Author + information
- Received September 8, 2017
- Revision received December 21, 2017
- Accepted December 23, 2017
- Published online May 6, 2019.
- Adam Leigh, MDa,
- John W. McEvoy, MBBCh, MHSb,
- Parveen Garg, MDc,
- J. Jeffrey Carr, MD, MScd,
- Veit Sandfort, MDe,
- Elizabeth C. Oelsner, MD, MPHf,
- Matthew Budoff, MDg,
- David Herrington, MD, MHSa and
- Joseph Yeboah, MD, MSa,∗ ()
- aHeart and Vascular Center of Excellence, Wake Forest University School of Medicine, Winston Salem, North Carolina
- bCiccarone Center for the Prevention of Heart Disease, Johns Hopkins University School of Medicine, Baltimore, Maryland
- cDivision of Cardiovascular Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California
- dDepartments of Cardiology and Radiology, Vanderbilt University School of Medicine, Nashville, Tennessee
- eClinical Center, National Institutes of Health, Bethesda, Maryland
- fDepartments of Medicine and Epidemiology, Columbia University, New York, New York
- gLos Angeles Biomedical Research Institute at Harbor–University of California, Los Angeles, Torrance California
- ↵∗Address for correspondence:
Dr. Joseph Yeboah, Heart and Vascular Center of Excellence, Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157.
Objectives This study assessed the utility of the pooled cohort equation (PCE) and/or coronary artery calcium (CAC) for atherosclerotic cardiovascular disease (ASCVD) risk assessment in smokers, especially those who were lung cancer screening eligible (LCSE).
Background The U.S. Preventive Services Task Force recommended and the Centers for Medicare & Medicaid Services currently pays for annual screening for lung cancer with low-dose computed tomography scans in a specified group of cigarette smokers. CAC can be obtained from these low-dose scans. The incremental utility of CAC for ASCVD risk stratification remains unclear in this high-risk group.
Methods Of 6,814 MESA (Multi-Ethnic Study of Atherosclerosis) participants, 3,356 (49.2% of total cohort) were smokers (2,476 former and 880 current), and 14.3% were LCSE. Kaplan-Meier, Cox proportional hazards, area under the curve, and net reclassification improvement (NRI) analyses were used to assess the association between PCE and/or CAC and incident ASCVD. Incident ASCVD was defined as coronary death, nonfatal myocardial infarction, or fatal or nonfatal stroke.
Results Smokers had a mean age of 62.1 years, 43.5% were female, and all had a mean of 23.0 pack-years of smoking. The LCSE sample had a mean age of 65.3 years, 39.1% were female, and all had a mean of 56.7 pack-years of smoking. After a mean of 11.1 years of follow-up 13.4% of all smokers and 20.8% of LCSE smokers had ASCVD events; 6.7% of all smokers and 14.2% of LCSE smokers with CAC = 0 had an ASCVD event during the follow-up. One SD increase in the PCE 10-year risk was associated with a 68% increase risk for ASCVD events in all smokers (hazard ratio: 1.68; 95% confidence interval: 1.57 to 1.80) and a 22% increase in risk for ASCVD events in the LCSE smokers (hazard ratio: 1.22; 95% confidence interval: 1.00 to 1.47). CAC was associated with increased ASCVD risk in all smokers and in LCSE smokers in all the Cox models. The C-statistic of the PCE for ASCVD was higher in all smokers compared with LCSE smokers (0.693 vs. 0.545). CAC significantly improved the C-statistics of the PCE in all smokers but not in LCSE smokers. The event and nonevent net reclassification improvements for all smokers and LCSE smokers were 0.018 and −0.126 versus 0.16 and −0.196, respectively.
Conclusions In this well-characterized, multiethnic U.S. cohort, CAC was predictive of ASCVD in all smokers and in LCSE smokers but modestly improved discrimination over and beyond the PCE. However, 6.7% of all smokers and 14.2% of LCSE smokers with CAC = 0 had an ASCVD event during follow-up.
- atherosclerotic cardiovascular disease
- cigarette smokers
- coronary artery calcium
- pooled cohort equation
This research was supported by grant T32HL076132 and contracts HHSN268201500003I, 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. Herrington is the principal investigator for grant T32HL076132 from the National Heart, Lung, and Blood Institute. Dr. Budoff has received grant support from the National Institutes of Health and GE Healthcare. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received September 8, 2017.
- Revision received December 21, 2017.
- Accepted December 23, 2017.
- 2019 American College of Cardiology Foundation
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