BACKGROUND: The coronary collateral circulation is an alternative source of blood supply to myocardium in the presence of advanced coronary artery disease and the therapeutic promotion of collateral growth appears to be a valuable treatment strategy in these patients. Although it has been shown in in-vivo studies that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) promote vasculogenesis and accelerate coronary collateral development in ischemic tissues, there are discordant results in clinical studies. Our aim was to investigate the effect of statin therapy, including dosage and duration of treatment, on coronary collateral growth in patients with advanced coronary artery disease. METHODS: Study population consisted of 400 (306 men, with the mean age of 62+/-10 years) consecutive patients who have undergone clinically indicated coronary angiography and had at least one major coronary artery stenosis of > or =95%. Coronary collaterals were graded from 0 to 3 according to the Cohen-Rentrop method and patients with grade 0-1 collateral development were regarded as having poor collateral and patients with grade 2-3 collateral development were regarded as having good collateral. RESULTS: Among 400 patients, 196 (48%) were on statin therapy. Patients with good collateral score were more likely to have stable angina pectoris as clinical presentation (P<0.001), and were on statin therapy (P=0.001), and have multivessel disease (P=0.003). Statin therapy for less than 3 months had no effect on collateral development (P=0.19); however, patients who were on statin therapy for more than 3 months had significantly better collateral development (P=0.002). Statin therapy had no effect on coronary collateral development in patients having <10 mg atorvastatin-equivalent dose (P=0.13); however, patients having > or =10 mg atorvastatin-equivalent dose had better collateral development (P<0.001). Diabetes mellitus was the only negative predictor for coronary collateral formation (P=0.03). On multivariate analysis, stable angina pectoris [odds ratio 2.88, 95% confidence interval (1.8-4.7), P<0.001], statin therapy with > or =10 mg atorvastatin-equivalent dose [odds ratio 2.06, 95% confidence interval (1.3-2.6), P<0.001] and having multivessel disease [odds ratio 1.86, 95% confidence interval (1.16-3), P=0.01] were found to be associated with rich collateralization. CONCLUSION: Statin therapy (> or =10 mg atorvastatin-equivalent dose), stable angina pectoris and having multivessel disease are associated with enhanced coronary collateral development in patients with advanced coronary artery disease.
BACKGROUND: The coronary collateral circulation is an alternative source of blood supply to myocardium in the presence of advanced coronary artery disease and the therapeutic promotion of collateral growth appears to be a valuable treatment strategy in these patients. Although it has been shown in in-vivo studies that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) promote vasculogenesis and accelerate coronary collateral development in ischemic tissues, there are discordant results in clinical studies. Our aim was to investigate the effect of statin therapy, including dosage and duration of treatment, on coronary collateral growth in patients with advanced coronary artery disease. METHODS: Study population consisted of 400 (306 men, with the mean age of 62+/-10 years) consecutive patients who have undergone clinically indicated coronary angiography and had at least one major coronary artery stenosis of > or =95%. Coronary collaterals were graded from 0 to 3 according to the Cohen-Rentrop method and patients with grade 0-1 collateral development were regarded as having poor collateral and patients with grade 2-3 collateral development were regarded as having good collateral. RESULTS: Among 400 patients, 196 (48%) were on statin therapy. Patients with good collateral score were more likely to have stable angina pectoris as clinical presentation (P<0.001), and were on statin therapy (P=0.001), and have multivessel disease (P=0.003). Statin therapy for less than 3 months had no effect on collateral development (P=0.19); however, patients who were on statin therapy for more than 3 months had significantly better collateral development (P=0.002). Statin therapy had no effect on coronary collateral development in patients having <10 mg atorvastatin-equivalent dose (P=0.13); however, patients having > or =10 mg atorvastatin-equivalent dose had better collateral development (P<0.001). Diabetes mellitus was the only negative predictor for coronary collateral formation (P=0.03). On multivariate analysis, stable angina pectoris [odds ratio 2.88, 95% confidence interval (1.8-4.7), P<0.001], statin therapy with > or =10 mg atorvastatin-equivalent dose [odds ratio 2.06, 95% confidence interval (1.3-2.6), P<0.001] and having multivessel disease [odds ratio 1.86, 95% confidence interval (1.16-3), P=0.01] were found to be associated with rich collateralization. CONCLUSION: Statin therapy (> or =10 mg atorvastatin-equivalent dose), stable angina pectoris and having multivessel disease are associated with enhanced coronary collateral development in patients with advanced coronary artery disease.
Authors: Ellen C Keeley; J Randall Moorman; Ling Liu; Lawrence W Gimple; Lewis C Lipson; Michael Ragosta; Angela M Taylor; Douglas E Lake; Marie D Burdick; Borna Mehrad; Robert M Strieter Journal: PLoS One Date: 2011-06-22 Impact factor: 3.240