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ORLANDO – Results from a head-to-head comparison of the two top statins on the U.S. market, rosuvastatin and atorvastatin, in more than 1,000 patients with coronary disease – a study apparently designed to more definitively prove rosuvastatin’s superiority – instead showed that atorvastatin was statistically indistinguishable from its somewhat more potent rival for the study’s primary end point.
With this finding coming just 2 weeks before atorvastatin’s expected availability as a substantially cheaper generic drug, the study – funded by AstraZeneca, the company that markets rosuvastatin (Crestor) – appeared to have the ironic consequence of convincing experts, as well as likely payers and patients, that generic atorvastatin will do just fine for most clinical situations.
And by testing maximum dosages of both drugs for 2 years of therapy and showing that both were "amazingly well tolerated" by patients, in the words of the study’s leader, Dr. Stephen J. Nicholls, the trial also added to existing evidence that intensive therapy using either agent was safe and should be accepted more readily by physicians and patients.
The results "add to the body of evidence that these two statins are safe and quite effective for reducing risk," commented Dr. Daniel J. Rader, professor of medicine and director of the preventive cardiology program at the University of Pennsylvania in Philadelphia.
"These were very high doses. Physicians don’t like to prescribe the highest doses, and patients don’t like to take them, because they don’t think they’re safe and that they don’t have added benefit. [This study] was a good opportunity to show, in more than 1,000 patients, that if you treat patients for 24 months, [these drugs] are actually very well tolerated, the safety profile looks very good, [and] you can regress disease and get very good lipid changes," said Dr. Nicholls, clinical director of the Cleveland Clinic Center for Clinical Research.
Dr. Nicholls also highlighted the "unprecedented" regression of coronary atheroma (the study’s primary efficacy measure) that was achieved in most study patients after 2 years of treatment with maximum dosages of either of the two statins. "It’s quite profound, the ability of the high doses of these therapies to remove lipid and reduce inflammation," he said at the annual scientific sessions of the American Heart Association. "It’s not a clinical marker," he acknowledged, "but it’s a reasonable surrogate, in that [coronary atheroma] is the pathology that ultimately causes events."
Until now, rosuvastatin was known to hold a modest but consistent edge over atorvastatin in its ability to lower blood levels of LDL cholesterol and also to produce a higher rise in HDL cholesterol, but the clinical meaning of these differences had not been established. Dr. Nicholls and his associates ran SATURN (Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin vs. Atorvastatin) to "compare the effect of maximal dosages of the most efficacious statin regimens on progression of coronary atherosclerosis," a 40-mg/day dosage or rosuvastatin and an 80-mg/day dosage of atorvastatin.
Simultaneously with Dr. Nicholls’ report at the meeting, the results appeared in an article online (N. Engl. J. Med. 2011 Nov. 15 [doi:10.1056/NEJMoa1110874]).
From January 2008 through June 2009, the researchers enrolled 1,578 patients with coronary disease at 208 centers. After randomization, patients underwent a 2-week run-in phase of treatment, receiving their assigned drug at half the study dose. This phase eliminated nearly 200 patients, although Dr. Nicholls said that most did not continue because of investigators’ inability to obtain a usable, baseline intravascular ultrasound (IVUS) image of the patient’s target artery, and not because of adverse effects of treatment. The 1,385 patients who remained in the study (691 on atorvastatin and 694 on rosuvastatin) had their dosage scaled up to the full study level and then remained on treatment for 104 weeks, after which they underwent follow-up IVUS imaging of their index coronary artery. The study’s primary end point was the change in percent atheroma volume from baseline to follow-up IVUS.
The results showed that this primary end point decreased by an average of 0.99% in the atorvastatin-treated patients, and by an average of 1.22% in those on rosuvastatin. Although each group had statistically significant atheroma shrinkage, compared with baseline, the two groups did not significantly differ from each other. The percentage of patients with atheroma shrinkage was 69% in the rosuvastatin group and 63% in the atorvastatin group, a difference that neared – but did not reach – statistical significance.
