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Background Periodontitis is a chronic inflammatory disease common among adults. It has been suggested that periodontal disease (PD) may be a contributing risk factor for cardiovascular disease; however, pathways underlying such a relationship require further investigation. Methods and Results A total of 665 men (mean age 68±9 years) and 611 women (mean age 67±9 years) enrolled in the MESA (Multiethnic Study of Atherosclerosis) underwent PD assessment using a 2‐item questionnaire at baseline (2000–2002) and had cardiovascular magnetic resonance 10 years later. PD was defined when participants reported either a history of periodontitis or gum disease or lost teeth caused by periodontitis or gum disease. Multivariable linear regression models were constructed to assess the associations of baseline self‐reported PD with cardiovascular magnetic resonance–obtained measures of interstitial myocardial fibrosis (IMF), including extracellular volume and native T1 time. Men with a self‐reported history of PD had greater extracellular volume percent (ß=0.6%±0.2, P=0.01). This association was independent of age, left ventricular mass, traditional cardiovascular risk factors, and history of myocardial infarction. In a subsequent model, substituting myocardial infarction for coronary artery calcium score, the association of PD with IMF remained significant (ß=0.6%±0.3, P=0.03). In women, a self‐reported history of PD was not linked to higher IMF. Importantly, a self‐reported history of PD was not found to be associated with myocardial scar independent of sex (odds ratio, 1.01 [95% CI, 0.62–1.65]; P=0.9). Conclusions In a community‐based setting, men but not women with a self‐reported PD history at baseline were found to be associated with increased measures of IMF. These findings support a plausible link between PD, a proinflammatory condition, and subclinical IMF.

Background Coronary artery calcium testing using noncontrast cardiac computed tomography is a guideline‐indicated test to help refine eligibility for aspirin in primary prevention. However, access to cardiac computed tomography remains limited, with carotid ultrasound used much more often internationally. We sought to update the role of aspirin allocation in primary prevention as a function of subclinical carotid atherosclerosis. Methods and Results The study included 11 379 participants from the MESA (Multi‐Ethnic Study of Atherosclerosis) and ARIC (Atherosclerosis Risk in Communities) studies. A harmonized carotid plaque score (range, 0–6) was derived using the number of anatomic sites with plaque from the left and right common, bifurcation, and internal carotid artery on ultrasound. The 5‐year number needed to treat and number needed to harm as a function of the carotid plaque score were calculated by applying a 12% relative risk reduction in atherosclerotic cardiovascular disease (ASCVD) events and 42% relative increase in major bleeding events related to aspirin use, respectively. The mean age was 57 years, 57% were women, 23% were Black, and the median 10‐year ASCVD risk was 12.8%. The 5‐year incidence rates (per 1000 person‐years) were 5.5 (4.9–6.2) for ASCVD and 1.8 (1.5–2.2) for major bleeding events. The overall 5‐year number needed to treat with aspirin was 306 but was 2‐fold lower for individuals with carotid plaque versus those without carotid plaque (212 versus 448). The 5‐year number needed to treat was less than the 5‐year number needed to harm when the carotid plaque score was ≥2 for individuals with ASCVD risk 5% to 20%, whereas the presence of any carotid plaque demarcated a favorable risk–benefit for individuals with ASCVD risk >20%. Conclusions Quantification of subclinical carotid atherosclerosis can help improve the allocation of aspirin therapy.

Background Pulse wave velocity (PWV) is a noninvasive measure of arterial stiffness and predictor of cardiovascular disease. However, the association between PWV and vascular calcification across different vascular beds has not been fully investigated. This study aimed to quantify the association between PWV and multiterritory calcification and to explore whether PWV can identify individuals with vascular calcification beyond traditional risk factors. Methods and Results Among 1351 older adults (mean age, 79.2 years [SD, 4.1]) from the ARIC (Atherosclerosis Risk in Communities) study, we measured segment‐specific PWVs: heart–carotid, heart–femoral, carotid–femoral, heart–ankle, brachial–ankle, and femoral–ankle. Dependent variables were high calcium score (≥75th percentile of Agatston score) across different vascular beds: coronary arteries, aortic valve ring, aortic valve, mitral valve, ascending aorta, and descending aorta. Quartiles of carotid–femoral, heart–femoral, heart–ankle, and brachial–ankle PWV were significantly associated with coronary artery calcium (eg, adjusted odds ratio [OR] for the highest versus lowest quartile of carotid–femoral PWV, 1.84 [95% CI, 1.24–2.74]). Overall, PWVs were most strongly associated with descending aorta calcification, with significant results for carotid–femoral, heart–femoral, heart–ankle, and brachial–ankle PWV (eg, adjusted OR for the highest versus lowest quartile of carotid–femoral PWV, 3.99 [95% CI, 2.61–6.17]). In contrast, femoral–ankle PWV was inversely associated with descending aorta calcification. Some PWVs improved the discrimination of coronary artery calcium and descending aorta calcification beyond traditional risk factors. Conclusions The associations of PWV with vascular calcification varied substantially across segments, with descending aorta calcification most closely linked to PWVs. Our study suggests that some PWVs, especially carotid–femoral PWV, are helpful to identify individuals with coronary artery calcium and descending aorta calcification.

Background Although there is research on the impact of social determinants of health (SDOHs) on cardiovascular health, most existing evidence is based on individual SDOH components. We evaluated the impact of cumulative SDOH burden on cardiovascular risk factors, subclinical atherosclerosis, and incident cardiovascular disease events. Methods and Results We included 6479 participants from the MESA (Multi‐Ethnic Study of Atherosclerosis). A weighted aggregate SDOH score representing the cumulative number of unfavorable SDOHs, identified from 14 components across 5 domains (economic stability, neighborhood and physical environment, community and social context, education, and health care system access) was calculated and divided into quartiles (quartile 4 being the least favorable). The impact of cumulative SDOH burden on cardiovascular risk factors (hypertension, diabetes, dyslipidemia, smoking, and obesity), systemic inflammation, subclinical atherosclerosis, and incident cardiovascular disease was evaluated. Increasing social disadvantage was associated with increased odds of all cardiovascular risk factors except dyslipidemia. Smoking was the risk factor most strongly associated with worse SDOH (odds ratio [OR], 2.67 for quartile 4 versus quartile 1 [95% CI, 2.13–3.34]). Participants within SDOH quartile 4 had 33% higher odds of increased high‐sensitivity C‐reactive protein (OR, 1.33 [95% CI, 1.11–1.60]) and 31% higher risk of all cardiovascular disease (hazard ratio, 1.31 [95% CI, 1.03–1.67]), yet no greater burden of subclinical atherosclerosis (OR, 1.01 [95% CI, 0.79–1.29]), when compared with those in quartile 1. Conclusions Increasing social disadvantage was associated with more prevalent cardiovascular risk factors, inflammation, and incident cardiovascular disease. These findings call for better identification of SDOHs in clinical practice and stronger measures to mitigate the higher SDOH burden among the socially disadvantaged to improve cardiovascular outcomes.

