reactive oxygen species hydrogen peroxide from D-amino acids. Vascular tissues contain L-amino acids, so yeast DAAO is quiescent until DAAO-TGTie2mice are provided with D-amino acids. Here we characterize the cellular and molecular consequences of vascular oxidative stress in DAAO-TGTie2mice.Hypothesis:Chronic oxidative stress in the vascular wall causes arterial dysfunction.Aim:To characterize the phenotype of DAAO-TGTie2mice after oxidative stress induction in vascular endothelium.To identify the mechanisms whereby vascular oxidative stress causes arterial dysfunction and hypertension.Methods:Systolic blood pressure and aortic sonography were measured weekly in D-alanine-fed DAAO-TGTie2. Proteomic analyses were used to identify mechanistic targets, which were validated using biochemical and immunohistochemical methods.Results:D-alanine-fed DAAO-TGTie2mice develop systolic hypertension and abdominal but not thoracic aortic aneurysms; treated mice die in >3 months with burst abdominal aortic aneurysms. Transgene expression is similar in abdominal and thoracic endothelium. Levels of oxidative stress markers (oxidized proteins, lipid, and DNA) were similar in thoracic and abdominal aorta. Proteomic analyses established phenotypic switching in abdominal but not thoracic aorta, and also revealed activation of the oxidant-activated kinase ASK1 and of the MAP kinase cascade in abdominal but not thoracic aorta. Immunoblot analyses showed a marked decrease in JNK1 phosphorylation by phosphatase DUSP3 and an increase in vascular KLF4, leading to phenotypic switching of contractile to synthetic VSMCs.Conclusion:Chronic chemogenetic oxidative stress induces hypertension and abdominal aortic aneurysm formation caused by KLF4-dependent VSMC phenotypic switching.

Circulation, Volume 150, Issue Suppl_1, Page A4142510-A4142510, November 12, 2024. Background:An acute hyperglycemic status is reportedly associated with poor prognosis in patients with acute cardiovascular diseases. Although the stress hyperglycemia ratio (SHR) is a novel index to accurately represent the hyperglycemic condition on admission, relations between SHR and clinical outcomes are not fully evaluated in a setting of acute myocardial infarction (MI).Methods:This retrospective, multicenter registry study included 2,386 patients with acute MI undergoing percutaneous coronary intervention. SHR was calculated as a blood glucose level on admission divided by the estimated average glucose derived from a glycated hemoglobin level. The co-primary endpoints of this study included heart failure (HF)-related events (a composite of all-cause death and worsening and hospitalized HF) and major atherosclerotic cardiovascular events (MACE) (a composite of all-cause death, recurrent MI, and ischemic stroke), during the index hospitalization and after discharge.Results:Of the 2,386 patients, 890 (37.3%) had diabetes, and the median SHR was 1.17 [0.99, 1.45]. HF events and MACE occurred in 680 (28.5%) and 233 (9.8%) during hospitalization. SHR was identified as a factor significantly associated with both in-hospital HF events (adjusted odds ratio 1.65, 95% confidence interval 1.18-2.29, p=0.003) and MACE (adjusted odds ratio 1.50, 95% confidence interval 1.10-2.03, p=0.009). Among 2,017 patients who survived to discharge and had follow-up information, 195 (9.7%) and 214 (10.6%) experienced HF events and MACE during the median of 536 days after discharge. Patients with the high SHR ( >1.45, 4th quartile) had an increased risk of HF events than those with SHR ≤1.45, while the incidence of MACE after discharge did not differ significantly between the two groups (Figure). The multivariable analysis confirmed the association of SHR with long-term HF events.Conclusions:In patients with acute MI, SHR was predictive of in-hospital outcomes including HF events and MACE, while after discharge, the higher SHR was associated with a higher HF risk but not with MACE. Further studies are needed to elucidate the underlying mechanisms and potential incremental benefit of SHR in stratifying patient risks after MI.

