Background: 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.
Methods and results: 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 > or =95% with Thrombolysis In Myocardial Infarction (TIMI) trial grade < or =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).
Conclusions: Statin therapy is associated with enhanced coronary collateral formation in patients with severely diseased coronary arteries.