Background Depression is a nontraditional risk factor for cardiovascular disease (CVD). Data on the association of depression and poor mental health with CVD and suboptimal cardiovascular health (CVH) among young adults are limited. Methods and Results We used data from 593 616 young adults (aged 18–49 years) from the 2017 to 2020 Behavioral Risk Factor Surveillance System, a nationally representative survey of noninstitutionalized US adults. Exposures were self‐reported depression and poor mental health days (PMHDs; categorized as 0, 1–13, and 14–30 days of poor mental health in the past 30 days). Outcomes were self‐reported CVD (composite of myocardial infarction, angina, or stroke) and suboptimal CVH (≥2 cardiovascular risk factors: hypertension, hypercholesterolemia, overweight/obesity, smoking, diabetes, physical inactivity, and inadequate fruit and vegetable intake). Using logistic regression, we investigated the association of depression and PMHDs with CVD and suboptimal CVH, adjusting for sociodemographic factors (and cardiovascular risk factors for the CVD outcome). Of the 593 616 participants (mean age, 34.7±9.0 years), the weighted prevalence of depression was 19.6% (95% CI, 19.4–19.8), and the weighted prevalence of CVD was 2.5% (95% CI, 2.4–2.6). People with depression had higher odds of CVD than those without depression (odds ratio [OR], 2.32 [95% CI, 2.13–2.51]). There was a graded association of PMHDs with CVD. Compared with individuals with 0 PMHDs, the odds of CVD in those with 1 to 13 PMHDs and 14 to 30 PHMDs were 1.48 (95% CI, 1.34–1.62) and 2.29 (95% CI, 2.08–2.51), respectively, after adjusting for sociodemographic and cardiovascular risk factors. The associations did not differ significantly by sex or urban/rural status. Individuals with depression had higher odds of suboptimal CVH (OR, 1.79 [95% CI, 1.65–1.95]) compared with those without depression, with a similar graded relationship between PMHDs and suboptimal CVH. Conclusions Depression and poor mental health are associated with premature CVD and suboptimal CVH among young adults. Although this association is likely bidirectional, prioritizing mental health may help reduce CVD risk and improve CVH in young adults.

Background Mobile health (mHealth) has an emerging role in the prevention of cardiovascular disease. This study evaluated possible inequities in mHealth access in older adults. Methods and Results mHealth access was assessed from 2019 to 2020 in MESA (Multi‐Ethnic Study of Atherosclerosis) telephone surveys of 2796 participants aged 62 to 102 years. A multivariable logistic regression model adjusted for general health status assessed associations of mHealth access measures with relevant demographic, socioeconomic, and cognitive characteristics. There were lower odds of all access measures with older age (odds ratios [ORs], 0.37–0.59 per 10 years) and annual income

Background The value of coronary artery calcium (CAC) in the allocation of PCSK9i (proprotein convertase subtilisin/kexin type 9 inhibitors) among individuals without clinically evident atherosclerotic cardiovascular disease (ASCVD) is unknown for indications that do not require confirmed familial hypercholesterolemia. We aimed to assess the ability of CAC to stratify ASCVD risk under 3 non–familial hypercholesterolemia PCSK9i allocation paradigms. Methods and Results We included participants without clinically evident ASCVD from MESA (Multi‐Ethnic Study of Atherosclerosis), CARDIA (Coronary Artery Risk Development in Young Adults) study, DHS (Dallas Heart Study), and HNR (Heinz Nixdorf Recall) study. Three PCSK9i eligibility scenarios were defined: a broad scenario informed only by high low‐density lipoprotein cholesterol levels (N=567), a restrictive one combining higher low‐density lipoprotein cholesterol levels and presence of ≥2 additional risk factors (N=127), and a high‐risk scenario where individuals with subclinical organ damage or high estimated risk would be treated to achieve low‐density lipoprotein cholesterol

Background Lipoprotein(a) (Lp(a)) is a potent causal risk factor for cardiovascular events and mortality. However, its relationship with subclinical atherosclerosis, as defined by arterial calcification, remains unclear. This study uses the ARIC (Atherosclerosis Risk in Communities Study) to evaluate the relationship between Lp(a) in middle age and measures of vascular and valvular calcification in older age. Methods and Results Lp(a) was measured at ARIC visit 4 (1996–1998), and coronary artery calcium (CAC), together with extracoronary calcification (including aortic valve calcium, aortic valve ring calcium, mitral valve calcification, and thoracic aortic calcification), was measured at visit 7 (2018–2019). Lp(a) was defined as elevated if >50 mg/dL and CAC/extracoronary calcification were defined as elevated if >100. Logistic and linear regression models were used to evaluate the association between Lp(a) and CAC/extracoronary calcification, with further stratification by race. The mean age of participants at visit 4 was 59.2 (SD 4.3) years, with 62.2% women. In multivariable adjusted analyses, elevated Lp(a) was associated with higher odds of elevated aortic valve calcium (adjusted odds ratio [aOR], 1.82; 95% CI, 1.34–2.47), CAC (aOR, 1.40; 95% CI, 1.08–1.81), aortic valve ring calcium (aOR, 1.36; 95% CI, 1.07–1.73), mitral valve calcification (aOR, 1.37; 95% CI, 1.06–1.78), and thoracic aortic calcification (aOR, 1.36; 95% CI, 1.05–1.77). Similar results were obtained when Lp(a) and CAC/extracoronary calcification were examined on continuous logarithmic scales. There was no significant difference in the association between Lp(a) and each measure of calcification by race or sex. Conclusions Elevated Lp(a) at middle age is significantly associated with vascular and valvular calcification in older age, represented by elevated CAC, aortic valve calcium, aortic valve ring calcium, mitral valve calcification, thoracic aortic calcification. Our findings encourage assessing Lp(a) levels in individuals with increased cardiovascular disease risk, with subsequent comprehensive vascular and valvular assessment where elevated.

Background Sodium‐glucose cotransporter‐2 inhibitors (SGLT2is) and glucagon‐like peptide‐1 receptor agonists (GLP‐1RAs) mitigate cardiovascular risk in individuals with type 2 diabetes, but most eligible patients do not receive them. We characterized temporal trends in SGLT2i and GLP‐1RA use by cardiologists compared with other groups of clinicians. Methods and Results We conducted a descriptive analysis of serial, cross‐sectional data derived from IQVIA’s National Prescription Audit, a comprehensive audit capturing ≈90% of US retail prescription dispensing and projected to population‐level data, to estimate monthly SGLT2is and GLP‐1RAs dispensed from January 2015 to December 2020, stratified by prescriber specialty and molecule. We also used the American Medical Association’s Physician Masterfile to calculate average annual SGLT2is and GLP‐1RAs dispensed per physician. Between January 2015 and December 2020, a total of 63.2 million SGLT2i and 63.4 million GLP‐1RA prescriptions were dispensed in the United States. Monthly prescriptions from cardiologists increased 12‐fold for SGLT2is (from 2228 to 25 815) and 4‐fold for GLP‐1RAs (from 1927 to 6981). Nonetheless, cardiologists represented only 1.5% of SGLT2i prescriptions and 0.4% of GLP‐1RA prescriptions in 2020, while total use was predominated by primary care physicians/internists (57% of 2020 SGLT2is and 52% of GLP‐1RAs). Endocrinologists led in terms of prescriptions dispensed per physician in 2020 (272 SGLT2is and 405 GLP‐1RAs). Cardiologists, but not noncardiologists, increasingly used SGLT2is over GLP‐1RAs, with accelerated uptake of empagliflozin and dapagliflozin coinciding with their landmark cardiovascular outcomes trials and subsequent US Food and Drug Administration label expansions. Conclusions While use of SGLT2is and GLP‐1RAs by cardiologists in the United States increased substantially over a 6‐year period, cardiologists still account for a very small proportion of all use, contributing to marked undertreatment of individuals with type 2 diabetes at high cardiovascular risk.

