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Background: Despite improvements in population health, marked racial and ethnic disparities in longevity and cardiovascular disease (CVD) mortality persist. This study aimed to describe risks for all-cause and CVD mortality by race and ethnicity, before and after accounting for socioeconomic status (SES) and other factors, in the MESA study (Multi-Ethnic Study of Atherosclerosis). Methods: MESA recruited 6814 US adults, 45 to 84 years of age, free of clinical CVD at baseline, including Black, White, Hispanic, and Chinese individuals (2000–2002). Using Cox proportional hazards modeling with time-updated covariates, we evaluated the association of self-reported race and ethnicity with all-cause and adjudicated CVD mortality, with progressive adjustments for age and sex, SES (neighborhood SES, income, education, and health insurance), lifestyle and psychosocial risk factors, clinical risk factors, and immigration history. Results: During a median of 15.8 years of follow-up, 22.8% of participants (n=1552) died, of which 5.3% (n=364) died of CVD. After adjusting for age and sex, Black participants had a 34% higher mortality hazard (hazard ratio [HR], 1.34 [95% CI, 1.19–1.51]), Chinese participants had a 21% lower mortality hazard (HR, 0.79 [95% CI, 0.66–0.95]), and there was no mortality difference in Hispanic participants (HR, 0.99 [95% CI, 0.86–1.14]) compared with White participants. After adjusting for SES, the mortality HR for Black participants compared with White participants was reduced (HR, 1.16 [95% CI, 1.01–1.34]) but still statistically significant. With adjustment for SES, the mortality hazards for Chinese and Hispanic participants also decreased in comparison with White participants. After further adjustment for additional risk factors and immigration history, Hispanic participants (HR, 0.77 [95% CI, 0.63–0.94]) had a lower mortality risk than White participants, and hazard ratios for Black participants (HR, 1.08 [95% CI, 0.92–1.26]) and Chinese participants (HR, 0.81 [95% CI, 0.60–1.08]) were not significantly different from those of White participants. Similar trends were seen for CVD mortality, although the age- and sex-adjusted HR for CVD mortality for Black participants compared with White participants was greater than all-cause mortality (HR, 1.72 [95% CI, 1.34–2.21] compared with HR, 1.34 [95% CI, 1.19–1.51]). Conclusions: These results highlight persistent racial and ethnic differences in overall and CVD mortality, largely attributable to social determinants of health, and support the need to identify and act on systemic factors that shape differences in health across racial and ethnic groups.

Background: Air pollution contributes to cardiovascular morbidity, including heart failure. Exposure to pollutants has been associated with hypertension and inflammation, which contribute to cardiac remodeling. Few studies have investigated long-term air pollution concentrations and measures of cardiac structure, and no large longitudinal analyses have investigated this association. Hypothesis: Long-term air pollution concentrations are associated with magnetic resonance imaging-derived measures of left ventricular structure and function. Methods: In the Multi-Ethnic Study of Atherosclerosis (MESA), we investigated cross-sectional and longitudinal associations between modeled fine particulate matter (PM2.5), oxides of nitrogen (NOX) and ozone (O3) concentrations and left ventricular mass index (LVMI), mass to volume ratio, ejection fraction, and circumferential strain by cardiac magnetic resonance imaging (CMR) at two time points roughly 10 years apart. Multivariable linear regression was used to estimate the association between pollutants and both cross-sectional and longitudinal CMR measures. Results: At MESA Exam 1 (2000-2002), 4,825 participants in our cross-sectional analysis sample had a mean age of 61 years (standard deviation: 10), 53% were women, 40% were white, 13% were Chinese-American, 25% were African-American, and 21% were Hispanic. At Exam 1, Higher concentrations of PM2.5 and NOX in the year prior to Exam 1 were associated with higher LVMI at Exam 1 (1.6% per 5ug/m3 higher PM2.5, 95% CI: 0.3, 2.9; 1.8% per 40 parts per billion [ppb] NOX, 95% CI: 0.3, 3.3) and higher O3 was associated with lower LVMI (-3.5% per 10ppb, 95% CI: -6.0, -1.0). In longitudinal analyses, higher NOX was associated with a worsening of LV circumferential strain (-0.87% per 40ppb, 95% CI: -1.69, -0.05). Conclusions: Our study offers mixed evidence of a cross-sectional association between higher PM2.5 and NOx concentrations and greater LVMI. We also found associations between greater O3 concentration and lower cross-sectional LVMI, though this association may be confounded by other pollutants. These findings suggest a role for NOX, PM2.5, and O3 in cardiac remodeling. Additional work is needed to clarify that role and better understand the biological underpinnings of these associations.

