Background:Black individuals have a lower incidence of atrial fibrillation (AF) than White individuals despite a higher burden of many traditional cardiovascular risk factors. Differences in left atrial (LA) structure and function by race could partly explain the observed pattern of AF risk. Methods:This analysis included 4,576 (978 Black and 3,598 White) participants from the Atherosclerosis Risk in Communities (ARIC) study, followed between 2011 and 2021. The association of selected echocardiographic measures of LA structure and function with AF incidence was evaluated with race-specific Cox proportional hazards models with adjustment for sociodemographic and clinical covariates. Additional analyses assessed whether LA measures attenuated the association between race and incident AF. Results:The analysis included 778 AF cases (113 in Black and 665 in White participants, mean age 75 years). Larger LA size and worse LA function were associated with higher AF risk in both Black and White individuals, with most associations of similar magnitude in both groups, except for a slightly stronger association of LA reservoir strain in Black than White participants (Black: hazard ratio (HR) 0.89, 95% CI 0.86-0.92 per 1% increase; White: HR 0.94, 95% CI 0.92-0.95, p for interaction = 0.01). In the overall sample, White participants showed higher AF risk compared to Black participants (HR 1.59, 95% CI 1.24-2.03). Adjustment for most individual LA measures did not attenuate the association between race and AF risk. Conclusion:Larger LA size and worse LA function were associated with incident AF in both Black and White ARIC participants. However, these measures did not explain the lower AF incidence observed among Black participants. LA remodeling appears to be an important predictor of AF risk, but it is not the primary explanation for the Black-White AF paradox.

Objective: Psychosocial stress is associated with increased cardiovascular disease (CVD) risk. The relationship between financial strain, a toxic form of psychosocial stress, and ideal cardiovascular health (CVH) is not well established. We examined whether financial strain was associated with poorer CVH in a multi-ethnic cohort free of CVD at baseline. Methods: This was a cross-sectional analysis of 6,453 adults aged 45-84 years from the Multi-Ethnic Study of Atherosclerosis. Financial strain was assessed by questionnaire and responses were categorized as yes or no. CVH was measured from 7 metrics (smoking, body mass index, physical activity, diet, total cholesterol, blood glucose and blood pressure). A CVH score of 14 was calculated by assigning points to the categories of each metric (poor = 0 points, intermediate = 1 point, ideal = 2 points). Multinomial logistic regression was used to examine the association of financial strain with the CVH score (inadequate 0-8, average 9-10, and optimal 11-14 points) adjusting for sociodemographic factors, depression and anxiety. Results: The mean age (SD) was 62 (10) and 53 % were women. Financial strain was reported by 25 % of participants. Participants who reported financial strain had lower odds of average (OR, 0.82 [95 % CI, 0.71, 0.94]) and optimal (0.73 [0.62, 0.87]) CVH scores. However, in the fully adjusted model, the association was only significant for optimal CVH scores (0.81, [0.68, 0.97]). Conclusion: Financial strain was associated with poorer CVH. More research is needed to understand this relationship so the burden of CVD can be decreased, particularly among people experiencing financial hardship.

Background Work‐related stress is a psychosocial risk factor linked to a higher risk of cardiovascular disease. However, the association between work‐related stress and cardiovascular health (CVH) is not well established. We estimated the association between work‐related stress and CVH in a multiethnic sample of adults free of cardiovascular disease at baseline. Methods and Results We performed a cross‐sectional analysis of 3579 community‐based men and women, aged 45 to 84 years, of the Multi‐Ethnic Study of Atherosclerosis from data collected between 2000 and 2002. Work‐related stress (yes/no) was assessed by a self‐administered questionnaire. CVH was measured by the American Heart Association's Life's Simple 7 metrics (smoking, physical activity, body mass index, diet, total cholesterol, blood pressure, and blood glucose). Each metric contributed 0, 1, or 2 points if in the poor, intermediate, or ideal range, respectively. The aggregated CVH score was 0 to 14 points and categorized as inadequate (0–8 points), average (9–10 points), and optimal (11–14 points). Polytomous logistic regression was used to estimate the association between work‐related stress and CVH, adjusting for sociodemographic factors. The mean±SD age was 57±8 years, and 48% were women. Work‐related stress was reported by 20% of participants. In fully adjusted models, participants with work‐related stress had lower odds of having average (adjusted odds ratio [OR], 0.75 [95% CI, 0.62–0.92]) and optimal (adjusted OR, 0.73 [95% CI, 0.58–0.92]) CVH scores compared with participants without work‐related stress. Conclusions Work‐related stress was associated with unfavorable CVH. These findings underscore the importance of workplace psychological well‐being and suggest the need for studies on interventions that may reduce work‐related stress and promote CVH.