Background Data are limited about young adults' characteristics and outcomes undergoing coronary artery bypass grafting (CABG). Methods and Results We used the National Inpatient Sample database to identify adults aged 18 to 45 years who underwent CABG between 2004 and 2018. The data were weighted to generate national estimates of the entire US hospitalized population. We identified 110 463 CABG cases, equivalent to 62.2 per 1 000 000 person‐years; 27.1% were women, and 70.2% were White adults. Overall, annual CABG volume per 1 000 000 significantly decreased from 87.3 in 2004 to 45.7 in 2018. The prevalence of obesity, diabetes mellitus, hypertension, drug abuse, and chronic medical conditions increased over time. Overall, inpatient mortality was 1.76%; ST‐segment–elevation myocardial infarction, non–ST‐segment–elevation myocardial infarction, heart failure, peripheral vascular disease, renal failure, and valvular surgery were associated with higher inpatient mortality. Women had higher inpatient mortality than men (2.29% versus 1.57%), and Black patients had higher deaths than White patients (2.86% versus 1.58%). Inpatient mortality remained stable overall, according to sex, race, or clinical indication of CABG. However, the mean length of stay (8.4 days in 2004 to 9.5 days in 2018) and inflation‐adjusted cost of care ($40 522.8 in 2004 to $52 434.2 in 2018) significantly increased during the study period. Conclusions Despite the increased burden of cardiometabolic risk factors, the inpatient mortality in young adults undergoing CABG remained stable during the last 15 years. However, CABG volumes have decreased, but length of stay and inflation‐adjusted costs have increased over time.

Background Atherosclerotic cardiovascular disease (ASCVD) results in high out‐of‐pocket healthcare expenditures predisposing to food insecurity. However, the burden and determinants of food insecurity in this population are unknown. Methods and Results Using 2013 to 2018 National Health Interview Survey data, we evaluated the prevalence and sociodemographic determinants of food insecurity among adults with ASCVD in the United States. ASCVD was defined as self‐reported diagnosis of coronary heart disease or stroke. Food security was measured using the 10‐item US Adult Food Security Survey Module. Of the 190 113 study participants aged 18 years or older, 18 442 (adjusted prevalence 8.2%) had ASCVD, representing ≈20 million US adults annually. Among adults with ASCVD, 2968 or 14.6% (weighted ≈2.9 million US adults annually) reported food insecurity compared with 9.1% among those without ASCVD (P

Background Randomized trials of pharmacologic strength omega‐3 fatty acid (n3‐FA)–based therapies suggest a dose‐dependent cardiovascular benefit. Whether blood n3‐FA levels also mediate safety signals observed in these trials, such as increased bleeding and atrial fibrillation (AF), remains uncertain. We hypothesized that higher baseline n3‐FA levels would be associated with incident bleeding and AF events in MESA (Multi‐Ethnic Study of Atherosclerosis), which included a population free of clinical cardiovascular disease at baseline. Methods and Results We examined the association between baseline plasma n3‐FA levels (expressed as percent mass of total fatty acid) with incident bleeding and AF in MESA, an ongoing prospective cohort study. Bleeding events were identified from review of hospitalization International Classification of Diseases, Ninth Revision (ICD‐9), and International Classification of Diseases, Tenth Revision (ICD‐10), codes, and AF from participant report, discharge diagnoses, Medicare claims data, and study ECGs performed at MESA visit 5. Separate multivariable Cox proportional hazard modeling was used to estimate hazard ratios of the association of continuous n3‐FA (log eicosapentaenoic acid [EPA], log docosahexaenoic acid [DHA], log [EPA+DHA]) and incident hospitalized bleeding events and AF. Among 6546 participants, the mean age was 62.1 years and 53% were women. For incident bleeding, consistent statistically significant associations with lower rates were seen with increasing levels of EPA and EPA+DHA in unadjusted and adjusted models including medications that modulate bleeding risk (aspirin, NSAIDS, corticosteroids, and proton pump inhibitors). For incident AF, a significant association with lower rates was seen with increasing levels of DHA, but not for EPA or EPA+DHA. Conclusions In MESA, higher plasma levels of n3‐FA (EPA and EPA+DHA, but not DHA) were associated with significantly fewer hospitalized bleeding events, and higher DHA levels (but not EPA or EPA+DHA) with fewer incident AF events.

Background Although Black adults are more likely to die from coronary heart disease (CHD) compared with White adults, few studies have examined the relationship between cigarette smoking and CHD risk among Black adults. We evaluated the relationship between cigarette smoking, incident CHD, and coronary artery calcification in the JHS (Jackson Heart Study). Methods and Results We classified JHS participants without a history of CHD (n=4432) by self‐reported baseline smoking status into current, former (smoked at least 400 cigarettes/life) or never smokers at baseline (2000–2004). We further classified current smokers by smoking intensity (number of cigarettes smoked per day [1–19 or ≥20]) and followed for incident CHD (through 2016). Hazard ratios (HR) for incident CHD for each smoking group compared with never smokers were estimated with adjusted Cox proportional hazard regression models. At baseline, there were 548 (12.4%) current, 782 (17.6%) former, and 3102 (70%) never smokers. During follow‐up (median, 13.8 years), 254 participants developed CHD. After risk factor adjustment, CHD risk was significantly higher in current smokers compared with never smokers (HR, 2.11; 95% CI, 1.39–3.18); the difference between former smokers and never smokers (HR, 1.37; 95% CI, 1.0–1.90) did not achieve statistical significance. Among current smokers, we did not observe a dose‐response effect for CHD risk. Additionally, in multivariable logistic regression models with a subset of our analytic cohort, current smokers had greater odds of coronary artery calcification score >0 compared with never smokers (odds ratio, 2.63; 95% CI, 1.88–3.68). Conclusions In a large prospective cohort of Black adults, current smoking was associated with a >2‐fold increased risk of CHD over a median follow‐up of greater than a decade.

Background The optimal method for communicating coronary heart disease (CHD) risk to individual patients is not yet clear. Recent research supports the concept of "coronary age" for more effective risk communication. We defined an individual's coronary age as the age at which an average healthy individual would have an equivalent estimated CHD risk as that calculated for the index individual, building on our previously validated MESA (Multi‐Ethnic Study of Atherosclerosis) 10‐year CHD Risk Score equations with and without coronary artery calcium (CAC). Methods and Results We derived a coronary age by (1) calculating the MESA 10‐year CHD risk; (2) mathematically setting this equal to an equation describing risk of an average healthy MESA participant, as a function of age; and (3) solving for age. The risk discrimination of the resultant coronary age was compared with that of chronological age, the MESA CHD Risk Score, and CAC alone. Approximately 95% of coronary age values ranged from 30 years less to 30 years higher than chronological age. Although the mean chronological age of individuals experiencing CHD events compared with those free of events was 67.4 versus 61.8 years, the difference in coronary age including CAC was larger (80.6 versus 62.8 years). Coronary age with CAC had identical predictive ability to that of MESA CHD Risk Score and outperformed chronological age and CAC alone. Conclusions The newly derived coronary age is a convenient transformation of MESA CHD Risk, retaining very good risk discrimination. This easy‐to‐communicate tool will be available for patients and clinicians, potentially facilitating risk communication in routine care.