In 2010, the American Heart Association published a statement concluding that the existing scientific evidence was consistent with a causal relationship between exposure to fine particulate matter and cardiovascular morbidity and mortality, and that fine particulate matter exposure is a modifiable cardiovascular risk factor. Since the publication of that statement, evidence linking air pollution exposure to cardiovascular health has continued to accumulate and the biological processes underlying these effects have become better understood. This increasingly persuasive evidence necessitates policies to reduce harmful exposures and the need to act even as the scientific evidence base continues to evolve. Policy options to mitigate the adverse health impacts of air pollutants must include the reduction of emissions through action on air quality, vehicle emissions, and renewable portfolio standards, taking into account racial, ethnic, and economic inequality in air pollutant exposure. Policy interventions to improve air quality can also be in alignment with policies that benefit community and transportation infrastructure, sustainable food systems, reduction in climate forcing agents, and reduction in wildfires. The health care sector has a leadership role in adopting policies to contribute to improved environmental air quality as well. There is also potentially significant private sector leadership and industry innovation occurring in the absence of and in addition to public policy action, demonstrating the important role of public-private partnerships. In addition to supporting education and research in this area, the American Heart Association has an important leadership role to encourage and support public policies, private sector innovation, and public-private partnerships to reduce the adverse impact of air pollution on current and future cardiovascular health in the United States.

Air pollution exposure is an important risk factor for cardiovascular morbidity and mortality. Acute exposure is associated with episodes of atrial fibrillation (AF), and long-term exposure may influence ventricular mass and volume. However, little is understood about the relationship between long-term pollution exposure and atrial structure and function, which may influence risk of AF and heart failure. We sought to determine the association of long-term exposure to oxides of nitrogen (NO X ), particulate matter smaller than 2.5 micrometers (PM 2.5 ), and ozone (O 3 ) with left atrial structure (LA) and function, as measured by LA volume, emptying fraction, and peak longitudinal strain. In the Multi-Ethnic Study of Atherosclerosis (MESA), a longitudinal study of 6,814 participants in six United States communities, we used estimated 5-year average exposure to PM 2.5 , NO X , and O 3 prior to outcome measurement from validated hierarchical spatio-temporal models developed from extensive monitoring of MESA participants. Left atrial measures were calculated from cardiac magnetic resonance imaging occurring between 2010 and 2012. Linear regression was used, adjusting for MESA study site and potential confounding characteristics. In 2,250 MESA participants, 5-year average exposure to PM 2.5 , NO X , and O 3 varied greatly by study site and was not associated with LA volume, emptying fraction, or peak longitudinal strain. Results were particularly sensitive to adjustment for study site, suggesting that there was substantial unmeasured confounding by US city/region. Using recently developed study-specific exposure estimation and highly accurate imaging, we did not find evidence to suggest an association between long-term exposure to several common pollutants and measures of left atrial structure and function. Additional analyses in areas of higher pollution may be useful in determining whether associations are consistent across exposure levels.

Objectives: Over half the US population experiences noise levels above WHO recommendations yet little research within the US has examined the health effects of these exposures. Our objective is to investigate the associations between community noise and blood pressure in residents of Chicago. Methods: Participants were from two prospective cohort studies: the Multi Ethnic Study of Atherosclerosis (MESA) and the Chicago Health and Aging Project (CHAP). MESA is a multi-site study of persons aged 45-84 years and free of clinical cardiovascular disease. CHAP is an open cohort initiated to study chronic conditions of aging among persons aged ≥65 years. This analysis focuses on the 5,167 participants of these cohorts living in Chicago with an average of 2.5 (CHAP) and 4.5 (MESA) assessments per participant, for systolic (SBP) and diastolic (DBP) blood pressure between 1999-2011. In both cohorts, hypertension was defined as taking antihypertensive medication, SBP ≥140 or DBP ≥ 90 mmHg. We estimated noise at participant addresses using land use regression models weighted according to participants’ 5-year residential history before each exam. Among those taking antihypertensive medication, blood pressure was adjusted using multiple imputation. Associations between noise and blood were estimated using linear mixed models. A Cox proportional hazards model was used to estimate relative risk (RR) of incident hypertension. All models included calendar time, age, sex, race, income, education, neighborhood socioeconomic score, smoking, cohort, interaction between cohort and age, race, and gender, and NO x (a traffic-related air pollutant). Findings : At baseline, MESA participants were younger (63 vs 73 years) and more educated (36 vs. 3% with ≥graduate degree) than CHAP participants. MESA participants had higher noise levels (60 vs 56 dB) and lower blood pressures (e.g. SBP: 124 vs 135 mmHg) than CHAP participants. After adjusting for cohort and other confounders, we found that 10 dB higher residential noise levels were associated with 0.9 (95% CI: -0.2, 0.2; p=0.1) and 0.5 mmHg greater (95% CI: -0.1, 0.11; p=0.08) SBP and DBP, respectively. Similar associations were found within each cohort. Noise was not associated with incident hypertension overall (RR: 1.00; 95% CI: 0.8, 1.3, p=0.98) or within cohort. Conclusions: We found a suggestive association between noise and blood pressure levels, but no association with hypertension. This could be due to the lack of nighttime noise information, which has been shown to be more strongly associated with blood pressure outcomes than daytime levels or with the selection of healthy older participants.

