Rachel H. Mackey

Heart Disease and Stroke Statistics—2014 Update A Report From the American Heart Association

Author(s): Go, Alan S; Mozaffarian, Dariush; Roger, Veronique L; Benjamin, Emelia J; Berry, Jarett D; Blaha, Michael J; Dai, Shifan; Ford, Earl S; Fox, Caroline S; Franco, Sheila; Fullerton, Heather J; Gillespie, Cathleen; Hailpern, Susan M; Heit, John A; Howard, Virginia J; Huffman, Mark D; Judd, Suzanne E; Kissela, Brett M; Kittner, Steven J; Lackland, Daniel T; Lichtman, Judith H; Lisabeth, Lynda D; Mackey, Rachel H; Magid, David J; Marcus, Gregory M; Marelli, Ariane; Matchar, David B; McGuire, Darren K; Mohler, Emile R; Moy, Claudia S; Mussolino, Michael E; Neumar, Robert W; Nichol, Graham; Pandey, Dilip K; Paynter, Nina P; Reeves, Matthew J; Sorlie, Paul D; Stein, Joel; Towfighi, Amytis; Turan, Tanya N; Virani, Salim S; Wong, Nathan D; Woo, Daniel; Turner, Melanie B; American Heart Association Statistics Committee and Stroke Statistics Subcommittee

Heart Disease and Stroke Statistics—2016 Update: A Report From the American Heart Association

Author(s): Writing Group Members; Mozaffarian, Dariush; Benjamin, Emelia J; Go, Alan S; Arnett, Donna K; Blaha, Michael J; Cushman, Mary; Das, Sandeep R; de Ferranti, Sarah; Despres, Jean-Pierre; Fullerton, Heather J; Howard, Virginia J; Huffman, Mark D; Isasi, Carmen R; Jimenez, Monik C; Judd, Suzanne E; Kissela, Brett M; Lichtman, Judith H; Lisabeth, Lynda D; Liu, Simin; Mackey, Rachel H; Magid, David J; McGuire, Darren K; Mohler, Emile R; Moy, Claudia S; Muntner, Paul; Mussolino, Michael E; Nasir, Khurram; Neumar, Robert W; Nichol, Graham; Palaniappan, Latha; Pandey, Dilip K; Reeves, Mathew J; Rodriguez, Carlos J; Rosamond, Wayne; Sorlie, Paul D; Stein, Joel; Towfighi, Amytis; Turan, Tanya N; Virani, Salim S; Woo, Daniel; Yeh, Robert W; Turner, Melanie B; American Heart Association Statistics Committee; Stroke Statistics Subcommittee

Heart Disease and Stroke Statistics—2015 Update A Report From the American Heart Association

STRIDE (Stanford Translational Research Integrated Database Environment) is a research and development project at Stanford University to create a standards-based informatics platform supporting clinical and translational research. STRIDE consists of three integrated components: a clinical data warehouse, based on the HL7 Reference Information Model (RIM), containing clinical information on over 1.3 million pediatric and adult patients cared for at Stanford University Medical Center since 1995; an application development framework for building research data management applications on the STRIDE platform and a biospecimen data management system. STRIDEs semantic model uses standardized terminologies, such as SNOMED, RxNorm, ICD and CPT, to represent important biomedical concepts and their relationships. The system is in daily use at Stanford and is an important component of Stanford Universitys CTSA (Clinical and Translational Science Award) Informatics Program.on behalf of the American Heart Association Statistics Committee and Stroke Statistics Nathan D. Wong, Daniel Woo and Melanie B. Turner Elsayed Z. Soliman, Paul D. Sorlie, Nona Sotoodehnia, Tanya N. Turan, Salim S. Virani, Claudia S. Moy, Dariush Mozaffarian, Michael E. Mussolino, Graham Nichol, Nina P. Paynter, Lynda D. Lisabeth, Diane M. Makuc, Gregory M. Marcus, Ariane Marelli, David B. Matchar, Lichtman, Virginia J. Howard, Brett M. Kissela, Steven J. Kittner, Daniel T. Lackland, Judith H. Caroline S. Fox, Heather J. Fullerton, Cathleen Gillespie, Susan M. Hailpern, John A. Heit, Benjamin, Jarett D. Berry, William B. Borden, Dawn M. Bravata, Shifan Dai, Earl S. Ford, Writing Group Members, Véronique L. Roger, Alan S. Go, Donald M. Lloyd-Jones, Emelia J. Association 2012 Update : A Report From the American Heart −− Heart Disease and Stroke StatisticsHeart Disease, Stroke and other Cardiovascular Diseases • Cardiovascular disease is the leading global cause of death, accounting for 17.3 million deaths per year, a number that is expected to grow to more than 23.6 million by 2030. • In 2008, cardiovascular deaths represented 30 percent of all global deaths, with 80 percent of those deaths taking place in lowand middle-income countries. • Nearly 787,000 people in the U.S. died from heart disease, stroke and other cardiovascular diseases in 2011. That’s about one of every three deaths in America. • About 2,150 Americans die each day from these diseases, one every 40 seconds. • Cardiovascular diseases claim more lives than all forms of cancer combined. • About 85.6 million Americans are living with some form of cardiovascular disease or the after-effects of stroke. • Direct and indirect costs of cardiovascular diseases and stroke total more than