Background Blacks are disproportionately affected by stroke compared with whites; however, less is known about the relationship between stroke and cigarette smoking in blacks. Therefore, we evaluated the relationship between cigarette smoking and all incident stroke in the JHS (Jackson Heart Study). Methods and Results JHS participants without a history of stroke (n=4410) were classified by self‐reported baseline smoking status into current, past (smoked at least 400 cigarettes/life), or never smokers at baseline (2000–2004). Current smokers were further classified by smoking intensity (number of cigarettes smoked per day [1–19 and ≥20]) and followed up for incident stroke (through 2015). Hazard ratios (HRs) for incident stroke for current and past smoking compared with never smoking were estimated with adjusted Cox proportional hazard regression models. After adjusting for cardiovascular risk factors, the risk for stroke in current smokers was significantly higher compared with never smokers (HR, 2.48; 95% CI, 1.60–3.83) but there was no significant difference between past smokers and never smokers (HR, 1.10; 95% CI, 0.74–1.64). There was a dose‐dependent increased risk of stroke with smoking intensity (HR, 2.28 [95% CI, 1.38–3.86] and HR, 2.78 [95% CI, 1.47–5.28] for current smokers smoking 1–19 and ≥20 cigarettes/day, respectively). Conclusions In a large cohort of blacks, current cigarette smoking was associated with a dose‐dependent higher risk of all stroke. In addition, past smokers did not have a significantly increased risk of all stroke compared with never smokers, which suggests that smoking cessation may have potential benefits in reducing the incidence of stroke in blacks.

Background Atherosclerotic cardiovascular disease (ASCVD) has a strong association with diabetes mellitus (DM), accounting for approximately two thirds of deaths in this patient population. Many individuals with ASCVD and DM are vulnerable to financial hardship associated with treatment‐related expenses. Therefore, we examined the burden of financial hardship from medical bills across the spectrum of ASCVD status with and without DM. Methods and Results Using data from the National Health Interview Survey from 2013 to 2017, we used logistic regression analysis to examine the association of ASCVD and DM status with financial hardship and an inability to pay medical bills from a representative sample of non‐elderly adults in the United States. Our study population consisted of 121 672 individuals. Approximately 3.1% of the weighted population had ASCVD, 5.6% had DM, and 1.3% had both ASCVD and DM. Nearly 50% of individuals with ASCVD and DM reported financial hardship from medical bills (23% being unable to pay medical bills at all), whereas ≈28% of those with neither ASCVD nor DM reported financial hardship from medical bills (8% being unable to pay medical bills at all). Individuals with concurrent ASCVD and DM had the highest relative odds of expressing an inability to pay at all when compared with those with neither condition (odds ratio, 2.69; 95% CI, 2.21–3.28). Conclusions Individuals with concurrent ASCVD and DM are at a disproportionately high risk of being unable to pay their medical bills. The findings provide strong evidence for developing more effective public health policies that protect vulnerable populations from financial hardship.

Background Coronary artery calcium (CAC) is a predictor for the development of cardiovascular disease (CVD) and to a lesser extent cancer. The age‐ and sex‐specific relationship of CAC with CVD and cancer mortality is unknown. Methods and Results Asymptomatic patients aged 40 to 75 years old without known CVD were included from the CAC Consortium. We calculated sex‐specific mortality rates per 1000 person‐years’ follow‐up. Using parametric survival regression modeling, we determined the age‐ and sex‐specific CAC score at which the risk of death from CVD and cancer were equal. Among the 59 502 patients included in this analysis, the mean age was 54.9 (±8.5) years, 34% were women, and 89% were white. There were 671 deaths attributable to CVD and 954 deaths attributable to cancer over a mean follow‐up of 12±3 years. Among patients with CAC=0, cancer was the leading cause of death, the total mortality rate was low (women, 1.8; men, 1.5), and the CVD mortality rate was exceedingly low for women (0.3) and men (0.3). The age‐specific CAC score at which the risk of CVD and cancer mortality were equal had a U‐shaped relationship for women, while the relationship was exponential for men. Conclusions The age‐ and sex‐specific relationship of CAC with CVD and cancer mortality differed significantly for women and men. Our age‐ and sex‐specific CAC score provides a more precise estimate and further facilitates the use of CAC as a synergistic tool in strategies for the prediction and prevention of CVD and cancer mortality.

Background Arsenic‐related cardiovascular effects at exposure levels below the US Environmental Protection Agency's standard of 10 μg/L are unclear. For these populations, food, especially rice, is a major source of exposure. We investigated associations of rice intake, a marker of arsenic exposure, with subclinical cardiovascular disease (CVD) markers in a multiethnic population. Methods and Results Between 2000 and 2002, MESA (Multi‐Ethnic Study of Atherosclerosis) enrolled 6814 adults without clinical CVD. We included 5050 participants with baseline data on rice intake and markers of 3 CVD domains: inflammation (hsCRP [high‐sensitivity C‐reactive protein], interleukin‐6, and fibrinogen), vascular function (aortic distensibility, carotid distensibility, and brachial flow‐mediated dilation), and subclinical atherosclerosis at 3 vascular sites (carotid intima‐media thickness, coronary artery calcification, and ankle‐brachial index). We also evaluated endothelial‐related biomarkers previously associated with arsenic. Rice intake was assessed by food frequency questionnaire. Urinary arsenic was measured in 310 participants. A total of 13% of participants consumed ≥1 serving of rice/day. Compared with individuals consuming

Background Low gait speed has been linked with impaired mood, cognition, and quality of life (QOL) in older adults. We examined whether low gait speed was associated with impaired mood, cognition, and QOL among older adults with atrial fibrillation (AF). Methods and Results Participants (n=1185) had a diagnosis of AF, aged ≥65 years, CHA2DS2VASc ≥2 and had no contraindications to anticoagulation. Participants completed a 15‐foot walk test, and low gait speed was categorized using cutoffs from the Fried Frailty Index. Participants self‐reported measures of depressive symptoms (Patient Health Questionnaire 9 ≥10), anxiety symptoms (Generalized Anxiety Disorder 7 ≥10), cognitive impairment (Montreal Cognitive Assessment ≤23), and potentially impaired Atrial Fibrillation Effect Quality‐of‐Life Questionnaire