Although the echocardiographic:derived ratio of tricuspid annular plane systolic excursion (TAPSE) to pulmonary arterial systolic pressure (PASP) is an important prognostic tool in heart failure (HF), the relation with 6-minute walk distance (6MWD) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) is less established. We sought to establish the normative values of TAPSE:PASP among older adults without cardiovascular disease (CVD) and evaluate the relation with NT-proBNP and 6MWD. Among 1,542 participants of the Multi-Ethnic Study of Atherosclerosis-HF ancillary study, the cross-sectional association of TAPSE:PASP with the outcomes of 6MWD and NT-proBNP was analyzed using multivariable linear regression, with progressive adjustment for sociodemographic and CVD risk factors. Our cohort had a mean age (SD) of 73 ± 8 years, 55% women, and a mean TAPSE:PASP ratio of 0.68 ± 0.16. In the unadjusted analysis, increasing tertiles of TAPSE:PASP were associated with younger age, less diabetes, higher estimated glomerular filtration rate, and less antihypertensive medication use. The TAPSE:PASP ratio significantly correlated with both 6MWD and NT-proBNP in the fully adjusted models. A 1-unit increment in TAPSE:PASP was associated with an adjusted 9.9% (4.8% to 15.2%) higher 6MWD, whereas a 1-unit increment in TAPSE:PASP was associated with an adjusted 38.0% (16.0% to 54.2%) lower NT-proBNP. There was a significant gender interaction of the association of TAPSE:PASP ratio and 6MWD, with stronger association seen in women. Among multiethnic older adults free of clinical CVD, the TAPSE:PASP ratio decreased with age, especially in women and was associated with decreased 6MWD and increasing NT-proBNP, the markers of subclinical HF.

Background:Hepatocyte growth factor (HGF) is a cytokine linked to incident heart failure (HF), particularly HF with preserved ejection fraction (HFpEF). Increases in left ventricular (LV) mass and concentric remodelling defined by increasing mass-to-volume (M:V) ratios are imaging risk markers for HFpEF. We aimed to determine if HGF is associated with adverse LV remodelling. Methods:We studied 4907 participants in the Multi-Ethnic Study of Atherosclerosis (MESA), free of cardiovascular disease and HF at baseline, who had HGF measured and cardiac magnetic resonance imaging (CMR) performed at baseline. Of these, 2921 completed a second CMR at 10 years. We examined the cross-sectional and longitudinal associations of HGF and LV structural parameters using multivariable-adjusted linear mixed-effect models, adjusting for cardiovascular disease risk factors and N-terminal pro B-type natriuretic peptide. Results:The mean (SD) for age was 62 (10) years; 52% were female. Median (interquartile range) for HGF level was 890 pg/mL (745-1070). At baseline, the highest HGF tertile, compared to the lowest, was associated with a greater M:V ratio (relative difference 1.94 [95% confidence interval [CI]: 0.72, 3.17]) and lower LV end-diastolic volume (-2.07 mL [95% CI: -3.72, -0.42)]. In longitudinal analysis, the highest HGF tertile was associated with increasing M:V ratio (10-year difference: 4.68 [95% CI: 2.64, 6.72]) and decreasing LV end-diastolic volume (-4.74 [95% CI: -6.87, -2.62]). Conclusions:In a community-based cohort, higher HGF levels were independently associated with a concentric LV remodelling pattern of increasing M:V ratio and decreasing LV end-diastolic volume by CMR over 10 years. These associations may reflect an intermediate phenotype explaining the association of HGF with HFpEF risk.