Circulation, Volume 150, Issue Suppl_1, Page A4139600-A4139600, November 12, 2024. Background:Cardiac injury after subarachnoid hemorrhage (SAH) is a well-recognized phenomenon with electrocardiogram (ECG) changes, arrhythmias and myocardial dysfunction. Neurocardiac injury has been commonly reported with increased severity of SAH, however much of the evidence has focused on high grade SAH requiring hemodynamic support or mechanical ventilation. In this study we focused on neurocardiac injury with high grade World Federation of Neurological Surgeons (WFNS) grade 3-5 SAH requiring intensive care management.Methods:Patients admitted to our intensive care unit from 2009-2019 with an WFNS 3-5 aneurysmal SAH with an echocardiogram within 7 days of admission were included in our study. Electrocardiogram, cardiac biomarkers and data regarding mortality and neurological complications were collected retrospectively.Results:A total of 242 patients were included in our study analysis with 11 (5%), 89 (37%), and 142 (59%) had WFNS grade 3, 4 or 5 SAH, respectively. Of the 95 patients that underwent echocardiography in the first week, 38 (40%) had a reduced ejection fraction, which was mild (LVEF 40-52%) in 13 (14%), moderate (LVEF 30-39%) in 14 (15%), and severe (LVEF < 30%) in 11 (12%). Independent predictors of reduced ejection fraction included a lower presenting GCS score (OR 1.2 per one point reduction in (Glasgow Coma Score) GCS, 95% CI 1.0-1.5, p = 0.03), elevated troponin T concentration (OR 6.1, 95% CI 1.2-31.3, p = 0.03) and T wave inversion on ECG (OR 9.1, 95% CI 1.6-52.3, p = 0.01). In patients with reduced ejection fraction, classical apical wall motion abnormality was more prevalent in older populations (median age 64 years (apical) vs 50 years (basal wall motion abnormality) and 52 years (other) p = 0.03). In all wall motion abnormality groups, there was a female predominance. Classic Takotsubo wall motion was associated with an anterior SAH aneurysm location (p = 0.03) and highest proportion of moderate to severe LV dysfunction (p = 0.04). ICU mortality did not differ based on the pattern of wall motion abnormalities.Conclusion:Predictors of neurocardiac injury in high grade SAH include troponin elevation, T wave abnormalities and lower presenting GCS. Aneurysm location was associated with wall motion abnormalities and degree of LV dysfunction. Patients with WFNS 3-5 SAH are at increased risk of neurocardiac injury. ECG changes, cardiac biomarker elevation and aneurysm location can help identify patients who warrant echocardiography.

Circulation, Volume 150, Issue Suppl_1, Page A4146135-A4146135, November 12, 2024. Background:Epicardial adipose tissue (EAT) is increasingly recognized as a key factor in the development of atrial fibrillation (AF). In addition to direct myocardial infiltration by adipocytes affecting conduction properties, EAT may also promote an arrhythmogenic substrate through paracrine and endocrine effects. EAT was shown to preferentially generate oxidase-dependent reactive oxygen species (ROS) when compared to subcutaneous fat. While a role for myocardial ROS in the development of AF is well established, a separate role for EAT oxidative stress remains unexplored.Hypothesis:Oxidative stress in the EAT contributes to atrial electrical remodeling and development of AF.Aims:Determine the effect of EAT-restricted gene therapy with NOX2 shRNA on atrial electrical remodeling in the short-term canine atrial tachypacing (ATP) model of AF.Methods:A single-chamber pacemaker was inserted for the ATP model. Animals developed persistent AF after 4-6 weeks, after which the atria were harvested. Unpaced animals were used as controls. Expression of NOX2 in the EAT was assessed by qPCR. EAT oxidative stress was determined by IHC for 8-OHdG, a marker of DNA oxidative damage. A subset of animals underwent an open-chest gene injection procedure restricted to the EAT (with a plasmid expressing NOX2 shRNA or a scrambled sequence) prior to initiation of ATP for 9 days. A terminal EP study determined regional atrial ERP and AF inducibility.Results:NOX2 expression was significantly increased in the EAT of animals with ATP-induced AF when compared to unpaced controls (Panel A, p

Circulation, Volume 150, Issue Suppl_1, Page A4144014-A4144014, November 12, 2024. Introduction:Lower socioeconomic status (SES) associates with greater MACE risk in part via stress-related mechanisms. Further, a higher polygenic risk score for neuroticism (nPRS), a marker linked to stress sensitivity and chronic stress conditions, is associated with greater MACE risk. Moreover, individuals with higher nPRS are more susceptible to the cardiovascular impacts of lower SES. Yet, it remains unknown whether individuals with higher nPRS experience greater adverse changes in autonomic and inflammatory intermediaries of stress in the setting of lower SES and whether these changes contribute to MACE risk. Accordingly, we tested the hypotheses that: 1) lower SES links to MACE risk via lower heart rate variability (HRV) and higher C-reactive protein (CRP), and 2) lower SES has a greater impact on HRV and CRP among those with higher nPRS.Methods:Individuals (N=18093; median age 64 years; 54% female) with nPRS and SES data were identified in the Mass General Brigham Biobank. SES was assessed as the median income of an individual’s residential zip code with lower income defined as the lowest tertile. Higher nPRS was defined as values ≥ population median. MACE data was collected for 10 years following enrollment using ICD-10 codes. CRP (N=4117) and HRV (N=4412) data were collected from available clinical lab values and electrocardiograms, respectively, with HRV assessed as the standard deviation of all normal RR intervals.Results:In the full cohort, both HRV and CRP mediated the relationship between lower SES and MACE risk (p