Heart Disease and Stroke Statistics'2017 Update: A Report from the American Heart Association

320.1 billion. That includes health expenditures and lost productivity. • Nearly half of all African-American adults have some form of cardiovascular disease, 48 percent of women and 46 percent of men. • Heart disease is the No. 1 cause of death in the world and the leading cause of death in the United States, killing over 375,000 Americans a year. • Heart disease accounts for 1 in 7 deaths in the U.S. • Someone in the U.S. dies from heart disease about once every 90 seconds.Author(s): Mozaffarian, Dariush; Benjamin, Emelia J; Go, Alan S; Arnett, Donna K; Blaha, Michael J; Cushman, Mary; de Ferranti, Sarah; Despres, Jean-Pierre; Fullerton, Heather J; Howard, Virginia J; Huffman, Mark D; Judd, Suzanne E; Kissela, Brett M; Lackland, Daniel T; Lichtman, Judith H; Lisabeth, Lynda D; Liu, Simin; Mackey, Rachel H; Matchar, David B; McGuire, Darren K; Mohler, Emile R; Moy, Claudia S; Muntner, Paul; Mussolino, Michael E; Nasir, Khurram; Neumar, Robert W; Nichol, Graham; Palaniappan, Latha; Pandey, Dilip K; Reeves, Mathew J; Rodriguez, Carlos J; Sorlie, Paul D; Stein, Joel; Towfighi, Amytis; Turan, Tanya N; Virani, Salim S; Willey, Joshua Z; Woo, Daniel; Yeh, Robert W; Turner, Melanie B; American Heart Association Statistics Committee and Stroke Statistics Subcommittee

Measures of Obesity Are Associated With Vascular Stiffness in Young and Older Adults

WRITING GROUP MEMBERS Emelia J. Benjamin, MD, SCM, FAHA Michael J. Blaha, MD, MPH Stephanie E. Chiuve, ScD Mary Cushman, MD, MSc, FAHA Sandeep R. Das, MD, MPH, FAHA Rajat Deo, MD, MTR Sarah D. de Ferranti, MD, MPH James Floyd, MD, MS Myriam Fornage, PhD, FAHA Cathleen Gillespie, MS Carmen R. Isasi, MD, PhD, FAHA Monik C. Jiménez, ScD, SM Lori Chaffin Jordan, MD, PhD Suzanne E. Judd, PhD Daniel Lackland, DrPH, FAHA Judith H. Lichtman, PhD, MPH, FAHA Lynda Lisabeth, PhD, MPH, FAHA Simin Liu, MD, ScD, FAHA Chris T. Longenecker, MD Rachel H. Mackey, PhD, MPH, FAHA Kunihiro Matsushita, MD, PhD, FAHA Dariush Mozaffarian, MD, DrPH, FAHA Michael E. Mussolino, PhD, FAHA Khurram Nasir, MD, MPH, FAHA Robert W. Neumar, MD, PhD, FAHA Latha Palaniappan, MD, MS, FAHA Dilip K. Pandey, MBBS, MS, PhD, FAHA Ravi R. Thiagarajan, MD, MPH Mathew J. Reeves, PhD Matthew Ritchey, PT, DPT, OCS, MPH Carlos J. Rodriguez, MD, MPH, FAHA Gregory A. Roth, MD, MPH Wayne D. Rosamond, PhD, FAHA Comilla Sasson, MD, PhD, FAHA Amytis Towfighi, MD Connie W. Tsao, MD, MPH Melanie B. Turner, MPH Salim S. Virani, MD, PhD, FAHA Jenifer H. Voeks, PhD Joshua Z. Willey, MD, MS John T. Wilkins, MD Jason HY. Wu, MSc, PhD, FAHA Heather M. Alger, PhD Sally S. Wong, PhD, RD, CDN, FAHA Paul Muntner, PhD, MHSc On behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee Heart Disease and Stroke Statistics—2017 Update