Objective To evaluate the association between ideal cardiovascular health (CVH) and adipokine levels. Adipokines are hormones implicated in obesity and its cardiometabolic consequences. The concept of ideal CVH was introduced to promote 7 key health factors and behaviors in the general population. Previous studies have found strong associations between obesity and ideal CVH. However, existing literature on the link between CVH and adipokines is scarce. Methods We studied 1842 Multi-Ethnic Study of Atherosclerosis participants free of cardiovascular disease who had 7 CVH metrics (smoking, body mass index, physical activity, diet, total cholesterol, blood pressure, and fasting blood glucose) measured at baseline and serum adipokine levels measured at a median of 2.4 years later. Each CVH metric was assigned a score of 0 (poor), 1 (intermediate), or 2 (ideal), and all scores were summed for a total CVH score (0-14). The total CVH scores of 0 to 8, 9 to 10, and 11 to 14 were considered inadequate, average, and optimal, respectively. We used multivariable linear regression models to assess the nonconcurrent associations between the CVH score and log-transformed adipokine levels. Results The mean age was 62.1 ± 9.8 years; 50.2% of participants were men. After adjusting for sociodemographic factors, a 1-unit higher CVH score was significantly associated with 4% higher adiponectin and 15% and 1% lower leptin and resistin levels. Individuals with optimal CVH scores had 27% higher adiponectin and 56% lower leptin levels than those with inadequate CVH scores. Similar trends were observed for those with average versus inadequate CVH scores. Conclusion In a multi-ethnic cohort free of cardiovascular disease at baseline, individuals with average and optimal CVH scores had a more favorable adipokine profile than those with inadequate CVH scores.

BACKGROUND:Female-specific factors of grand multiparity (≥5 births) and early menopause age are associated with an increased risk of cardiovascular disease (CVD). However, mechanisms are incompletely understood. Carotid plaque is a marker of subclinical atherosclerosis and associated with increased CVD risk. We evaluated the association of female-specific factors with plaque burden.METHODS:We included 2,313 postmenopausal women in the Multi-Ethnic Study of Atherosclerosis, free of clinical CVD, whose parity and menopause age were ascertained by questionnaires and carotid plaque measured by ultrasound at baseline and 10 years later. Parity was categorized as nulliparity (reference), 1-2, 3-4 and ≥5 live births. Menopause age was categorized as <45, 45-49, 50-54 (reference) and ≥55 years. Multivariable regression was performed to evaluate the association of parity and menopause age with carotid plaque presence (yes/no) and extent [carotid plaque score (CPS)].RESULTS:The mean age was 64±9 years; 52.3% had prevalent carotid plaque at baseline. Compared to nulliparity, grand multiparity was significantly associated with prevalent carotid plaque after adjustment for CVD risk factors (prevalence ratio 1.17 (95% CI 1.03-1.35)) and progression of CPS over 10 years [percent difference 13% (95% CI 3-23)]. There was not any significant association of menopause age with carotid plaque presence or progression in fully-adjusted models.CONCLUSION:In a multiethnic cohort, grand multiparity was independently associated with carotid plaque presence and progression. Early menopause, a known risk factor for CVD, was not captured by carotid plaque in this study. These findings may have implications for refining CVD risk assessment in women.

Background Although there has been a decrease in the incidence of ST-segment-elevation myocardial infarction (STEMI) in the United States, this trend might be stagnant or increasing in young women. We assessed the trends, characteristics, and outcomes of STEMI in women aged 18 to 55 years. Methods and Results We identified 177 602 women aged 18 to 55 with the primary diagnosis of STEMI from the National Inpatient Sample during years 2008 to 2019. We performed trend analyses to assess hospitalization rates, cardiovascular disease (CVD) risk factor profile, and in-hospital outcomes stratified by three age subgroups (18-34, 35-44, and 45-55 years). We found STEMI hospitalization rates were decreased in the overall study cohort from 52 per 100 000 hospitalizations in 2008 to 36 per 100 000 in 2019. This was driven by decreased proportion of hospitalizations in women aged 45 to 55 years (74.2% to-71.7%; P<0.001). Proportion of STEMI hospitalizationincreased in women aged 18-34 (4.7%-5.5%; P<0.001) and 35-44 years (21.2%-22.7%; P<0.001). The prevalence of traditional and non-traditional female-specific or female-predominant CVD risk factors increased in all age subgroups. The adjusted odds of in-hospital mortality in the overall study cohort and age subgroups were unchanged throughout the study period. Additionally, we observed an increase in the adjusted odds of cardiogenic shock, acute stroke, and acute kidney injury in the overall cohort over the study period. Conclusions STEMI hospitalizations are increasing among women aged <45 years, and in-hospital mortality has not changed over the past 12 years in women aged <55 years. Future studies on the optimization of risk assessment and management of STEMI in young women are urgently needed.