Background The relationship between lowering LDL (low‐density lipoprotein) cholesterol with contemporary lipid‐lowering therapies and incident diabetes mellitus (DM) remains uncertain. Methods and Results Thirty‐three randomized controlled trials (21 of statins, 12 of PCSK9 [proprotein convertase subtilisin/kexin type 9] inhibitors, and 0 of ezetimibe) were selected using Medline, Embase, and the Cochrane Central Register of Controlled Trials (inception through November 15, 2018). A total of 163 688 nondiabetic patients were randomly assigned to more intensive (83 123 patients) or less intensive (80 565 patients) lipid‐lowering therapy. More intensive lipid‐lowering therapy was defined as the more potent pharmacological strategy (PCSK9 inhibitors, higher intensity statins, or statins), whereas less intensive therapy corresponded to active control group or placebo/usual care of the trial. Metaregression and meta‐analyses were conducted using a random‐effects model. No significant association was noted between 1‐mmol/L reduction in LDL cholesterol and incident DM for more intensive lipid‐lowering therapy (risk ratio: 0.95; 95% CI, 0.87–1.04; P=0.30; R2=14%) or for statins or PCSK9 inhibitors. More intensive lipid‐lowering therapy was associated with a higher risk of incident DM compared with less intensive therapy (risk ratio: 1.07; 95% CI, 1.03–1.11; P

Background The predictive value of coronary artery calcium (CAC) has been widely studied; however, little is known about specific characteristics of CAC that are most predictive. We aimed to determine the independent associations of Agatston score, CAC volume, CAC area, CAC mass, and CAC density score with major adverse cardiac events in patients with suspected coronary artery disease. Methods and Results A total of 379 symptomatic participants, aged 45 to 85 years, referred for invasive coronary angiography, who underwent coronary calcium scanning and computed tomography angiography as part of the CORE320 (Combined Noninvasive Coronary Angiography and Myocardial Perfusion Imaging Using 320 Detector Computed Tomography) study, were included. Agatston score, CAC volume, area, mass, and density were computed on noncontrast images. Stenosis measurements were made on contrast‐enhanced images. The primary outcome of 2‐year major adverse cardiac events (30 revascularizations [>182 days of index catheterization], 5 myocardial infarctions, 1 cardiac death, 9 hospitalizations, and 1 arrhythmia) occurred in 32 patients (8.4%). Associations were estimated using multivariable proportional means models. Median age was 62 (interquartile range, 56–68) years, 34% were women, and 56% were white. In separate models, the Agatston, volume, and density scores were all significantly associated with higher risk of major adverse cardiac events after adjustment for age, sex, race, and statin use; density was the strongest predictor in all CAC models. CAC density did not provide incremental value over Agatston score after adjustment for diameter stenosis, age, sex, and race. Conclusions In symptomatic patients, CAC density was the strongest independent predictor of major adverse cardiac events among CAC scores, but it did not provide incremental value beyond the Agatston score after adjustment for diameter stenosis.

Background Prevalence of peripheral artery disease (PAD) is significantly higher among blacks as compared with non‐Hispanic whites, but the role of cigarette smoking in PAD is understudied in blacks. We aimed to evaluate the relationship between cigarette smoking and PAD in blacks in the (JHS) Jackson Heart Study. Methods and Results JHS participants (n=5306) were classified by self‐reported baseline smoking status into current, past (smoked at least 400 cigarettes/life), or never smokers. We examined multivariable logistic and robust linear regression models to estimate the associations between baseline smoking status, smoking intensity, and measures of subclinical PAD (ankle‐brachial index [visit 1] and aortic calcium by computed tomography [visit 2]) to yield odds ratios and β‐coefficients (estimated adjusted difference) to compare each smoking status with never smokers (reference group). There were 3579 (68%) never smokers, 986 (19%) past smokers, and 693 (13%) current smokers self‐identified at baseline. After adjustment for covariates, current smokers had increased risk of ankle‐brachial index

Background Coronary artery calcium (CAC) predicts cardiovascular disease (CVD) events; however, less is known about how its prognostic implications vary by race/ethnicity. Methods and Results A total of 38 277 whites, 1621 Asians, 977 blacks, and 1349 Hispanics from the CAC Consortium (mean age 55 years, 35% women) were followed over a median of 11.7 years. Modeling CAC in continuous and categorical (CAC=0; CAC 1–99; CAC 100–399; CAC ≥400) forms, we assessed its predictive value for all‐cause and CVD mortality by race/ethnicity using Cox proportional hazards and Fine and Gray competing‐risk regression, respectively. We also assessed the impact of race/ethnicity on risk within individual CAC strata, using whites as the reference. Models were adjusted for traditional cardiovascular risk factors. Increased CAC was associated with higher total and CVD mortality risk in all race/ethnicity groups, including Asians. However, the risk gradient with increasing CAC was more pronounced in blacks and Hispanics. In Fine and Gray subdistribution hazards models adjusted for traditional cardiovascular risk factors and CAC (continuous), blacks (subdistribution hazard ratio 3.4, 95% confidence interval, 2.5–4.8) and Hispanics (subdistribution hazard ratio 2.3, 95% confidence interval, 1.6–3.2) showed greater risk of CVD mortality when compared with whites, while Asians had risk similar to whites. These race/ethnic differences persisted when CAC=0. Conclusions CAC predicts all‐cause and CVD mortality in all studied race/ethnicity groups, including Asians and Hispanics, who may be poorly represented by the Pooled Cohort Equations. Blacks and Hispanics may have greater mortality risk compared with whites and Asians after adjusting for atherosclerosis burden, with potential implications for US race/ethnic healthcare disparities research.

Background To examine the prevalence and patterns of recent electronic cigarette (e‐cigarette) use in a nationally representative sample of US adults and adolescents. Methods and Results Using tobacco information from NHANES (National Health and Nutrition Examination Survey) 2013–2014, 5423 adults and 895 adolescents (aged 13–17 years) were included in this analysis. Demographic, tobacco use, and drug use information were self‐reported. Recent e‐cigarette use (within the previous 5 days) was stratified by smoking status. Of 125 e‐cigarette users, 116 participants were aged ≥18 years, corresponding to 2.6% (95% confidence interval [CI], 2.0–3.1) and 1.21% (95% CI, 0.3–2.1) prevalence of e‐cigarette use among US adults and adolescents, respectively. E‐cigarette adult users were current smokers (68.1%), former smokers (23.7%), and never smokers (8.2%). The highest prevalence of e‐cigarette use was among current smokers (8.2%; 95% CI, 6.3–10.1), followed by former smokers (2.7%; 95% CI, 1.4–4.1), and then never smokers (0.4%; 95% CI, 0.2–0.6). After adjusting for age, sex, and ethnicity, e‐cigarette users had higher odds of being exposed to secondhand smoke (odds ratio: 6.3; 95% CI, 3.6–11.1) and drinking alcohol (odds ratio: 4.2; 95% CI, 1.8–10.0) and lower odds of having at least a college education or a higher income, compared with tobacco nonusers. Conclusions Between 2013 and 2014, e‐cigarette use in the United States was more common among younger people, those with low socioeconomic status, and current and former smokers. These findings will help inform future research as well as public policy and regulatory actions.