After 2 years of treatment, average LDL cholesterol levels were 70.2 mg/dL on atorvastatin and 62.6 mg/dL on rosuvastatin, a statistically significant difference. By the end of the study, the mean HDL cholesterol levels in the two groups stood at 48.6 mg/dL for those on atorvastatin and 50.4 mg/dL for those on rosuvastatin. Although this difference in HDL also was statistically significant, "we were somewhat surprised [that] the difference in HDL was not quite as large as we suspected," Dr. Nicholls said. "At the highest doses, the difference in HDL effect appears to dissipate."
Based on the primary end point results, "the study provides no basis to infer differential clinical benefit between atorvastatin and rosuvastatin," commented Dr. Darwin R. Labarthe, professor of preventive medicine at Northwestern University in Chicago and the designated discussant for the report at the meeting.
The study showed "a low number of clinical and biochemical adverse events in both groups," said Dr. Nicholls. An elevated ALT level occurred in 2.0% of the atorvastatin patients and in 0.7% of the rosuvastatin patients, a statistically significant difference. Proteinuria occurred in 3.8% of the rosuvastatin patients and in 1.7% of those on atorvastatin, also a statistically significant difference. No patient had rhabdomyolysis, and the two groups did not differ significantly in their rates of major adverse cardiovascular events, which occurred in 7.1% of the atorvastatin patients and in 7.5% of those on rosuvastatin.
Although Dr. Nicholls highlighted the high level of coronary-atheroma regression seen among most patients in both study arms, some experts dismissed the immediate importance of this finding without evidence for the association of this regression with clinical end points.
"The question is whether plaque stability is any different," commented Dr. Robert H. Eckel, professor of medicine and an atherosclerosis specialist at the University of Colorado at Denver, Aurora. "It is possible that with regression the plaque is more stable, but it is a surrogate marker. We don’t know whether that will translate into a clinical benefit." The U.S. cholesterol-treatment goals set by the National Heart, Lung, and Blood Institute, which are now in late stages of revision, "are directed by evidence-based outcomes," and hence the findings from SATURN "will not influence" goal revisions, he said in an interview.
Dr. Eckel and other experts also said they believe that the results would prod insurers and patients to focus more on treatment with generic atorvastatin and less on treatment with a pricier, proprietary rosuvastatin. "Price will drive treatment decisions," Dr. Eckel said. "In many cases, third-party payers and patients won’t pay for Crestor."
The SATURN study was sponsored by AstraZeneca, which markets rosuvastatin (Crestor). Dr. Nicholls said that he has been a consultant to and has received honoraria from AstraZeneca, Eli Lilly, Anthera, Omthera, Merck, Takeda, Resverlogix, Sanofi-Aventis, CSL Behring, Esperion, and Boehringer Ingelheim. He said he has received research support from AstraZeneca, Anthera, Eli Lilly, Novartis, Resverlogix, Roche, and LipoScience. Dr. Rader has been a consultant or advisor to Genentech, Merck, and Roche, and he has spoken on behalf of and has received research grants from Merck. Dr. Labarthe, Dr. Eckel, and Dr. Lloyd-Jones said that they had no relevant disclosures.
One of the most important things we can do for patients with cardiovascular disease is to get them on an intensive dosage of a potent statin. That’s the most effective way to reduce their risk for secondary events.
We already have substantial evidence on the safety of high-dose statins, particularly atorvastatin and increasingly with rosuvastatin as well. My hope is that by piling on here with additional safety data, physicians will become increasingly comfortable with using these medications at potent doses to achieve maximal LDL cholesterol lowering and really benefit patients. In SATURN, we see that intensive dosages of very potent statins are safe and effective [for lowering LDL cholesterol]. In SATURN, we did not see incremental benefit from one of the tested statins over the other.
Having generic atorvastatin available soon will be a real game changer. If payers then include atorvastatin among their class 1 medications that we can easily prescribe to patients, we’ll be able to get more patients to lower [LDL cholesterol levels] with a safe and well-tolerated drug.
The SATURN results don’t really change anything in clinical practice. The study looked at an intermediate marker of coronary disease – plaque volume – that does not really correlate well with the risk for secondary events. I would be more interested in seeing data on changes in the quality of the coronary plaque [such as] changes in the fibrous cap and lipid core. Those measures tend to correlate with events.