High-density lipoprotein cholesterol and particle concentrations, carotid atherosclerosis, and coronary events: MESA (Multi-Ethnic Study of Atherosclerosis)

Abstract—Obesity has reached epidemic levels and carries a risk for cardiovascular disease. Obesity’s effects on the vascular systems of young adults and African Americans have not been well characterized. The aim of this study was to assess the association between measures of obesity and aortic stiffness in 186 young adults (20 to 40 years, 50% African American) and 177 older adults (41 to 70 years, 33% African American). Aortic stiffness was measured by aortic pulse-wave velocity. The median pulse-wave velocity value was 468 cm/s for young adults and 627 cm/s for older adults (P <0.001). Higher body weight, body mass index, waist and hip circumferences, and waist-hip ratio were strongly correlated with higher pulse-wave velocity, independent of age, systolic blood pressure, race, and sex overall and among both age groups (P <0.01 for all). Even among the 20- to 30-year-olds, obese individuals (body mass index>30) had a mean pulse-wave velocity value 47 cm/s higher than did nonobese individuals (P <0.001). Obesity measures were among the strongest independent predictors of pulse-wave velocity overall and for both age groups. Results were consistent by race. In conclusion, excess body weight is associated with higher aortic stiffness in whites and African Americans as young as 20 to 30 years. The strength of the association, the early age at which it appears, and the prevalence of obesity among the young warn of substantially increased cardiovascular disease incidence as this cohort ages.

Clinical implications of discordance between low-density lipoprotein cholesterol and particle number

OBJECTIVES The purpose of this study was to evaluate independent associations of high-density lipoprotein cholesterol (HDL-C) and particle (HDL-P) concentrations with carotid intima-media thickness (cIMT) and incident coronary heart disease (CHD). BACKGROUND HDL-C is inversely related to CHD, and also to triglycerides, low-density lipoprotein particles (LDL-P), and related metabolic risk. HDL-P associations with CHD may be partially independent of these factors. METHODS In a multiethnic study of 5,598 men and women ages 45 to 84 years old, without baseline CHD, excluding subjects on lipid-lowering medications, triglycerides >400 mg/dl, or missing values, we evaluated associations of HDL-C and nuclear magnetic resonance spectroscopy-measured HDL-P with cIMT and incident CHD (myocardial infarction, CHD death, and angina, n = 227 events; mean 6.0 years follow-up). All models were adjusted for age, sex, ethnicity, hypertension, and smoking. RESULTS HDL-C and HDL-P correlated with each other (ρ = 0.69) and LDL-P (ρ = -0.38, -0.25, respectively, p < 0.05 for all). For (1 SD) higher HDL-C (15 mg/dl) or HDL-P (6.64 μmol/l), cIMT differences were - 26.1 (95% confidence interval [CI]: -34.7 to -17.4) μm and -30.1 (95% CI: -38.8 to - 21.4) μm, and CHD hazard ratios were 0.74 (95% CI: 0.63 to 0.88) and 0.70 (95% CI: 0.59 to 0.82), respectively. Adjusted for each other and LDL-P, HDL-C was no longer associated with cIMT (2.3; 95% CI: - 9.5 to 14.2 μm) or CHD (0.97; 95% CI: 0.77 to 1.22), but HDL-P remained independently associated with cIMT (-22.2; 95% CI: - 33.8 to -10.6 μm) and CHD (0.75; 95% CI: 0.61 to 0.93). Interactions by sex, ethnicity, diabetes, and high-sensitivity C-reactive protein were not significant. CONCLUSIONS Adjusting for each other and LDL-P substantially attenuated associations of HDL-C, but not HDL-P, with cIMT and CHD. Potential confounding by related lipids or lipoproteins should be carefully considered when evaluating HDL-related risk.