Background The potential impact of the 2016 United States Preventive Services Task Force (USPSTF) guidelines on statins for primary prevention of atherosclerotic cardiovascular disease (ASCVD) warrants further analysis. Methods and Results We studied participants from MESA (Multi‐Ethnic Study of Atherosclerosis) aged 40 to 75 years and not on statins. We compared statin eligibility at baseline (2000–2002) and over follow‐up between USPSTF and the 2013 American College of Cardiology/American Heart Association (ACC/AHA) guidelines. Coronary artery calcium (CAC) was measured at baseline. Absolute ASCVD event rates were calculated according to eligibility categories for each guideline. Among 4962 MESA participants (aged 59.3±8.8 years, 47.2% female), compared with ACC/AHA guidelines, baseline statin eligibility by USPSTF was significantly lower (34.4% versus 49.1%) and increased less over time (39.1% versus 59.1%) at examination 5 [years 2010–2012]). Compared with ACC/AHA, participants eligible by USPSTF were less likely to have zero CAC at baseline (36.6% versus 41.2%) and had higher rates of hard ASCVD events per 1000 person‐years (11.6 [95% confidence interval, 10.2–13.3] versus 10.0 [8.9–11.3]). The hard ASCVD event rate in those eligible by ACC/AHA but not USPSTF was 6.5 (4.9–8.5) events per 1000 person‐years, with the rate varying significantly according to baseline CAC (4.2 [2.7–6.7] events in those with CAC=0, 12.8 [8.3–19.9] events in those with CAC >100). Conclusions In MESA, compared with ACC/AHA, the USPSTF statin guidelines resulted in a 15% absolute decrease in eligibility. Participants with discordant eligibility had ASCVD rates that varied significantly according to baseline CAC, suggesting CAC could aid clinical decision making for statins in these individuals.

BackgroundAtherosclerotic cardiovascular disease (ASCVD) and cancer are among the leading causes of economic burden, morbidity, and mortality in the United States. We aimed to quantify the overall impact of cardiovascular modifiable risk factor (CRF) profile on healthcare expenditures among those with and without ASCVD and/or cancer. Methods and ResultsThe 2012–2013 Medical Expenditure Panel Survey, a nationally representative adult sample (≥40 years), was utilized for the study. Variables included ASCVD, CRF (hypertension, diabetes mellitus, hypercholesterolemia, smoking, physical activity and/or obesity), and cancer (all). Two‐part econometric models analyzed cost data. Medical Expenditure Panel Survey participants (n=27 275, 59±9 years, 52% female) were studied and 14% had cancer, translating to 25.6 million US adults over 40 years of age. A higher prevalence of ASCVD was noted in those with versus without cancer (25% versus 14%). Absence of ASCVD and a more favorable CRF profile were associated with significantly lower expenditures across the spectrum of cancer diagnosis. Among cancer patients, the adjusted mean annual cost for those with and without ASCVD were $10 852 (95% confidence interval [8917, 12 788]) and $6436 (95% confidence interval [5531, 7342]). Among cancer patients without ASCVD, adjusted annual healthcare expenditures among those with optimal versus poor CRF profile were $4782 and $7256. ConclusionsIn a nationally representative US adult population, absence of ASCVD and a favorable CRF profile were associated with significantly lower medical expenditure among cancer patients. This provides estimates to continue better cardiovascular management and prevention practices, while contextualizing the burden of cancer.

BackgroundPrevious reports on whether smoking is associated with insulin resistance and diabetes mellitus have yielded inconsistent findings. We aimed to evaluate the relationship between cigarette smoking and incident diabetes mellitus in the Jackson Heart Study. Methods and ResultsJackson Heart Study participants enrolled at baseline without prevalent diabetes mellitus (n=2991) were classified by self‐report as current smokers, past smokers (smoked ≥400 cigarettes/life and no longer smoking), or never smokers. We quantified smoking intensity by number of cigarettes smoked daily; we considered ≥20 cigarettes per day (1 pack) “high‐intensity.” We defined diabetes mellitus as fasting glucose ≥126 mg/dL, hemoglobin A1c ≥6.5% or International Federation of Clinical Chemistry units HbA1c 48 mmol/mol, or use of diabetes mellitus medication. We estimated the adjusted associations of smoking status, intensity, and dose (pack‐years) with incident diabetes mellitus using Poisson regression models. At baseline there were 361 baseline current (1–10 cigarettes per day [n=242]; ≥20 [n=119]), 502 past, and 2128 never smokers. From Visit 1 to Visit 3 (mean 8.0±0.9 years), 479 participants developed incident diabetes mellitus. After adjustment for covariates, baseline current smokers who smoked less than a pack/d and past smokers had similar rates of incident diabetes mellitus compared with never smokers (incidence rate ratios 1.04, 95% confidence interval, 0.69–1.58 and 1.08, 95% confidence interval, 0.82–1.42, respectively). Baseline current high‐intensity smokers had a 79% (95% confidence interval, 1.14–2.81) higher incidence of diabetes mellitus compared with never smokers. Smoking dose (per 10 pack‐years) was also associated with a higher incidence of diabetes mellitus (incidence rate ratios 1.10, 95% confidence interval, 1.03–1.19) in adjusted models. ConclusionsHigh‐intensity cigarette smoking and smoking pack‐years are associated with an increased risk of developing diabetes mellitus in blacks.

BackgroundEvidence supporting nonstatin lipid‐lowering therapy in atherosclerotic cardiovascular disease risk reduction is variable. We aim to examine nonstatin utilization and expenditures in the United States between 2002 and 2013. Methods and ResultsWe used the Medical Expenditure Panel Survey database to estimate national trends in nonstatin use and cost (total and out‐of‐pocket, adjusted to 2013 US dollars using a gross domestic product deflator) among adults 40 years or older. Nonstatin users increased from 3 million (2.5%) in 2002‐2003 (20.1 million prescriptions) to 8 million (5.6%) in 2012‐2013 (45.8 million prescriptions). Among adults with atherosclerotic cardiovascular disease, nonstatin use increased from 7.5% in 2002‐2003 to 13.9% in 2012‐2013 after peaking at 20.3% in 2006‐2007. In 2012‐2013, 15.9% of high‐intensity statin users also used nonstatins, versus 9.7% of low/moderate‐intensity users and 3.6% of statin nonusers. Nonstatin use was significantly lower among women (odds ratio 0.80; 95% confidence interval 0.75‐0.86), racial/ethnic minorities (odds ratio 0.41; 95% confidence interval 0.36‐0.47), and the uninsured (odds ratio 0.47; 95% confidence interval 0.40‐0.56). Total nonstatin expenditures increased from $1.7 billion (out‐of‐pocket cost, $0.7 billion) in 2002‐2003 to $7.9 billion (out‐of‐pocket cost $1.6 billion) in 2012‐2013, as per‐user nonstatin expenditure increased from $550 to $992. Nonstatin expenditure as a proportion of all lipid‐lowering therapy expenditure increased 4‐fold from 8% to 32%. ConclusionsBetween 2002 and 2013, nonstatin use increased by 124%, resulting in a 364% increase in nonstatin‐associated expenditures.