Circulation, Volume 150, Issue Suppl_1, Page A4141934-A4141934, November 12, 2024. Introduction:Heightened psychosocial stress is a CVD risk factor. While stressors are common and often co-occur, identifying sources and patterns of psychosocial stress exposure may provide insight into individual susceptibility to CVD. Therefore, we sought to identify and examine the longitudinal associations of baseline psychosocial stress subgroups with CVD events in MESA.Methods:Data from 6,349 adults (aged: 62.2±10.2 years; 52.9% women) from the MESA cohort with no prior CVD event at baseline (years 2000-2002) were used in this analysis. Latent class analysis (LCA) was used to specify distinct stress subgroups based on 6 variables: chronic burden, neighborhood safety, adequate food shopping, neighborhood noise, lifetime- and past-year discrimination. Five classes were determined after examining traditional fit indices. Adjudicated fatal and nonfatal CVD events were ascertained in annual follow-up visits through the year 2019. Cox proportional hazards models with sequential adjustment of baseline variables were used to examine the associations between subgroup membership and CVD events.Results:Five distinct stress subgroups were identified via LCA and were labeled “moderate neighborhood noise” (12.1%), “excessive noise/crime” (6.4%), “elevated on all” (6.3%), “high discrimination/safe neighborhood” (21.4%), “optimal” (53.8%) (see figure). By the year 2019, 1,121 participants had experienced a CVD event. Membership in the “elevated on all” and “high discrimination/safe neighborhood” subgroups (see table) were associated with higher risk of a CVD event when adjusted for sociodemographic characteristics and cardiovascular health metrics. However, when adjusted for measures of anxiety and depression, possible mediators, only membership in the “high discrimination/safe neighborhood” subgroup was associated with increased risk of a CVD event.Conclusions:Among 5 distinct stress subgroups those experiencing high discrimination had higher risk for CVD events.

Circulation, Volume 150, Issue Suppl_1, Page A4140555-A4140555, November 12, 2024. Background:Psychological stress and poor sleep quality are interrelated and disproportionately affect adults who have multiple risk factors of cardiovascular disease (CVD). Sleep hygiene practices, such as maintaining an optimal household environment and engaging in healthy bedtime behaviors, are essential to sleep health. These practices may also impact psychological stress; however, their relationships remain under-studied. This study aimed to examine the associations among sleep hygiene practices, sleep quality, and psychological stress in adults with multiple CVD risk factors.Methods:Adults diagnosed with hypertension and type 2 diabetes completed an online survey (N = 300). Psychological stress and sleep quality were assessed using the Perceived Stress Scale 4 and the Pittsburgh Sleep Quality Index, respectively. A sleep hygiene instrument was used to examine 8 individual factors focusing on negative household environment (safety, physical comfort, temperature, and light) and poor in-bed behaviors (watching TV, playing video games, using screens, and eating). Multiple regression was employed to examine the association of each sleep hygiene factor with sleep quality and psychological stress. Subsequently, mediation analyses were conducted to examine the mediating role of sleep in the association between the composite sleep hygiene score and psychological stress.Results:Of the sample, 78% reported poor sleep quality and 44% reported high psychological stress. Individual sleep hygiene factors (e.g., unsafe household and eating at bedtime), as well as the composite sleep hygiene score, were significantly associated with poorer sleep quality and higher psychological stress. Sleep quality partially mediated the association between the composite sleep hygiene score and psychological stress (Indirect effect: 0.183; 95% bootstrap confidence interval: 0.057-0.339).Conclusions:The findings showed strong links between sleep hygiene practices, sleep quality, and psychological stress. Although causality cannot be inferred, current evidence suggests that promoting sleep hygiene education and implementing strategies to enhance sleep quality may alleviate psychological burdens in adults with multiple CVD risk factors.