Correlates of aortic stiffness in elderly individuals: A subgroup of the Cardiovascular Health Study

BACKGROUND The amount of cholesterol per low-density lipoprotein (LDL) particle is variable and related in part to particle size, with smaller particles carrying less cholesterol. This variability causes concentrations of LDL cholesterol (LDL-C) and LDL particles (LDL-P) to be discordant in many individuals. METHODS LDL-P measured by nuclear magnetic resonance spectroscopy, calculated LDL-C, and carotid intima-media thickness (IMT) were assessed at baseline in the Multi-Ethnic Study of Atherosclerosis, a community-based cohort of 6814 persons free of clinical cardiovascular disease (CVD) at entry and followed for CVD events (n = 319 during 5.5-year follow-up). Discordance, defined as values of LDL-P and LDL-C differing by ≥ 12 percentile units to give equal-sized concordant and discordant subgroups, was related to CVD events and to carotid IMT in models predicting outcomes for a 1 SD difference in LDL-C or LDL-P, adjusted for age, gender, and race. RESULTS LDL-C and LDL-P were associated with incident CVD overall: hazard ratios (HR 1.20, 95% CI [CI] 1.08-1.34; and 1.32, 95% CI 1.19-1.47, respectively, but for those with discordant levels, only LDL-P was associated with incident CVD (HR 1.45, 95% CI 1.19-1.78; LDL-C HR 1.07, 95% CI 0.88-1.30). IMT also tracked with LDL-P rather than LDL-C, ie, adjusted mean IMT of 958, 932, and 917 microm in the LDL-P > LDL-C discordant, concordant, and LDL-P < LDL-C discordant subgroups, respectively, with the difference persisting after adjustment for LDL-C (P = .002) but not LDL-P (P = .60). CONCLUSIONS For individuals with discordant LDL-C and LDL-P levels, the LDL-attributable atherosclerotic risk is better indicated by LDL-P.

Weight Change Is Associated With Change in Arterial Stiffness Among Healthy Young Adults

BACKGROUND Arterial stiffness has been associated with aging, hypertension, and diabetes; however, little data has been published examining risk factors associated with arterial stiffness in elderly individuals. METHODS Longitudinal associations were made between aortic stiffness and risk factors measured approximately 4 years earlier. Aortic pulse wave velocity (PWV), an established index of arterial stiffness, was measured in 356 participants (53.4% women, 25.3% African American), aged 70 to 96 years, from the Pittsburgh site of the Cardiovascular Health Study during 1996 to 1998. RESULTS Mean aortic pulse wave velocity (850 cm/sec, range 365 to 1863) did not differ by ethnicity or sex. Increased aortic stiffness was positively associated with higher systolic blood pressure (SBP), age, fasting and 2-h postload glucose, fasting and 2-h insulin, triglycerides, waist circumference, body mass index, truncal fat, decreased physical activity, heart rate, and common carotid artery wall thickness (P < .05). After controlling for age and SBP, the strongest predictors of aortic stiffness in men were heart rate (P = .001) and 2-h glucose (P = .063). In women, PWV was positively associated with heart rate (P = .018), use of antihypertensive medication (P = .035), waist circumference (P = .030), and triglycerides (P = .081), and was negatively associated with physical activity (P = .111). Results were similar when the analysis was repeated in nondiabetic individuals and in those free of clinical or subclinical cardiovascular disease in 1992 to 1993. CONCLUSIONS In these elderly participants, aortic stiffness was positively associated with risk factors associated with the insulin resistance syndrome, increased common carotid intima-media thickness, heart rate, and decreased physical activity measured several years earlier.

Volumetric BMD and vascular calcification in middle-aged women : The study of women's health across the nation

Risk factors for arterial stiffness progression have not been well characterized. We examined the relationship between arterial stiffness progression and body weight and weight gain in a group of healthy young adults. Aortic pulse-wave velocity was assessed at 2 time points approximately 2 years apart in 152 white and black adults aged 20 to 40 years, and was standardized by the time between visits to obtain annualized pulse-wave velocity changes. Blacks had 15.5 cm/s per year larger annual pulse-wave velocity increases compared with whites (P=0.02), even after multivariable adjustment for weight and blood pressure changes. Larger annual pulse-wave velocity increases were also associated with larger baseline body weight (P=0.02), waist girth (P=0.003), and body mass index (P<0.001), and greater annual weight gain (P=0.02), after adjustment for baseline pulse-wave velocity. After multivariable adjustment that included blood pressure changes, larger baseline waist girth (P=0.009), baseline body mass index (P=0.001), body mass index increase (P=0.037), and weight gain (P=0.017) remained significantly associated with larger annual pulse-wave velocity progression. Weight change showed a direct relationship with pulse-wave velocity change; mean annual pulse-wave velocity changes were −29.9 cm/s per year (regression) for those with ≥4.5 kg annual weight loss and 18.2 cm/s per year (progression) for those with ≥4.5 kg annual weight gain. These data show strong associations between weight gain and arterial stiffness progression, as well as between weight loss and arterial stiffness regression. These data greatly underscore the vascular benefit of weight loss. Successful weight loss programs in young adults, particularly blacks, are needed.