Introduction: Adipokines are hormones implicated in obesity and its cardiometabolic consequences. The concept of ideal cardiovascular health (CVH) was introduced to monitor and promote 7 (now 8) key health factors and behaviors in the general population. Although prior studies have found strong associations between obesity and ideal CVH, the link between CVH and adipokines has not been elucidated. We examined the associations between CVH and adipokine levels in MESA. Methods: We studied 1,842 MESA participants who were free of cardiovascular disease at baseline, had 7 CVH metrics (smoking, body mass index, physical activity, diet, total cholesterol, blood pressure and fasting blood glucose) measured at exam 1 (2000-2002) and adipokine levels measured at either exam 2 or 3 (2002-2004 or 2004-2005). Each metric was assigned a score of 0(poor), 1(intermediate) and 2(ideal), and summed to obtain a total CVH score (0 -14). We used multivariable linear regression models to assess the non-concurrent cross-sectional associations between CVH score and log-transformed serum adipokine levels, adjusting for sociodemographic factors. Results: The mean ± SD age was 62.1 ± 9.8 years and 50.2% of participants were men. Median (IQR) adiponectin, leptin and resistin levels were 17.4 (11.8 - 26.3) mcg/mL,13.3 (5.6 - 28.2) ng/mL and 15.0 (11.9 - 19.0) ng/mL, respectively. A 1 unit higher CVH score was significantly associated with 4% higher adiponectin, 15% and 1% lower leptin and resistin levels respectively, after adjusting for sociodemographic factors. Individuals with optimal CVH scores had 27% higher adiponectin and 56% lower leptin levels compared to those with inadequate CVH scores. Similar results were obtained for those with average scores (Table). Conclusion: In a multi-ethnic cohort free of cardiovascular disease at baseline, individuals with average and optimal CVH scores had higher adiponectin and lower leptin and resistin levels compared to those with inadequate CVH scores.

Background: Obesity leads to adipocyte hypertrophy and adipokine dysregulation and is an independent risk factor for venous thromboembolism (VTE). However, the asso-ciation between adipokines and VTE is not well established.Objectives: To examine whether adipokines are associated with increased risk of incident VTE.Methods: We studied 1888 participants of the Multi-Ethnic Study of Atherosclerosis cohort who were initially free of VTE and had adipokine (adiponectin, leptin, and resistin) levels measured at either examination 2 or 3 (2002-2004 or 2004-2005, respectively). During follow-ups, VTE was ascertained through hospitalization records and death certificates by using ICD-9 and 10 codes. We used multivariable Cox pro-portional hazards regression to assess the association between 1 standard deviation (SD) log-transformed increments in adipokines and incident VTE.Results: The mean & PLUSMN; SD age was 64.7 & PLUSMN; 9.6 years, and 49.8% of participants were women. Medians (interquartile range) of adiponectin, leptin, and resistin were 17.3 (11.8-26.2) mcg/mL, 13.5 (5.6-28.2) ng/mL, and 15.0 (11.9-19.0) ng/mL, respectively. There were 78 incident cases of VTE after a median of 9.7 (5.0-12.4) years of follow-up. After adjusting for sociodemographics, smoking, and physical activity, the hazard ratios (95% CIs) per 1 SD increment of adiponectin, leptin, and resistin were 1.14 (0.90-1.44), 1.29 (1.00-1.66), and 1.38 (1.09-1.74), respectively. The association for resistin per-sisted after further adjustments for body mass index and computed tomography- derived total visceral adipose tissue area. Conclusion: Higher resistin levels were independently associated with greater risk of incident VTE. Larger prospective cohort studies are warranted to confirm this association.