In 2004, the first American Heart Association scientific statement on “Air Pollution and Cardiovascular Disease” concluded that exposure to particulate matter (PM) air pollution contributes to cardiovascular morbidity and mortality. In the interim, numerous studies have expanded our understanding of this association and further elucidated the physiological and molecular mechanisms involved. The main objective of this updated American Heart Association scientific statement is to provide a comprehensive review of the new evidence linking PM exposure with cardiovascular disease, with a specific focus on highlighting the clinical implications for researchers and healthcare providers. The writing group also sought to provide expert consensus opinions on many aspects of the current state of science and updated suggestions for areas of future research. On the basis of the findings of this review, several new conclusions were reached, including the following: Exposure to PM 2.5 ) over a few hours to weeks can trigger cardiovascular disease–related mortality and nonfatal events; longer-term exposure (eg, a few years) increases the risk for cardiovascular mortality to an even greater extent than exposures over a few days and reduces life expectancy within more highly exposed segments of the population by several months to a few years; reductions in PM levels are associated with decreases in cardiovascular mortality within a time frame as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM 2.5 exposure and cardiovascular morbidity and mortality. This body of evidence has grown and been strengthened substantially since the first American Heart Association scientific statement was published. Finally, PM 2.5 exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality.

Background: While CAC=0 is associated with excellent prognosis, progression to CAC>0 has been shown to confer increased risk. The time interval at which a repeat CAC scan would be reasonable - the “warranty period” of CAC=0 - is currently poorly defined. Methods: We studied 3116 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) with baseline CAC=0 and at least 1 follow-up CAC scan per MESA protocol (up to 10 years after baseline). Cumulative incidence of incident CAC was calculated yearly. Cumulative survival fee of CAC was calculated using Kaplan-Meier statistics and additionally modeled using a parametric survival model with Weibull distribution. The warranty period of CAC=0 was defined distribution as the time needed for 15%, 20%, or 25% (number needed to scan [NNS] 6, 5, or 4) to progress to detectable CAC. Results: The mean age of the subjects was 58 ± 9 years with 63% women and mean FRS of 8 ± 6%. Cumulative prevalence of CAC>0 increased with time, from 11% at 2 years to nearly 50% at 10 years. The cumulative incidence rate of CAC>0 was non-linear, increasing from approximately 2.5 per 100 person-years at 2 years to 5-6 per 100 person-years from years 4 to 10. The table shows the estimated warranty period of CAC=0 by gender and baseline FRS CHD risk. Among men, using an acceptable detection rate of 25% (NNS=4 to detect CAC>0), the estimated warranty period of a low, intermediate, and high risk man was 6, 5, and 3 years. For women, the equivalent warranty period was 7, 5, and 4 years. In general, rescanning at 5 years will enable selection of 50% of the individuals with baseline CAC=0 who will go on to have CHD events following their repeat scan over 10-year follow-up. Conclusions: Although limited by lack of yearly CAC scanning, modeling in MESA allows estimation of the warranty period of CAC=0. A general rule would be to rescan low risk CAC=0 patients at 6-7 years and intermediate risk at 4-5 years, although exact warranty periods vary by gender and desired yield of repeat testing.

