Influence of serum cholesterol and cholesterol subfractions on restenosis after successful coronary angioplasty. A quantitative angiographic analysis of 3336 lesions.

BACKGROUND

Previous reports have suggested that hyperlipidemia may be associated with increased restenosis after successful coronary angioplasty. These studies have been compromised, however, by their retrospective nature, the small numbers involved, differences in the definition of restenosis, and inadequate quantitative angiographic follow-up at a prespecified time interval. The objective of the study was to examine the relation between serum cholesterol and long-term restenosis after coronary angioplasty, using quantitative angiography, at a predetermined time interval.

METHODS AND RESULTS

The study population comprised 2753 patients (3336 lesions) prospectively enrolled and successfully completing four major restenosis trials. Cineangiographic films were processed and analyzed at a central angiographic core laboratory with the use of an automated interpolated edge-detection technique. Serum total cholesterol was measured at trial entry and at 6 months. Hypercholesterolemia was defined as total cholesterol > 7.8 mmol.L-1 at trial entry. Two approaches were used to assess restenosis: first, a categorical approach using the cutoff point of > 50% diameter stenosis at follow-up and second, a continuous approach examining changes in minimal luminal dimensions, the absolute loss (change in minimum luminal diameter after PTCA to follow-up, in mm) and relative loss (absolute loss corrected for vessel size), which may give a better understanding of the underlying pathological process involved. One hundred sixty patients with 191 lesions (5.73%) had hypercholesterolemia (total cholesterol, > 7.8 mmol.L-1; mean +/- SD, 8.46 +/- 0.75 mmol.L-1) and 2593 patients with 3145 lesions (94.27%) normal cholesterol (5.67 +/- 1.06 mmol.L-1). The restenosis rate was similar in patients with and without hypercholesterolemia (31.9% versus 33.7%, respectively; relative risk, 0.975; 95% CI, 0.882 to 1.077; P = .68). Similarly, there was no difference in either the absolute or relative loss between patients with and without hypercholesterolemia (0.31 +/- 0.53 versus 0.32 +/- 0.53 mm and 0.12 +/- 0.20 versus 0.13 +/- 0.21, respectively, P = NS for both). Conversely, the total serum cholesterol in patients with restenosis (using the categorical definition) was similar to those without restenosis (5.84 +/- 1.24 versus 5.81 +/- 1.22 mmol/L, respectively, P = NS). Dividing the population into deciles according to total cholesterol and examining the categorical restenosis rate (by chi 2) as well as the absolute and relative loss by ANOVA again revealed no significant differences between deciles. Subgroup analysis of 579 patients (667 lesions) with HDL and LDL cholesterol levels available again revealed no differences in the categorical restenosis rate (by chi 2) or the absolute or relative loss between deciles according to LDL, HDL, or LDL:HDL ratio, suggesting no influence of these cholesterol subfractions on restenosis.

CONCLUSIONS

Our results indicate that there is no association between cholesterol and restenosis by either a categorical or continuous approach, suggesting that measures aimed at reducing total cholesterol are unlikely to significantly influence postangioplasty restenosis.