Author + information
- Lewis H. Kuller, MD, PhD⁎ ( and )
- Daniel Edmundowicz, MD, MS
- ↵⁎Department of Epidemiology, University of Pittsburgh, GSPH, 130 North Bellefield Avenue, Room 550, Pittsburgh, Pennsylvania 15213
In a recent issue of the Journal, Lauer (1) suggested that the lack of effect of prostate-specific antigen (PSA) screening for prostate cancer is an important reason to be cautious about screening for subclinical coronary artery disease. Unfortunately, his argument might be fallacious. First, he states that prostate cancer death rates have not declined, despite widespread screening. Quite the contrary is true. Death rates due to prostate cancer have substantially declined in the U.S. from 39.2 to 23.6/100,000 from 1992 to 2006 (2–4). This is an age-adjusted decline of approximately 4%/year. From 1991 to 2004, prostate cancer mortality has declined much more rapidly in the U.S. with the frequent use of PSA testing than in the United Kingdom, where there is less screening (4.2%/year in the U.S. vs. 1.1%/year in the United Kingdom) (5).
Second, he points to the recent report of the PLCO (Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial) that failed to document benefit of prostate cancer screening with PSA (6). Unfortunately, the PLCO trial was contaminated by high screening rates in the comparison group and a lack of control for therapies for prostate cancer. It is estimated that probably 50% of men 50 years of age and older in the U.S. have a PSA test. Most recently, PSA testing was evaluated in a population that was previously unexposed to PSA testing. A randomized trial of 20,000 men in Göteborg, Sweden, 50 to 64 years of age at entry were followed an average of 14 years (7). The reduction of prostate cancer deaths was 40% (range 0.17 to 64) in the PSA screening versus control group, p = 0.002. Approximately 293 men needed to be screened and 12 needed to be diagnosed to prevent 1 prostate cancer death—44 deaths in the intervention versus 78 in the control group. The effect of PSA testing on reducing mortality in this study was of similar magnitude as mammography screening for breast cancer.
A trial to evaluate screening of asymptomatic individuals for the prevention of subsequent clinical coronary artery disease events (i.e., screening asymptomatic individuals with coronary calcium detection) is impractical. The technology is widely available; its prognostic implications are well-published; and preventive therapies such as lipid lowering, antihypertensive therapy, and lifestyle modifications are now accessible and affordable. Such a trial, like the PLCO trial, will be contaminated by crossovers, use or lack of use of statins and other effective therapies, and poor compliance with dietary and pharmacological therapies. The trial of hard end points (i.e., coronary heart disease [CHD] deaths or myocardial infarction), will require long follow-up because of the early stage of incubation of atherosclerosis in which these individuals will be detected. Do we really need to prove that lipid lowering is effective in individuals with atherosclerosis for reducing CHD mortality? Do we need to waste another 7 to 10 years and millions of dollars of valuable research funds? The key is maximizing the use of proven effective preventive pharmacological and nonpharmacological therapies by targeting the population most likely to benefit from them and thereby substantially reducing CHD incidence, mortality, and costs of health care.
- American College of Cardiology Foundation
- Lauer M.S.
- Kinsey T.,
- Jemal A.,
- Liff J.,
- Ward E.,
- Thun M.
- DeLancey J.O.L.,
- Thun M.J.,
- Jemal A.,
- Ward E.M.