BackgroundThe American Heart Association introduced the Life's Simple 7 (LS7) metrics to assess and promote cardiovascular health. We sought to examine the association between the LS7 metrics and incident heart failure (HF) in a multiethnic cohort. Methods and ResultsWe analyzed data from 6506 participants of the Multi‐Ethnic Study of Atherosclerosis free of cardiovascular disease at baseline. The LS7 metrics (smoking, physical activity, body mass index, diet, blood pressure, total cholesterol, and blood glucose) were graded on a scale of 0 to 2, with 2 indicating “ideal” status, 1 “intermediate” status, and 0 “poor” status. Points were summed, thus the LS7 score ranged from 0 to 14. Cox proportional hazard ratios and incidence rates of HF per 1000 person‐years were calculated. During a median follow‐up of 12.2 years, 262 (4%) participants developed HF. Incidence of HF decreased as the number of ideal LS7 metrics increased; 5.9 per 1000 person‐years for participants with 0 to 1 ideal metrics and 0.6 per 1000 person‐years for those with 6 to 7 ideal metrics. Compared with inadequate scores (0–8 points), hazard ratios for HF were 0.57 (0.43–0.76) and 0.31 (0.19–0.49) for average (9–10 points) and optimal (11–14 points) scores, respectively. A similar pattern was observed when the results were stratified by 4 racial/ethnic groups: white, Chinese American, black, and Hispanic. ConclusionsA lower risk of HF with more favorable LS7 status regardless of race/ethnicity suggests that efforts to achieve ideal cardiovascular health may reduce the burden of HF, a major source of morbidity and mortality.

BackgroundAtherosclerotic cardiovascular disease (ASCVD) causes most deaths in the United States and accounts for the highest healthcare spending. The association between the modifiable risk factors (MRFs) of ASCVD and pharmaceutical expenditures are largely unknown. Methods and ResultsWe examined the association between MRFs and pharmaceutical expenditures among adults with ASCVD using the 2012 and 2013 Medical Expenditure Panel Survey. A 2‐part model was used while accounting for the survey's complex design to obtain nationally representative results. All costs were adjusted to 2013 US dollars using the gross domestic product deflator. The annual total pharmaceutical expenditure among those with ASCVD was $71.6 billion, 33% of which was for medications for cardiovascular disease and 14% medications for diabetes mellitus. The adjusted relationship between MRFs and pharmaceutical expenditures showed significant marginal increase in average annual pharmaceutical expenditure associated with inadequate physical activity ($519 [95% confidence interval (CI), $12–918; P=0.011]), dyslipidemia ($631 [95% CI, $168–1094; P=0.008]), hypertension: ($1078 [95% CI, $697–1460; P

BackgroundThere is a need to identify sensitive biomarkers of early tobacco‐related cardiovascular disease. We examined the association of smoking status, burden, time since quitting, and intensity, with markers of inflammation and subclinical atherosclerosis. Methods and ResultsWe studied 14 103 participants without clinical cardiovascular disease in ELSA‐Brasil (Brazilian Longitudinal Study of Adult Health). We evaluated baseline cross‐sectional associations between smoking parameters and inflammation (high‐sensitivity C‐reactive protein [hsCRP]) and measures of subclinical atherosclerosis (carotid intima–media thickness, ankle‐brachial index, and coronary artery calcium [CAC]). The cohort included 1844 current smokers, 4121 former smokers, and 8138 never smokers. Mean age was 51.7±8.9 years; 44.8% were male. After multivariable adjustment, compared with never smokers, current smokers had significantly higher levels of hsCRP (β=0.24, 0.19–0.29 mg/L; P0 (odds ratio: 1.83; 95% confidence interval, 1.46–2.30; P0 were lower with increasing time since quitting (P0 (P=0.03) after adjusting for duration of smoking. ConclusionsStrong associations were observed between smoking status, burden, and intensity with inflammation (hsCRP) and subclinical atherosclerosis (carotid intima–media thickness, ankle‐brachial index, CAC). These markers of early cardiovascular disease injury may be used for the further study and regulation of traditional and novel tobacco products.

BackgroundInflammation is suggested to be a central feature of atherosclerosis, particularly among smokers. We studied whether inflammatory biomarkers GlycA and high‐sensitivity C‐reactive protein are associated with cigarette smoking. Methods and ResultsA total of 11 509 participants, 6774 from the MESA (Multi‐Ethnic Study of Atherosclerosis) and 4735 from ELSA‐Brasil (The Brazilian Longitudinal Study of Adult Health) were included. We evaluated the cross‐sectional association between multiple measures of smoking behavior and the inflammatory biomarkers, GlycA and high‐sensitivity C‐reactive protein, using regression models adjusted for demographic, anthropometric, and clinical characteristics. Participants were 57.7±11.1 years old and 46.4% were men. Never, former, and current smokers comprised 51.7%, 34.0%, and 14.3% of the population, respectively. Multivariable‐adjusted mean absolute difference in GlycA levels (μmol/L) with 95% confidence interval (CI) were higher for former (4.1, 95% CI, 1.7–6.6 μmol/L) and current smokers (19.9, 95% CI, 16.6–23.2 μmol/L), compared with never smokers. Each 5‐unit increase in pack‐years of smoking was associated with higher GlycA levels among former (0.7, 95% CI, 0.3–1.1 μmol/L) and current smokers (1.6, 95% CI, 0.8–2.4 μmol/L). Among former smokers, each 5‐year increase in time since quitting smoking was associated with lower GlycA levels (−1.6, 95% CI, −2.4 to −0.8 μmol/L) and each 10‐unit increase in number of cigarettes/day was associated with higher GlycA among current smokers (2.8, 95% CI, 0.5–5.2 μmol/L). There were similar significant associations between all measures of smoking behavior, and both log‐transformed GlycA and high‐sensitivity C‐reactive protein. ConclusionsAcute and chronic exposure to tobacco smoking is associated with inflammation, as quantified by both GlycA and high‐sensitivity C‐reactive protein. These biomarkers may have utility for the study and regulation of novel and traditional tobacco products.

BackgroundCoronary artery calcium (CAC) predicts coronary heart disease (CHD) events better than carotid wall plaque presence; however, differences in the utility of CAC burden and carotid plaque burden across the spectrum of cardiovascular disease (CVD) events is unknown. Methods and ResultsCVD, CHD and stroke/transient ischemic attack (TIA) events were evaluated prospectively in a multiethnic cohort without CVD at baseline. Carotid plaque score was determined by the number of ultrasound‐detected plaques in the common, bifurcation, and internal carotid artery segments. CAC was detected by computed tomography. Predictive values were compared using Cox proportional hazards models, C‐statistics, and net reclassification, adjusting for traditional CVD risk factors. At baseline, the 4955 participants were mean (SD) 61.6 (10.1) years old and 52.8% female; 48.9% had CAC >0 and 50.8% had at least 1 carotid plaque. After 11.3 (3.0) years of follow‐up, 709 CVD, 498 CHD, and 262 stroke/TIA events occurred. CAC score compared to carotid plaque score was a stronger predictor of CVD (hazard ratio [HR], 1.78; 95% CI, 1.16–1.98; P

BackgroundFew studies have evaluated the association between secondhand smoke (SHS) and subclinical cardiovascular disease among ethnically diverse populations. This study assesses the impact of SHS on inflammation and atherosclerosis (carotid intima‐media thickness, coronary artery calcification, and peripheral arterial disease). Methods and ResultsWe examined 5032 nonsmoking adults aged 45 to 84 years without prior cardiovascular disease participating in the Multi‐Ethnic Study of Atherosclerosis (MESA) from 2000 to 2002. SHS exposure was determined by self‐report, and urinary cotinine was measured in a representative subset (n=2893). The multi‐adjusted geometric mean ratios (95% CIs) for high‐sensitivity C‐reactive protein and interleukin‐6 comparing 407 participants with SHS ≥12 h/wk versus 3035 unexposed participants were 1.13 (1.02–1.26) and 1.04 (0.98–1.11), respectively. The multi‐adjusted geometric mean ratio for carotid intima‐media thickness was 1.02 (0.97–1.07). Fibrinogen and coronary artery calcification were not associated with SHS. The prevalence of peripheral arterial disease (ankle‐brachial index ≤0.9 or ≥1.4) was associated with detectable urinary cotinine (odds ratio, 2.10; 95% CI, 1.09–4.04) but not with self‐reported SHS. Urinary cotinine was not associated with inflammation or carotid intima‐media thickness. ConclusionsDespite limited exposure assessment, this study supports the association of SHS exposure with inflammation and peripheral arterial disease.

