Relative risk for cardiovascular atherosclerotic events after

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Abstract

Background:
Smoking history is often di- or trichotomized into for example never, ever or current smoking". However, smoking must be treated as a time-dependent covariate when lifetime data is available. In particular, individuals do not smoke at birth, there is usually a wide variation with respect to smoking history, and smoking cessation must also be considered.

Methods:
Therefore we analyzed smoking as a time-dependent risk factor for cardiovascular atherosclerotic events in a cohort of 2400 individuals with familial hypercholesterolemia who were followed from birth until 2004. Excess risk after smoking-cessation was modelled in a Cox regression model with linear and exponential decaying trends. The model with the highest likelihood value was used to estimate the decay of the excess risk of smoking.

Results:
Atherosclerotic events were observed in 779 patients with familial hypercholesterolemia and 1569 individuals had a smoking history. In the model with the highest likelihood value the risk reduction of smoking after cessation follows a linear pattern with time and it appears to take 6 to 9 years before the excess risk is reduced to zero. The risk of atherosclerotic events due to smoking was estimated as 2.1 (95% confidence interval 1.5; 2.9).

Conclusion:
It was concluded that excess risk due to smoking declined linearly after cessation in at least six to nine years.

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Background
Smoking is one of the most important risk factors for disease, particularly for lung, and cardiovascular disease(CVD) 1. In many studies where lifetime smoking data is not available, a patient's smoking history is dichotomized into yes or no smoking", or trichotomized into "never, ever, or current smoking". Subsequently, odds ratios or relative risks are calculated in a case-control study or cohort study, respectively. Although likely crude, the untoward effect of smoking is clearly illustrated in suchanalyses, provided that smoking occurred before development of disease in the case-control study, or that followup in the cohort study started at some point in time at which smoking history could be determined. Many prognostic models have been developed with smoking as a time-independent factor, i.e. not changing in time. Examples of such models for cardiovascular disease are the Framingham risk score 2, the Procam risk score 3, and recently the score developed by Yusuf et al. 1. It is challenging to collect reliable data on smoking from decades ago, and this may be the reason why di- or trichotomization, is often used to summarize smoking history. But this s often suboptimal since it is likely that a person who ceased smoking ten years ago is at a different risk for developing cardiovascular disease, for instance, than a person who ceased smoking at the day follow-up started in a cohort study./>

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