Objectives: Smoking exposure can be measured in a variety of ways including duration, intensity (cigarettes /day), and the product of these known as pack-years. How these variables should be combined to best model smoking as an exposure in cardiovascular (CVD) studies is not clear. Methods: The MESA study is a cohort of 6814 participants initially free of clinical heart disease at baseline in 2000-2002. MESA collected questionnaire data on smoking duration, intensity, and pack-years. Initial models were stratified by current versus former smoking status, with a second set of models that pooled all participants and controlled for status. Generalized additive models for time to incident CVD (myocardial infarction, stroke, and CVD death) were used to investigate the functional form of each aspect of smoking. Cox models were used to investigate the hazard ratio (HR) of each exposure definition of smoking on time to event. Models were compared which used intensity and duration alone, in combination, and expressed as pack-years. The interaction between duration and intensity was also tested. All models were adjusted for age, sex, and race/ethnicity. We summarized model performance using the pseudo- R 2 statistic and the area under the receiver-operator characteristic curve (AUC). Results: There were 2487 former and 887 current smokers at baseline, with 370 incident CVD events over a median of 8.5 years. There was no significant non-linearity detected for intensity, duration or pack-years with respect to CVD risk. Among the former smokers none of duration, intensity, and pack-years was significant. Among the current smokers, only intensity was significant (HR for cigarettes/day 1.03, p=0.005). There was no evidence of an interaction between intensity and duration. Among current smokers, the model including intensity alone had an R 2 of 0.24 and AUC of 0.697. The model adding duration had very similar results with an R 2 of 0.24 and AUC of 0.698. The model with pack-years had worse performance than the model with intensity alone, with an R 2 of 0.19 and AUC of 0.662. In the model pooling all participants, former smoking and duration were non-significant, while current smoking (HR 2.0, p Other outcomes were also examined including coronary heart disease (CHD) and the findings were very consistent. Conclusions: For CVD risk, only current smoking intensity at baseline is significant. Adding duration to the model does not add information, and use of the pack-years variable results in a loss of information since it does not estimate the intensity effect as accurately. These results suggest that lowering or limiting current smoking would lower CVD risk, regardless of cumulative smoking exposure.

Coronary artery calcium (CAC) progression has previously been observed to predict coronary events above and beyond its association with baseline CAC. Prior studies show associations between CAC progression and risk factors, but were limited by short follow-up or restriction to individuals with advanced disease. We examined the relationship between risk factors for clinical events and the progression of CAC in MESA, a prospective cohort study. Participants were 6810 adults without CVD at recruitment in 2000-2002. Agatston scores for extent of calcification were assessed 1-4 times (mean 2.5) over a 10-year period with interim exams spaced at approximately 2-4 years. Mean follow-up time for those with at least 2 scans was 5.0 years. An innovative approach to mixed effects models jointly modeled the associations between risk factors and CAC both at baseline and with CAC progression rate. This method is less biased than controlling for baseline CAC, since the same risk factors are associated with both baseline and progression. Hence, time-varying factors can adjust progression rate, and data from participants with varying follow-up time and number of measurements_even those measured only at baseline_are incorporated. Mean CAC progression rate was 25 CAC units/year. All models were adjusted for age, sex, site, and race/ethnicity. Strong effects were observed for age, male sex, hypertension, and diabetes. Effects for statins likely reflect poor health status, rather than a causal effect of medication. Simultaneous adjustment for all risk factors produced similar results except the effect of statin use was not observed. See table for estimates and confidence intervals. In conclusion, CAC progression is associated with risk factors for clinical coronary events, confirming that processes involved in CAC progression mirror development of clinical atherosclerosis. The methods applied for the analysis of repeated continuous noninvasive measures of atherosclerosis extent can also be applied to evaluating novel risk factors.

Objective: To determine whether long-term exposure to oxides of nitrogen (NO x ) is associated with left ventricular mass index (LVMI) in adults without known cardiovascular disease (CVD). Background: An association between very close (x , a specific, gaseous traffic related pollutant and more reliable surrogate for traffic-related pollution, has not been examined. Methods: This study included 4125 participants free of clinical cardiovascular disease in the Multi-Ethnic Study of Atherosclerosis (MESA) who underwent cardiac MRI, cardiac computed tomography (CT), and an extensive air pollution exposure assessment campaign to determine long-term individual residential exposure to NO x . This study used year 2000 average exposure to estimate long term exposure to NO x . LVMI was calculated by indexing cardiac MRI measures of left ventricular mass to body surface area measured at the exam. Agatston score was calculated based on cardiac CT. Multiple linear regression was used to examine the association between long-term exposure to NO x and LVMI, adjusted for multiple potential confounders including study site. To examine whether such relationships may be mediated by atherosclerosis or blood pressure, additional adjustment for Agatston score and blood pressure was performed. Results: An interquartile range (44 ppb) increase in estimated residential NO x was associated with significantly higher LVMI (1.6 g/m 2 , 95% CI: 0.1 to 3.1, p=0.03). Such estimates were comparable to prior associations observed for the relationship between close residential proximity to major roadways and LVMI (comparing individuals living 150m away). Additional adjustment for Agatston score and blood pressure had no effect on estimates of association. Stratified analyses suggested interactions with age, with younger individuals demonstrating larger associations than older individuals (p for interaction = 0.05). No significant evidence of effect modification by race, gender, other cardiovascular risk factors, or study site was observed. Conclusions: This study further supports the observation that long-term exposure to traffic-related air pollution is associated with higher left ventricular mass, and suggests that such associations may be independent of effects on blood pressure or atherosclerotic disease.