Introduction: Obesity leads to adipocyte hypertrophy and adipokine dysregulation, with implications for cardiovascular disease. Prior studies have linked adipokines to many obesity-related pathologies, with higher adiponectin levels considered cardioprotective whereas higher leptin and resistin are generally considered deleterious to cardiovascular health. In this regard, obesity is an independent risk factor for incident venous thromboembolism [VTE (deep vein thrombosis or pulmonary embolus)]. However, the associations of adipokines with VTE are not well established. Methods: We studied 1,888 MESA participants who were initially free of VTE and had adipokine levels measured at either visit 2 or 3. VTE was ascertained through hospitalization records and death certificates using ICD-9 and 10 codes. We used multivariable Cox proportional hazards regression to assess the association between 1 standard deviation (SD) log-transformed increments in adipokines and incident VTE. Results: The mean ± SD age was 64.7 ± 9.6 years; 50% women, 40% White, 20% Black, 26% Hispanic, and 13% Chinese - American participants. Median (IQR) of adiponectin, leptin and resistin were 17.3 (11.8 - 26.2) mcg/mL ,13.5 (5.6 - 28.2) ng/mL, and 15.0 (11.9 - 19.0) ng/mL respectively. There were 78 incident cases of VTE after a median of 9.7 (5.0 - 12.4) years of follow-up. The adjusted hazard ratio (95%) per 1 SD increment of adiponectin, leptin and resistin were 1.10 (0.86 - 1.42), 1.30 (0.97 - 1.74) and 1.39 (1.10 - 1.75), respectively (Table 1, Model 1 ). Associations for resistin persisted after adjustment for body mass index (Model 2) and computed tomography derived total visceral and subcutaneous adipose tissue area (Model 3). Conclusions: In this multi-ethnic cohort of adults free of cardiovascular disease at baseline, higher resistin levels were independently associated with greater risk of incident VTE. Larger prospective cohort studies are warranted to confirm this association.

Introduction Multiparity has been associated with increased risk of cardiovascular disease (CVD). Inflammation may be a mechanism linking parity to CVD. We investigated the association between parity and later-life markers of inflammation. Methods We studied 3,454 female MESA participants aged 45–84, free of CVD, who had data on parity and inflammatory markers. Parity was categorized as 0 (reference), 1–2, 3–4, or ≥5. Linear regression was used to evaluate the association between parity and natural log-transformed levels of fibrinogen, D-dimer, GlycA, high sensitivity C-reactive protein (hsCRP), and interleukin-6 (IL-6). Results Mean age was 62 ± 10 years. The proportion of women with nulliparity, 1–2, 3–4, and ≥5 live births were 18, 39, 29, and 14%, respectively. There was no association between parity and fibrinogen. Women with grand multiparity (≥5 live births) had 28, 10, and 18% higher levels of hsCRP, IL-6 and D-dimer, respectively, compared to nulliparous women, after adjustment for demographic factors. After additional adjustment for CVD risk factors, women with 1–2 and 3–4 live births had higher hsCRP and women with 1–2 live births had higher GlycA. Conclusion In this diverse cohort of middle-to-older aged women, we found that higher parity was associated with some inflammatory markers; however, these associations were largely attenuated after adjustment for CVD risk factors. There was no clear dose-response relationship between parity and these inflammatory markers. Future studies are needed to evaluate how inflammation may influence the link between parity and CVD and whether healthy lifestyle/pharmacotherapies targeting inflammation can reduce CVD risk among multiparous women. Clinical trial registration The MESA cohort design is registered at clinicaltrials.gov as follows: https://clinicaltrials.gov/ct2/show/NCT00005487.

Background: Ideal cardiovascular health (CVH) is associated with a lower incidence of cardiovascular disease. Extracoronary calcification (ECC)—measured at the aortic valve, mitral annulus, ascending thoracic aorta, and descending thoracic aorta—is an indicator of systemic atherosclerosis. This study examined whether favorable CVH was associated with a lower risk of ECC. Methods: We analyzed data from MESA (Multi-Ethnic Study of Atherosclerosis) participants aged 45 to 84 years without cardiovascular disease at baseline. ECC was measured by noncontrast cardiac computed tomography scan at baseline and after an average of 2.4 years. Prevalent ECC was defined as an Agatston score >0 at the baseline scan. Incident ECC was defined as Agatston score >0 at the follow-up scan among participants with Agatston score of 0 at the baseline scan. Each CVH metric (smoking, physical activity, body mass index, diet, blood pressure, total cholesterol, and blood glucose) was scored 0 to 2 points, with 2 indicating ideal; 1, intermediate; and 0, poor. The aggregated CVH score was 0 to 14 points (0–8, inadequate; 9–10, average; 11–14, optimal). We used Poisson and linear mixed-effects regression models to examine the association between CVH and ECC adjusted for sociodemographic factors. Results: Of 6504 participants, 53% were women with a mean age (SD) of 62 (10) years. Optimal and average CVH scores were associated with lower ECC prevalence, incidence, and extent. For example, optimal CVH scores were associated with 57%, 56%, 70%, and 54% lower risk of incident aortic valve calcification, mitral annulus calcification, ascending thoracic aorta calcification, and descending thoracic aorta calcification, respectively. In addition, optimal and average CVH scores were associated with lower ECC progression at 2 years, although these associations were only significant for mitral annulus calcification and descending thoracic aorta calcification. Conclusions: In this multiethnic cohort, favorable CVH was associated with a lower risk of extracoronary atherosclerosis. These findings emphasize the importance of primordial prevention as an intervention to reduce the burden of cardiovascular disease.

