Determinants of carotid endarterectomy anatomic durability: effects of serum lipids and lipid-lowering drugs.

OBJECTIVES: Carotid endarterectomy (CEA) remains the gold standard for treatment of carotid stenosis. With inevitable comparisons of catheter-based therapy to all aspects of CEA, this study of a large contemporary series was undertaken to evaluate the determinants of anatomic durability of CEA.
METHODS: During the interval (1989 through 1999), 2,127 primary, isolated CEAs with selective patching (50.2%) were performed in 1,853 patients (61.8% male, 36.1% symptomatic). End points included patient longevity and perioperative morbidity as well as evidence of CEA anatomic durability as defined by duplex evaluation: CEA restenosis (moderate, >50%, or greater recurrent stenosis), which included CEA anatomic failure (severe, >70%, restenosis/carotid occlusion). The incidence of CEA recurrent stenosis was temporally assessed early (<2 years) and late (>2 years) after operation. Clinical and surgical variables potentially associated with the study endpoints were analyzed by univariate and multivariate methods.
RESULTS: The perioperative stroke and death rate was 1.4% and the 2-year and 10-year survival was 88.1% and 44.9%, respectively. Anatomic failure after CEA developed in 3.9% at 2 years and in 8.5% at 5 years; only 3.2% of CEA patients underwent reoperation during a mean follow-up of 73.4 months. Early (<2 years) analysis revealed 12.2% restenosis, whereas late (>2 years) results identified 9.8% progression of carotid stenosis and a 5.8% rate of anatomic failure. Multivariate analysis determined elevated creatinine (odds ratio [OR], 1.719, P < .001) and female gender (OR, 1.564; P < .02) correlated with early restenosis. Surgical patch closure and lipid-lowering drugs were protective for both early restenosis, with ORs of 0.543 (P < .0.001) and 0.601 (P < .007) and early anatomic failure ORs of 0.469 (P < .02) and 0.517 (P < .03), respectively. Although only elevated serum cholesterol (OR, 1.009; P < .03) correlated with late anatomic failure, only lipid-lowering drugs were protective for both late freedom from progression of disease (OR, 0.202; P < .0002) or late CEA anatomic failure (OR, 0.128; P < .0003).
CONCLUSIONS: The association of female gender and elevated cholesterol with recurrent carotid stenosis is confirmed, elevated creatinine is introduced as a risk factor, and surgical patch repair is protective for early CEA recurrent carotid stenosis. The unique findings of the significant, beneficial effects of lipid-lowering drugs on both early and late CEA anatomic durability and patient survival indicate that such therapy should be instituted in most patients after CEA.