The cardiovascular event reduction tool (CERT)—a simplified cardiac risk prediction model developed from the West of Scotland Coronary Prevention Study (WOSCOPS)

doi:10.1016/S0002-9149(99)00847-4

The American Journal of Cardiology

Volume 85, Issue 6, 15 March 2000, Pages 720-724

https://doi.org/10.1016/S0002-9149(99)00847-4 Get rights and content

Abstract

The clinical decision to treat hypercholesterolemia is premised on an awareness of patient risk, and cardiac risk prediction models offer a practical means of determining such risk. However, these models are based on observational cohorts where estimates of the treatment benefit are largely inferred. The West of Scotland Coronary Prevention Study (WOSCOPS) provides an opportunity to develop a risk-benefit prediction model from the actual observed primary event reduction seen in the trial. Five-year Cox model risk estimates were derived from all WOSCOPS subjects (n = 6,595 men, aged 45 to 64 years old at baseline) using factors previously shown to be predictive of definite fatal coronary heart disease or nonfatal myocardial infarction. Model risk factors included age, diastolic blood pressure, total cholesterol/high-density lipoprotein ratio (TC/HDL), current smoking, diabetes, family history of fatal coronary heart disease, nitrate use or angina, and treatment (placebo/40-mg pravastatin). All risk factors were expressed as categorical variables to facilitate risk assessment. Risk estimates were incorporated into a simple, hand-held slide rule or risk tool. Risk estimates were identified for 5-year age bands (45 to 65 years), 4 categories of TC/HDL ratio (<5.5, 5.5 to <6.5, 6.5 to <7.5, ≥7.5), 2 levels of diastolic blood pressure (<90, ≥90 mm Hg), from 0 to 3 additional risk factors (current smoking, diabetes, family history of premature fatal coronary heart disease, nitrate use or angina), and pravastatin treatment. Five-year risk estimates ranged from 2% in very low-risk subjects to 61% in the very high-risk subjects. Risk reduction due to pravastatin treatment averaged 31%. Thus, the Cardiovascular Event Reduction Tool (CERT) is a risk prediction model derived from the WOSCOPS trial. Its use will help physicians identify patients who will benefit from cholesterol reduction.

Section snippets

Methods

The design of WOSCOPS has been previously described.3, 7 In the present analysis, Cox proportional hazards regression8 was performed for the entire study population (intention-to-treat), placebo and treated groups (n = 6,595 men, aged 45 to 64 years old at baseline) using factors previously shown to be predictive of the primary event for the trial population.9 Model risk factors included age, diastolic blood pressure, total cholesterol/high-density lipoprotein ratio (TC/HDL), current smoking,

Results

The CERT model results are shown in Table Ifor all model variables. All continuous risk factors (diastolic blood pressure, TC/HDL, age) were expressed as categorical variables that were defined as terms corresponding to combinations of any 1, 2, or 3 of these risk factors. To assess the benefit of therapy, a term for treatment was included in the model. The inclusion of treated patients and a treatment variable did not appreciably change the hazard ratios for the other variables. The hazard

Discussion

This study was not intended to elucidate or identify specific predictors of cardiovascular disease among WOSCOPS patients. This study has been done previously for both cohorts using more appropriate epidemiologic methods.9 The goal of this study was to develop a utilitarian risk model for deriving risk and risk reduction estimates associated with an intervention. Existing risk prediction models are based primarily on observational epidemiologic cohorts,1, 2 not interventional trials, and

References (13)

P.W.F. Wilson et al.
Prediction of coronary heart disease using risk factor categories
Circulation
(1998)
K.M. Anderson et al.
An updated coronary risk profilea statement for health professionals
Circulation
(1991)
Influence of pravastatin and plasma lipids on clinical events in the West of Scotland Coronary Prevention trial
Circulation
(1998)
G. Fager
Cholesterol reduction and clinical benefit. Are there limits to our expectations?
Arterioscler Thromb Vasc Biol
(1997)
P. Greenland et al.
Problems on the pathway from risk assessment to risk reduction
Circulation
(1998)
F.H. Muldoon et al.
The emerging role of statins in the prevention of coronary heart disease. Statins are effective but we need better ways of assessing risk
BMJ
(1997)

There are more references available in the full text version of this article.

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Preventive CardiologyThe cardiovascular event reduction tool (CERT)—a simplified cardiac risk prediction model developed from the West of Scotland Coronary Prevention Study (WOSCOPS)

Abstract

Section snippets

Methods

Results

Discussion

Prediction of coronary heart disease using risk factor categories

Circulation

An updated coronary risk profilea statement for health professionals

Circulation

Influence of pravastatin and plasma lipids on clinical events in the West of Scotland Coronary Prevention trial

Circulation

Cholesterol reduction and clinical benefit. Are there limits to our expectations?

Arterioscler Thromb Vasc Biol

Problems on the pathway from risk assessment to risk reduction

Circulation

The emerging role of statins in the prevention of coronary heart disease. Statins are effective but we need better ways of assessing risk

BMJ

Preventive Cardiology
The cardiovascular event reduction tool (CERT)—a simplified cardiac risk prediction model developed from the West of Scotland Coronary Prevention Study (WOSCOPS)