Background: Polycystic ovary syndrome (PCOS) is a common endocrine pathology affecting women of reproductive age characterized by chronic anovulation, hyperandrogenism, and polycystic ovaries. Coronary artery calcification (CAC) is a marker of subclinical atherosclerosis and prognostic of cardiovascular disease (CVD) risk. Some studies have shown that women with PCOS have a greater risk of CAC; however, a few others report contrary findings. The objective of this study is to examine and quantify the association between PCOS and CAC.Materials and Methods: We searched EMBASE, Google Scholar, PubMed, and Web of Science from inception to November 2021 to identify studies that provided information on PCOS and CAC. We used a random-effects model to aggregate the odds ratios (ORs) for CAC (score >0) among women with PCOS compared with controls adjusted for sociodemographic characteristics and CVD risk factors.Results: From the 36 articles reviewed, 3 prospective cohort and 4 cross-sectional studies met the inclusion criteria with a total of 2341 participants. Six studies used CAC > 0 as an outcome and were included in the pooled analysis. Using the Hartung-Knapp-Sidik-Jonkman method, the pooled adjusted ORs for the associations between PCOS and the presence of CAC were 2.48 (95% confidence interval: 2.11-2.84) with no significant heterogeneity (I-2 = 0.10%, p = 0.97) for the cohort studies and 1.88 (0.71-3.06) with no significant heterogeneity (I-2 = 13.95%, p = 0.87) for the cross-sectional studies.Conclusion: In pooled analyses, women with PCOS had approximately twofold greater odds of having CAC compared with women without PCOS. However, additional prospective studies will be needed to further understand the relationship between PCOS and CAC.

Background Hepatocyte growth factor (HGF) is a biomarker with potential for use in the diagnosis, treatment and prognostication of cardiovascular disease (CVD). Elevated HGF is associated with calcification in the coronary arteries. However, knowledge is limited on the role HGF may play in extracoronary calcification (ECC). This study examined whether HGF is associated with ECC in the aortic valve (AVC), mitral annulus (MAC), ascending thoracic aorta and descending thoracic aortic (DTAC).Methods At baseline, adults aged 45–84 years, free of CVD, in the Multi-Ethnic Study of Atherosclerosis had HGF and ECC measured by ELISA and cardiac CT scan, respectively. ECC measurements were repeated after an average of 2.4 years of follow-up. Prevalent ECC was defined as Agatston score >0 at baseline. Incident ECC was defined as Agatston score >0 at follow-up among participants with Agatston score=0 at baseline. We used Poisson and linear mixed-effects regression models to estimate the association between HGF and ECC, adjusted for sociodemographic and CVD risk factors.Results Of 6648 participants, 53% were women. Mean (SD) age was 62 (10) years. Median (IQR) of HGF was 905 (757-1087) pg/mL. After adjustment for CVD risk factors, the highest HGF levels (tertile 3) were associated with greater prevalence and extent of AVC, MAC and DTAC at baseline compared with the lowest tertile (tertile 1). Additionally, the risk of incident AVC and MAC increased by 62% and 45%, respectively, in demographic-adjusted models. However, the associations were not statistically significant in fully adjusted models. The highest HGF levels were also associated with 10% and 13% increase in MAC and DTAC progression, respectively, even after adjustment for CVD risk factors.Conclusion Higher HGF levels were significantly associated with a greater risk of calcification at some extracoronary sites, suggesting an alternate biological pathway that could be targeted to reduce CVD risk.

