BACKGROUND: The American Heart Association, in conjunction with the National Institutes of Health, annually reports the most up-to-date statistics related to heart disease, stroke, and cardiovascular risk factors, including core health behaviors (smoking, physical activity, diet, and weight) and health factors (cholesterol, blood pressure, and glucose control) that contribute to cardiovascular health. The Statistical Update presents the latest data on a range of major clinical heart and circulatory disease conditions (including stroke, congenital heart disease, rhythm disorders, subclinical atherosclerosis, coronary heart disease, heart failure, valvular disease, venous disease, and peripheral artery disease) and the associated outcomes (including quality of care, procedures, and economic costs). METHODS: The American Heart Association, through its Statistics Committee, continuously monitors and evaluates sources of data on heart disease and stroke in the United States to provide the most current information available in the annual Statistical Update. The 2021 Statistical Update is the product of a full year’s worth of effort by dedicated volunteer clinicians and scientists, committed government professionals, and American Heart Association staff members. This year’s edition includes data on the monitoring and benefits of cardiovascular health in the population, an enhanced focus on social determinants of health, adverse pregnancy outcomes, vascular contributions to brain health, the global burden of cardiovascular disease, and further evidence-based approaches to changing behaviors related to cardiovascular disease. RESULTS: Each of the 27 chapters in the Statistical Update focuses on a different topic related to heart disease and stroke statistics. CONCLUSIONS: The Statistical Update represents a critical resource for the lay public, policy makers, media professionals, clinicians, health care administrators, researchers, health advocates, and others seeking the best available data on these factors and conditions.

Extracellular vesicles (EVs) are cell-derived nanoparticles that facilitate transport of proteins, lipids, and genetic material, playing important roles in intracellular communication. They have remarkable potential as non-toxic and non-immunogenic nanocarriers for drug delivery to unreachable organs and tissues, in particular, the central nervous system (CNS). Herein, we developed a novel platform based on macrophage-derived EVs to treat Parkinson disease (PD). Specifically, we evaluated the therapeutic potential of EVs secreted by autologous macrophages that were transfected ex vivo to express glial-cell-line-derived neurotrophic factor (GDNF). EV-GDNF were collected from conditioned media of GDNF-transfected macrophages and characterized for GDNF content, size, charge, and expression of EV-specific proteins. The data revealed that, along with the encoded neurotrophic factor, EVs released by pre-transfected macrophages carry GDNF-encoding DNA. Four-month-old transgenic Parkin Q311(X)A mice were treated with EV-GDNF via intranasal administration, and the effect of this therapeutic intervention on locomotor functions was assessed over a year. Significant improvements in mobility, increases in neuronal survival, and decreases in neuroinflammation were found in PD mice treated with EV-GDNF. No offsite toxicity caused by EV-GDNF administration was detected. Overall, an EV-based approach can provide a versatile and potent therapeutic intervention for PD.

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Introduction: Recent work has suggested that there is some association between acute exposures to fine particulate matter with aerodynamic diameter less than or equal to 2.5 micrometers (PM2.5) and ischemic stroke; however, the evidence is conflicting. Thus, we assessed whether PM2.5 was associated with ischemic stroke in participants in the Reasons for Geographic And Racial Differences in Stroke (REGARDS) cohort. Methods: We used a time-stratified case-crossover design to determine if exposure to PM2.5 was associated with an increased risk of ischemic stroke. We fit conditional logistic regression models to determine the odds ratio of ischemic stroke for those exposed to moderate (PM2.5 15-40 μg/m3) relative to good (PM2.5 ≤ 15 μg/m3) levels of PM2.5. We adjusted for temperature at the time of exposure, and assessed whether the association differed by region of residence (stroke belt vs. non-belt regions). Results: Among 442 participants who experienced an incident ischemic stroke in REGARDS, we found that there was no association with PM2.5 exposure (OR: 0.89, 95% CI: 0.69-1.15), and that there was no impact of region of residence on these results (p for interaction=0.14). Conclusions: We did not confirm earlier research indicating that there is an acute association between PM2.5 and ischemic stroke. More research is needed to understand these conflicting results, and to assess the impact of longer term exposures of PM2.5 on stroke incidence.

Introduction: The Atherosclerosis Risk In Communities (ARIC) study conducted community surveillance of hospitalized myocardial infarction (MI) from 1987 to 2014 among four US communities (Jackson MS, Forsyth County NC, Washington County MD, and Minneapolis MN). Surveillance of MI during the troponin era (1996 - ) has been complicated by increasing sensitivity of troponin I assays. It is unclear to what extent increased assay sensitivity has affected the validity of event classification. We hypothesized that among events that would have been classified as a definite/probable MI or a suspect/no MI regardless of cardiac biomarkers, the sensitivity and specificity of troponin I assays to identify abnormal enzyme levels (ARIC community surveillance criterion: 2x upper limit of normal) has changed over time in hospitals participating in ARIC community surveillance. Methods and results: From 33,995 community hospitalizations with suspicion of MI or coronary heart disease with a troponin I measurement that occurred between 1996 and 2014, 2,143 met ARIC criteria as MI cases (ARIC computer algorithm classification of definite or probable MI regardless of cardiac biomarker levels) and 9,909 we considered noncases (ARIC computer algorithm classification of no or suspect MI regardless of cardiac biomarker levels). In order to be an MI case, the event had to include an evolving diagnostic ECG. To be an noncase, the event had to include no chest pain and an equivocal or absent/uncodable ECG. We used survey-weighted logistic regression models to predict sensitivity and specificity from 1996 - 2014. The sensitivity of troponin I assay being abnormal was approximately 50% for most of the time period, with a potential increase to 70% after 2010. The specificity was approximately 90% in the late 1990s and early 2000s, but fell to 68% (95% confidence interval: 63% - 73%) by 2014. The median upper limit normal (ULN) for troponin I among all 33,995 hospitalizations dropped from 1.4 ng/mL in 1996 to 0.045 ng/mL in 2014. Conclusions: For most of the troponin era among the four ARIC communities, hospitalizations that were classified as an MI regardless of cardiac biomarker levels were equally likely to have or not have abnormal troponin I. In recent years, the likelihood that hospitalizations that were classified as no MI regardless of cardiac biomarker levels had normal troponin I decreased, potentially affecting the usefulness of troponin I measurements to separate hospitalized MIs from non-MIs in the context of community surveillance, particularly among hospitalizations with few other signs of MI. These shifts in assay validity were likely due in part to a decrease in ULN for troponin I in the four ARIC communities.