Statin Use Appears to Enhance Coronary Collateral Formation

Collateralization of severely diseased coronary arteries is greater in patients on statin therapy than in those who are not, researchers report. As Dr. Richard H. Karas put it in comments to Reuters Health, “Patients who are taking statins might, in effect, grow their own ‘bypass’ blood vessels.”

Dr. Karas and colleagues at Tufts University School of Medicine in Boston, Massachusetts, note in their paper in the November issue of the American Heart Journal that “animal experiments have shown that hydroxymethyl glutaryl coenzyme A reductase inhibitors (statins) can promote angiogenesis in ischemic tissues in a cholesterol-independent manner.”

To investigate any similar effect in humans, the researchers studied 94 patients with at least one major coronary artery occlusion who were undergoing clinically indicated coronary angiography. Prior to admission, 51 patients were taking statins, and 43 were not.

The team graded coronary collaterals on the angiograms from 0 to 3 based on the degree of side vessel filling and epicardial perfusion. Univariate analysis showed that the mean collateral score was significantly higher among statin-treated patients than those not taking statins (2.05 versus 1.52, p = 0.005). The association remained significant on multivariate analysis (p = 0.008).

Moreover, compared with patients not taking statins, those in the statin-treated group had a significantly higher mean left ventricular ejection fraction (51% versus 44%, p < 0.05). The investigators found that there was no association between collateral score and low-density lipoprotein levels. “These findings lend further support to the concept that statins can have benefits in addition to those derived directly from cholesterol lowering,” Dr. Karas commented. He and his colleagues say the “association noted in this observational study requires confirmation from a study of a randomized patient population.” Am Heart J 2003;146:876-881.