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Secondary prevention of heart disease with statins

Editor—There is no substitute for properly randomised controlled trials in evaluating the effects of drug treatments. But trial selection criteria may make patients studied substantially different from those who will receive treatment in clinical practice. For example, in the Medical Research Council's mild hypertension trial cardiovascular mortality rates were similar to those of normotensive men in the general population.1 Examining the associations between treatment and outcome in typical patients is potentially useful in understanding generalisability of effects. 
 
Fair comparisons of people treated with statins and people not treated with statins, who have all had a cardiovascular event, are possible despite their demographic and comorbidity differences. Multivariable logistic regression is a standard and robust statistical technique for making adjustments for measured confounding factors but, as Fleetcroft and Steel point out, an inherent weakness of observational methods is that unmeasured confounders cannot be taken into account. Penston thinks our analyses are invalid as the all cause mortality effect is bigger than the recurrence effect of cardiovascular disease. The 95% confidence intervals of these effects overlap, indicating that any apparent difference between these outcomes may simply represent the play of chance. In randomised controlled trials of statins, all cause mortality and recurrence effects of cardiovascular disease are remarkably similar as the latter drive the all cause mortality effect.2,3 
 
Improvements in treatment and survival prospects of patients have occurred over the period of the study, and our Cox regressions, using a time dependent statin variable, allow for this. However, simple stratified analyses of statin use in the first and second halves of our study showed similar associations—relative risks for all cause mortality was 0.62 (95% confidence interval 0.49 to 0.77) for the period 1993-7 and 0.73 (0.54 to 0.98) for the period 1998-2001, showing that temporal trends do not explain our findings. 
 
Mills is correct, but in cardiovascular disease idiosyncratic terminology has arisen and is widely used. The American Heart Association defines secondary prevention as “identifying and treating people with established disease and those at very high risk of developing cardiovascular disease,”4 as does the World Health Organization.5