To The Editor:
The editorial by Professor Grundy1 on the statin trials has prompted this letter, which is based on personal observations on treatment of atherosclerotic ischemic heart disease2 that has reduced non-HDL to “subnormal” levels and halted atherosclerosis.
Professor Grundy’s editorial1 on the 3 major statin trials has failed to resolve the question of how low LDL should be reduced to have the maximum effect in halting atherosclerosis.
It is now accepted that the severity of atherosclerosis is related to the LDL level. However, at any particular level, the degree of atherosclerosis can vary enormously.3 The study by Cullen and Assmann3 implicates a factor, probably inherited, possibly located in vascular endothelium and/or the platelets but perhaps elsewhere, that augments the atherogenic action of LDL and that, for convenience, I have called the coronary atherosclerotic index (CAI).
Those individuals with a high CAI would be prone to develop atherosclerosis when LDL levels might be considered normal and would correspond to Grundy’s Figure 2, linear model A; those with moderate CAI to Figure 2, curvilinear model C; and those with low CAI to Figure 2, threshold model B. A consideration of the statin trials would show that most of the patients in the WOSCOPS trial would have a low CAI and thus be expected to have a threshold for LDL. However, in the CARE and 4S trials, a small proportion of patients with a high CAI would be diluted with a larger proportion of patients with moderate and low CAIs, and the results would thus be confounded. It would be instructive to stratify patients in the CARE and 4S trials into the 3 CAI groups and to compare risks with LDL levels. It would also be interesting to compare the relative risks of maintaining 1 group of patients with a high CAI at a mean LDL level <2.0 mmol/L with a similar group maintained at <3.0 mmol/L.
- Copyright © 1999 by American Heart Association