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Shah NS, Lloyd-Jones DM, O’Flaherty M, et al. Trends in Cardiometabolic Mortality in the United States, 1999-2017. JAMA. 2019;322(8):780–782. doi:10.1001/jama.2019.9161
While cardiovascular disease (CVD) death rates declined by approximately 36% from 2000 to 2014,1 CVD remains the leading cause of mortality among US adults.2 Annual declines in CVD mortality slowed between 2011 and 2014 (0.7% fewer CVD deaths per year),1,3 and it appears unlikely that strategic goals from the American Heart Association (20% reduction by 2020) will be achieved.4 To clarify the most recent national trends, we investigated CVD and other key cardiometabolic disease mortality rates overall, by sex, and by race from 1999 to 2017.
We determined mortality rates attributed to cardiometabolic diseases using death certificates from the Centers for Disease Control and Prevention’s Wide-Ranging Online Data for Epidemiologic Research (WONDER) from January 1, 1999, to December 31, 2017.2 Mortality rates in which the underlying cause of death was listed as heart disease (International Classification of Diseases, Tenth Revision [ICD-10] codes I00-I09, I11, I13, I20-I51), stroke (ICD-10 codes I60-I69), diabetes (ICD-10 codes E10-E14), or essential hypertension and hypertensive renal disease (ICD-10 codes I10, I12, I15) were age adjusted using the 2000 US standard population.1,2 Age-adjusted mortality rates (AAMRs) were examined overall (all decedents) and by sex-race (black and white only) groups. AAMR ratios quantifying racial disparities were calculated as number of deaths per 100 000 population in black individuals for every 1 death per 100 000 population in white individuals. The Joinpoint Regression Program (National Cancer Institute)5 was used to identify up to 1 inflection point in AAMR trends. Statistical trends and AAMR annual rate of change were identified using linear regression (SPSS version 21). Two-sided statistical significance was defined as P < .05. This study was determined to be exempt from review by the institutional review board at Northwestern University Feinberg School of Medicine.
In 1999, total deaths by cause (AAMR per 100 000 population) were 725 192 (266.5) from heart disease, 167 366 (61.6) from stroke, 68 399 (25.0) from diabetes, and 16 968 (6.2) from hypertension. In 2017, total deaths by cause (AAMR per 100 000 population) were 647 457 (165.0) from heart disease, 146 383 (37.6) from stroke, 83 564 (21.5) from diabetes, and 35 316 (9.0) from hypertension. During 1999-2017, 12.3% of fatal cardiometabolic events occurred in black individuals and 85.1% in white individuals, and 51.3% occurred in women.
AAMRs from 1999-2017 experienced an inflection point in 2010 for deaths due to heart disease, stroke, and diabetes (Table). The rate of AAMR decline for heart disease before 2010 was β = −8.3 (95% CI, −8.8 to −7.8; P < .001), indicating 8.3 fewer deaths per 100 000 population per year, vs β = −1.8 (95% CI, −2.5 to −1.0; P = .001) after 2010. AAMR declines between 1999-2010 for stroke were β = −2.3 (95% CI, −2.5 to −2.1; P < .001) and for diabetes were β = −0.4 (95% CI, −0.6 to −0.3; P < .001). AAMRs did not significantly change for stroke or diabetes between 2010 and 2017. The hypertension AAMR experienced an inflection point in 2003 and increased less rapidly thereafter (1999-2003: β = 0.3 [95% CI, 0.3 to 0.4]; P = .001 and 2003-2017: β = 0.1 [95% CI, 0.04 to 0.1]; P < .001).
Between 1999 and 2017, the AAMRs for heart disease, stroke, and diabetes declined, but the AAMR for hypertension increased in most sex-race groups except in black women, for whom the hypertension AAMR remained generally unchanged. Black individuals consistently had higher AAMRs compared with whites. In 2017, the highest AAMR ratios were in black compared with white women due to diabetes (2.09) and in black compared with white men due to hypertension (2.18). Black men consistently had the highest AAMRs across all underlying causes of death.
These findings demonstrate a continued but slower decline in AAMR for heart disease, a plateau in mortality rates from stroke and diabetes, and an increasing AAMR for hypertension (although hypertension as underlying cause of death remained relatively infrequent) between 2010 and 2017. Racial disparities in cardiometabolic causes of death persisted. Strengths of this study include up-to-date trends in cardiometabolic AAMRs and quantitative evaluation of slope change. Limitations include use of death certificate data, which may be subject to miscoding. Furthermore, these data do not identify if changes in AAMRs are due to changing disease incidence or case-fatality rates.
Clinical and public health efforts focusing on primordial and primary prevention throughout the life course, with an emphasis on identifying and addressing the causes of racial disparities, are needed to reverse the slowing of cardiometabolic mortality rate declines.
Accepted for Publication: June 6, 2019.
Correction: This article was corrected on October 1, 2019, for an incomplete author name.
Corresponding Author: Sadiya S. Khan, MD, MSc, Division of Cardiology, Department of Medicine and Preventive Medicine, Northwestern University Feinberg School of Medicine, 680 N Lake Shore Dr, 14-002, Chicago, IL 60611 (email@example.com).
Author Contributions: Dr Khan had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Concept and design: Shah, Lloyd-Jones, O'Flaherty, Capewell, Khan.
Acquisition, analysis, or interpretation of data: Shah, O'Flaherty, Kershaw, Carnethon, Khan.
Drafting of the manuscript: Shah.
Critical revision of the manuscript for important intellectual content: All authors.
Statistical analysis: Shah, Khan.
Obtained funding: O'Flaherty.
Administrative, technical, or material support: Lloyd-Jones.
Supervision: Lloyd-Jones, O'Flaherty, Capewell, Carnethon, Khan.
Conflict of Interest Disclosures: None reported.
Funding/Support: Research reported in this publication was supported by the National Institutes of Health (NIH) National Center for Advancing Translational Sciences (KL2TR001424).
Role of the Funder/Sponsor: The National Center for Advancing Translational Sciences did not contribute to design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.
Disclaimer: The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
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