The presence of coronary collateral vessels has been associated with improved clinical outcome in patients with coronary artery disease. Animal experiments have shown that hydroxymethyl glutaryl coenzyme A reductase inhibitors (statins) can promote angiogenesis in ischemic tissues in a cholesterol-independent manner. We hypothesized that statin therapy is associated with increased coronary collateral formation in patients with severe coronary artery disease.

Patients undergoing clinically indicated coronary angiography at the Tufts–New England Medical Center from September 2000 to April 2001 who had at least 1 major coronary artery occlusion, or a stenosis of ≥95% with Thrombolysis In Myocardial Infarction (TIMI) trial grade ≤1 anterograde flow on their angiograms, were included. Fifty-one patients were taking statins before admission, and 43 patients were not. Their angiograms were reviewed and coronary collaterals were graded from 0 to 3 according to the Cohen-Rentrop method. The statin-treated group had a significantly higher mean collateral score compared with the patients not taking statins (2.05 vs 1.52, P = .005). Multivariate analysis supported the significance of the effect of statin therapy on the collateral score. There was no relation between collateral score and low-density lipoprotein levels (r = −0.06, P = .64). The statin-treated group also had a significantly higher left ventricular ejection fraction compared to the patients not taking statins (51% vs 44%, P < .05).

Statin therapy is associated with enhanced coronary collateral formation in patients with severely diseased coronary arteries.