Background: Multiparity is a risk factor for cardiovascular disease (CVD). However, the mechanisms of this relationship are unknown. Adipokines may predispose multiparous women to certain cardiometabolic complications that can increase their risk of future CVD. Materials and Methods: We studied 973 female participants of the Multi-Ethnic Study of Atherosclerosis free of CVD, who had complete data on parity and adipokines measured at Examination 2 or 3 (randomly assigned). Parity was categorized as nulliparity, 1-2, 3-4, and ≥5 live births. Multivariable linear regression was used to evaluate the association of parity with leptin, resistin, and adiponectin levels. Results: The women had mean age of 65 ± 9 years. After adjustment for age, race/ethnicity, study site, education, menopause status, smoking, physical activity, use of hormone therapy, and waist circumference, a history of grand multiparity (≥5 live births) was associated with 11% higher resistin levels (95% confidence interval [CI] 0-23) and 3-4 live births was associated with 23% higher leptin levels (95% CI 7-42), compared with nulliparity. After adjustment for computed tomography-measured visceral fat, the association of 3-4 live births with leptin remained significant. There were no significant associations of parity with adipokines after further adjustment for additional CVD risk factors. Multigravidity (but not parity) was inversely associated with adiponectin levels. Conclusions: In a multiethnic cohort of women, greater parity was associated with resistin and leptin; however, this association was attenuated after accounting for CVD risk factors. Dysregulation of adipokines could contribute to the excess CVD risk associated with multiparity. Further studies are needed to determine whether adipokines independently mediate the relationship between multiparity and CVD. Clinical trials registration: The MESA cohort is registered at NCT00005487.

Background: Psychosocial stress is associated with an increased risk of cardiovascular disease (CVD). The relationship between financial strain, a toxic form of psychosocial stress, and ideal cardiovascular health (CVH) is not well established. This study examined whether financial strain was associated with poorer CVH in a multi-ethnic cohort free of CVD at baseline. Methods: This is a cross-sectional analysis of 6,468 men and women aged 45-84 years. Two measures of financial strain were assessed: ongoing financial strain and ongoing financial strain for >6 months. Responses to both measures were categorized as yes or no. CVH was measured from 7 metrics (smoking, physical activity, body mass index, diet, total cholesterol, blood pressure, and blood glucose). A CVH score was calculated from points assigned to the categories of each metric (poor = 0 points; intermediate = 1 point; ideal = 2 points) for a total of 14 points. Multinomial logistic regression was used to examine the association of financial strain with the CVH score (inadequate 0-8, average 9-10, and optimal 11-14 points) and number of ideal metrics, adjusting for sociodemographic factors. Results: The mean age (SD) was 62 (10) and 53% were women. Ongoing financial strain was reported by 25% of participants while 23% reported ongoing financial strain for > 6 months. Participants who reported ongoing financial strain had lower odds of having average (0.82 [0.71, 0.94]) and optimal (0.73 [0.62, 0.87]) CVH scores ( Table ). Likewise, ongoing financial strain for >6 months was associated with lower odds of having average (0.81 [0.70, 0.93]) and optimal (0.70 [0.58, 0.83]) CVH scores. Similar results were observed for the association of financial strain with the number of ideal metrics. Conclusions: Financial strain was associated with poorer CVH. More research is needed to understand this relationship so the burden of CVD can be decreased, particularly among people experiencing financial hardship.

Background: Multiparity may be associated with an increased risk of cardiovascular disease (CVD); however, responsible mechanisms are incompletely understood. Carotid artery plaque is a marker of subclinical atherosclerosis and an indicator of CVD risk. We hypothesized that multiparity would be independently associated with greater atherosclerosis, as measured by carotid plaque. Methods: We included women in MESA free of CVD who had data on parity ascertained by questionnaire and carotid plaque measured by B-mode ultrasound at baseline. Parity was categorized as nulliparity (ref), 1-2, 3-4 and ≥5 live births. Multivariable logistic and linear regression were performed to evaluate the association of parity categories with carotid plaque presence (yes/no) and extent [carotid plaque score (CPS)], respectively. Results: Of 2789 women included, 38% were White, 29% Black, 12% Chinese, and 22% Hispanic with a mean (SD) age of 62±10 yrs. Carotid plaque prevalence increased with greater parity ( Figure) . Compared to nulliparity, a history of 1-2 live births, 3-4 live births, and grand multiparity (≥5 live births) were significantly associated with carotid plaque presence after adjustment for demographics ( Table, Model 1 ) . Grand multiparity remained significantly associated with carotid plaque presence after full covariate adjustment [OR 1.42 (95% 1.01-2.01), Model 2]. In addition, a history of 1-2 live births and grand multiparity was associated with a greater CPS compared to nulliparity after adjustment for demographics (Model 1). The association of parity with CPS was attenuated and no longer significantly associated with CPS after further adjustment for lifestyle and CVD risk factors (Model 2). Conclusion: In a multiethnic cohort of US women, grand multiparity was independently associated with carotid plaque presence. Further studies are needed to understand the increased risk and prognostic significance of subclinical atherosclerosis among parous women.