Author + information
- Received August 4, 2015
- Revision received August 31, 2015
- Accepted September 3, 2015
- Published online May 1, 2016.
- Catherine E. Handy, MD, MPHa,
- Chintan S. Desai, MDa,
- Zeina A. Dardari, MSa,
- Mouaz H. Al-Mallah, MDb,
- Michael D. Miedema, MDc,
- Pamela Ouyang, MDa,
- Matthew J. Budoff, MDd,
- Roger S. Blumenthal, MDa,
- Khurram Nasir, MDa,e,f,g and
- Michael J. Blaha, MD, MPHa,∗ ()
- aThe Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, Maryland
- bHeart and Vascular Institute, Henry Ford Hospital, Detroit, Michigan
- cMinneapolis Heart Institute and Minneapolis Heart Institute Foundation, Minneapolis, Minnesota
- dDivision of Cardiology, Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, California
- eCenter for Healthcare Advancement & Outcomes, Baptist Health South Florida, Miami, Florida
- fDepartment of Medicine, Herbert Wertheim College of Medicine, Florida International University, Miami, Florida
- gDepartment of Epidemiology, Robert Stempel College of Public Health, Florida International University, Miami, Florida
- ↵∗Reprint requests and correspondence:
Dr. Michael J. Blaha, The Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Carnegie 565A, 600 North Wolfe Street, Baltimore, Maryland 21287.
Objectives This study sought to determine if coronary artery calcium (CAC) is associated with incident noncardiovascular disease.
Background CAC is considered a measure of vascular aging, associated with increased risk of cardiovascular and all-cause mortality. The relationship with noncardiovascular disease is not well defined.
Methods A total of 6,814 participants from 6 MESA (Multi-Ethnic Study of Atherosclerosis) field centers were followed for a median of 10.2 years. Modified Cox proportional hazards ratios accounting for the competing risk of fatal coronary heart disease were calculated for new diagnoses of cancer, pneumonia, chronic obstructive pulmonary disease (COPD), chronic kidney disease (CKD), deep vein thrombosis/pulmonary embolism, hip fracture, and dementia. Analyses were adjusted for age; sex; race; socioeconomic status; health insurance status; body mass index; physical activity; diet; tobacco use; number of medications used; systolic and diastolic blood pressure; total and high-density lipoprotein cholesterol; antihypertensive, aspirin, and cholesterol medication; and diabetes. The outcome was first incident noncardiovascular disease diagnosis.
Results Compared with those with CAC = 0, those with CAC >400 had an increased hazard of cancer (hazard ratio [HR]: 1.53; 95% confidence interval [CI]: 1.18 to 1.99), CKD (HR: 1.70; 95% CI: 1.21 to 2.39), pneumonia (HR: 1.97; 95% CI: 1.37 to 2.82), COPD (HR: 2.71; 95% CI: 1.60 to 4.57), and hip fracture (HR: 4.29; 95% CI: 1.47 to 12.50). CAC >400 was not associated with dementia or deep vein thrombosis/pulmonary embolism. Those with CAC = 0 had decreased risk of cancer (HR: 0.76; 95% CI: 0.63 to 0.92), CKD (HR: 0.77; 95% CI: 0.60 to 0.98), COPD (HR: 0.61; 95% CI: 0.40 to 0.91), and hip fracture (HR: 0.31; 95% CI: 0.14 to 0.70) compared to those with CAC >0. CAC = 0 was not associated with less pneumonia, dementia, or deep vein thrombosis/pulmonary embolism. The results were attenuated, but remained significant, after removing participants developing interim nonfatal coronary heart disease.
Conclusions Participants with elevated CAC were at increased risk of cancer, CKD, COPD, and hip fractures. Those with CAC = 0 are less likely to develop common age-related comorbid conditions, and represent a unique population of “healthy agers.”
This research was supported by contracts N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, and N01-HC-95169 from the National Heart, Lung, and Blood Institute, and by grants UL1-TR-000040 and UL1-TR-001079 from the National Center for Research Resources. Dr. Nasir is on the Advisory Board of Quest Diagnostic and is a consultant for Regeneron. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Drs. Handy and Desai contributed equally to this work.
- Received August 4, 2015.
- Revision received August 31, 2015.
- Accepted September 3, 2015.
- American College of Cardiology Foundation