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J Am Coll Cardiol, 2001; 38:56-63 © 2001 by the American College of Cardiology Foundation |
a NHMRC Clinical Trials Center, University of Sydney, Sydney, Australia
Core Research Group, University of Queensland, Brisbane, Australia
Department of Social and Preventive Medicine, University of Queensland, Brisbane, Australia
Royal Prince Alfred Hospital, Sydney, Australia
|| Launceston General Hospital, Launceston, Australia
¶ Waikato Hospital, Hamilton, New Zealand, Australia
# Greenlane Hospital, Auckland, New Zealand
** Sir Charles Gairdner Hospital, Perth, Australia
National Heart Foundation, Melbourne, Australia
Manuscript received October 10, 2000; revised manuscript received March 22, 2001, accepted April 5, 2001.
Reprint requests and correspondence: Dr. Ian Marschner, NHMRC Clinical Trials Center, Level 5, Building F, 88 Mallett Street, P.O.B. Locked Bag 77, Camperdown, NSW 2050, Australia
ian{at}ctc.usyd.edu.au
OBJECTIVES
We developed a prognostic strategy for quantifying the long-term risk of coronary heart disease (CHD) events in survivors of acute coronary syndromes (ACS).
BACKGROUND
Strategies for quantifying long-term risk of CHD events have generally been confined to primary prevention settings. The Long-term Intervention with Pravastatin in Ischemic Disease (LIPID) study, which demonstrated that pravastatin reduces CHD events in ACS survivors with a broad range of cholesterol levels, enabled assessment of long-term prognosis in a secondary prevention setting.
METHODS
Based on outcomes in 8,557 patients in the LIPID study, a multivariate risk factor model was developed for prediction of CHD death or nonfatal myocardial infarction. Prognostic indexes were developed based on the model, and low-, medium-, high- and very high-risk groups were defined by categorizing the prognostic indexes.
RESULTS
In addition to pravastatin treatment, the independently significant risk factors included: total and high density lipoprotein cholesterol, age, gender, smoking status, qualifying ACS, prior coronary revascularization, diabetes mellitus, hypertension and prior stroke. Pravastatin reduced coronary event rates in each risk level, and the relative risk reduction did not vary significantly between risk levels. The predicted five-year coronary event rates ranged from 5% to 19% for those assigned pravastatin and from 6.4% to 23.6% for those assigned placebo.
CONCLUSIONS
Long-term prognosis of ACS survivors varied substantially according to conventional risk factor profile. Pravastatin reduced coronary risk within all risk levels; however, absolute risk remained high in treated patients with unfavorable profiles. Our risk stratification strategy enables identification of ACS survivors who remain at very high risk despite statin therapy.
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