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J Am Coll Cardiol, 2008; 51:91-92, doi:10.1016/j.jacc.2007.08.053 © 2008 by the American College of Cardiology Foundation |
* Department of Public Health and General Practice, University of Oulu and University Hospital, P.O. Box 5000, FIN-90014 Oulun Yliopisto, Finland (Email: timo.strandberg{at}oulu.fi).
Consequently, I made further simple calculations based on Table 2 in the study by Alsheikh-Ali et al. (1). There was a significant correlation between achieved LDL and cancer per 100,000 person-years (r = –0.75, p = 0.003), but also between mean age in trials (median age 65 years for the HPS [Heart Protection Study]) and cancer incidence (r = 0.82, p = 0.0006). This is naturally expected as cancer risk increases with age. In multivariate analyses, adjusted for sample size, achieved LDL was a significant predictor of cancer incidence (p = 0.03). However, when age was included in the model, age (p = 0.008)—but not achieved LDL (p = 0.42)—was a significant predictor of cancer risk.
I think that these findings, together with totality of evidence including data from the TNT (Treating to New Targets) study (2) and also from the IDEAL (Incremental Decrease in Clinical Endpoints Through Aggressive Lipid Lowering) study (3), at this stage refute a true link between achieved LDL and cancer risk.
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