BackgroundThe American Heart Association introduced the Life's Simple 7 (LS7) metrics to assess and promote cardiovascular health. We examined the association between the LS7 metrics and noncardiovascular disease. Methods and ResultsWe studied 6506 men and women aged between 45 and 84 years, enrolled in the Multi‐Ethnic Study of Atherosclerosis. Median follow‐up time was 10.2 years. Each component of the LS7 metrics (smoking, body mass index, physical activity, diet, total cholesterol, blood pressure, and blood glucose) was assigned points, 0 indicates “poor” category; 1, “intermediate,” and 2, “ideal.” The LS7 score, ranged from 0 to 14, was created from the points and categorized as optimal (11–14), average (9–10), and inadequate (0–8). Hazard ratios and event rates per 1000 person‐years were calculated for outcomes based on self‐reported hospitalizations with the International Classification of Diseases, 9th Revision, diagnoses of cancer, chronic kidney disease, pneumonia, deep venous thromboembolism/pulmonary embolism, chronic obstructive pulmonary disease, dementia, and hip fracture. Analyses were adjusted for age, sex, race/ethnicity, income, and education. Overall, noncardiovascular disease event rates were lower with increasing LS7 scores. With the inadequate LS7 score as reference, an optimal score was associated with a decreased risk for noncardiovascular disease events. The hazard ratio for cancer was, 0.80 (0.64–0.98); chronic kidney disease, 0.38 (0.27–0.54); pneumonia, 0.57 (0.40–0.80); deep venous thromboembolism/pulmonary embolism, 0.52 (0.33–0.82), and chronic obstructive pulmonary disease, 0.51 (0.31–0.83). ConclusionsThe American Heart Association's LS7 score identified individuals who were vulnerable to multiple chronic nonvascular conditions. These results suggest that improving cardiovascular health will also reduce the burden of cancer and other chronic diseases.

Background Physical activity (PA) has an established favorable impact on cardiovascular disease (CVD) outcomes and quality of life. In this study, we aimed to estimate the economic effect of moderate‐vigorous PA on medical expenditures and utilization from a nationally representative cohort with and without CVD. Methods and Results The 2012 Medical Expenditure Panel Survey data were analyzed. Our study population was limited to noninstitutionalized US adults ≥18 years of age. Variables of interest included CVD (coronary artery disease, stroke, heart failure, dysrhythmias, or peripheral artery disease) and cardiovascular modifiable risk factors (CRFs; hypertension, diabetes mellitus, hypercholesterolemia, smoking, and/or obesity). Two‐part econometric models were utilized to study cost data; a generalized linear model with gamma distribution and link log was used to assess expenditures per capita. The final study sample included 26 239 surveyed individuals. Overall, 47% engaged in moderate‐vigorous PA ≥30 minutes, ≥5 days/week, translating to 111.5 million adults in the United States stratifying by CVD status; 32% reported moderate‐vigorous PA among those with CVD versus 49% without CVD. Generally, participants reporting moderate‐vigorous PA incurred significantly lower health care expenditures and resource utilization, displaying a step‐wise lower total annual health care expenditure as moving from CVD to non‐CVD (and each CRF category). Conclusions Moderate‐vigorous PA ≥30 minutes, ≥5 days/week is associated with significantly lower health care spending and resource utilization among individuals with and without established CVD.

BackgroundRemnant lipoproteins (RLPs), the triglyceride‐enriched precursors to low‐density lipoprotein, are an emerging risk factor for coronary heart disease (CHD). We sought to determine the association of RLP cholesterol (RLP‐C) levels with incident CHD in 2 diverse, prospective, longitudinal observational US cohorts. Methods and ResultsWe analyzed cholesterol levels from serum lipoprotein samples separated via density gradient ultracentrifugation in 4114 US black participants (mean age 53.8 years, 64% women) from the Jackson Heart Study and a random sample of 818 predominantly white participants (mean age 57.3 years, 52% women) from the Framingham Offspring Cohort Study. Multivariable‐adjusted hazard ratios (HRs) for RLP‐C (the sum of very low‐density lipoprotein3 cholesterol and intermediate‐density lipoprotein cholesterol) were derived to estimate associations with incident CHD events consisting of myocardial infarction, CHD death, and revascularizations for each cohort separately and as a combined population. There were 146 CHD events in the combined population. After adjustments for age, sex, body mass index, smoking, blood pressure, diabetes, and lipid‐lowering therapy for the combined population, RLP‐C (HR 1.23 per 1‐SD increase, 95% CI 1.06–1.42, P

Background The prognostic significance of modest elevations in exercise systolic blood pressure response has not been extensively examined. Methods and Results We examined the association between systolic blood pressure response and all‐cause death and incident myocardial infarction (MI) in 44 089 (mean age 53±13 years, 45% female, 26% black) patients who underwent exercise treadmill stress testing from the Henry Ford ExercIse Testing (FIT) Project (1991–2010). Exercise systolic blood pressure response was examined as a categorical variable (>20 mm Hg: referent; 1 to 20 mm Hg, and ≤0 mm Hg) and per 1 SD decrease. Cox regression was used to compute hazard ratios (HR) and 95% CI for the association between systolic blood pressure response and all‐cause death and incident MI. Over a median follow‐up of 10 years, a total of 4782 (11%) deaths occurred and over 5.2 years, a total of 1188 (2.7%) MIs occurred. In a Cox regression analysis adjusted for demographics, physical fitness, and cardiovascular risk factors, an increased risk of death was observed with decreasing systolic blood pressure response (>20 mm Hg: HR=1.0, referent; 1 to 20 mm Hg: HR=1.13, 95% CI=1.05, 1.22; ≤0 mm Hg: HR=1.21, 95% CI=1.09, 1.34). A trend for increased MI risk was observed (>20 mm Hg: HR=1.0, referent; 1 to 20 mm Hg: HR=1.09, 95% CI=0.93, 1.27; ≤0 mm Hg: HR=1.19, 95% CI=0.95, 1.50). Decreases in systolic blood pressure response per 1 SD were associated with an increased risk for all‐cause death (HR=1.08, 95% CI=1.05, 1.11) and incident MI (HR=1.09, 95% CI=1.03, 1.16). Conclusions Our results suggest that modest increases in exercise systolic blood pressure response are associated with adverse outcomes.