Donald M. Lloyd-Jones, M.D., is a cardiologist and chairman of the department of preventive medicine at Northwestern University in Chicago. He said that he has no disclosures. He made these comments in an interview.
One of the most important things we can do for patients with cardiovascular disease is to get them on an intensive dosage of a potent statin. That’s the most effective way to reduce their risk for secondary events.
We already have substantial evidence on the safety of high-dose statins, particularly atorvastatin and increasingly with rosuvastatin as well. My hope is that by piling on here with additional safety data, physicians will become increasingly comfortable with using these medications at potent doses to achieve maximal LDL cholesterol lowering and really benefit patients. In SATURN, we see that intensive dosages of very potent statins are safe and effective [for lowering LDL cholesterol]. In SATURN, we did not see incremental benefit from one of the tested statins over the other.
Having generic atorvastatin available soon will be a real game changer. If payers then include atorvastatin among their class 1 medications that we can easily prescribe to patients, we’ll be able to get more patients to lower [LDL cholesterol levels] with a safe and well-tolerated drug.
The SATURN results don’t really change anything in clinical practice. The study looked at an intermediate marker of coronary disease – plaque volume – that does not really correlate well with the risk for secondary events. I would be more interested in seeing data on changes in the quality of the coronary plaque [such as] changes in the fibrous cap and lipid core. Those measures tend to correlate with events.
Donald M. Lloyd-Jones, M.D., is a cardiologist and chairman of the department of preventive medicine at Northwestern University in Chicago. He said that he has no disclosures. He made these comments in an interview.
One of the most important things we can do for patients with cardiovascular disease is to get them on an intensive dosage of a potent statin. That’s the most effective way to reduce their risk for secondary events.
We already have substantial evidence on the safety of high-dose statins, particularly atorvastatin and increasingly with rosuvastatin as well. My hope is that by piling on here with additional safety data, physicians will become increasingly comfortable with using these medications at potent doses to achieve maximal LDL cholesterol lowering and really benefit patients. In SATURN, we see that intensive dosages of very potent statins are safe and effective [for lowering LDL cholesterol]. In SATURN, we did not see incremental benefit from one of the tested statins over the other.
Having generic atorvastatin available soon will be a real game changer. If payers then include atorvastatin among their class 1 medications that we can easily prescribe to patients, we’ll be able to get more patients to lower [LDL cholesterol levels] with a safe and well-tolerated drug.
The SATURN results don’t really change anything in clinical practice. The study looked at an intermediate marker of coronary disease – plaque volume – that does not really correlate well with the risk for secondary events. I would be more interested in seeing data on changes in the quality of the coronary plaque [such as] changes in the fibrous cap and lipid core. Those measures tend to correlate with events.
Donald M. Lloyd-Jones, M.D., is a cardiologist and chairman of the department of preventive medicine at Northwestern University in Chicago. He said that he has no disclosures. He made these comments in an interview.
ORLANDO – Results from a head-to-head comparison of the two top statins on the U.S. market, rosuvastatin and atorvastatin, in more than 1,000 patients with coronary disease – a study apparently designed to more definitively prove rosuvastatin’s superiority – instead showed that atorvastatin was statistically indistinguishable from its somewhat more potent rival for the study’s primary end point.
With this finding coming just 2 weeks before atorvastatin’s expected availability as a substantially cheaper generic drug, the study – funded by AstraZeneca, the company that markets rosuvastatin (Crestor) – appeared to have the ironic consequence of convincing experts, as well as likely payers and patients, that generic atorvastatin will do just fine for most clinical situations.
And by testing maximum dosages of both drugs for 2 years of therapy and showing that both were "amazingly well tolerated" by patients, in the words of the study’s leader, Dr. Stephen J. Nicholls, the trial also added to existing evidence that intensive therapy using either agent was safe and should be accepted more readily by physicians and patients.
The results "add to the body of evidence that these two statins are safe and quite effective for reducing risk," commented Dr. Daniel J. Rader, professor of medicine and director of the preventive cardiology program at the University of Pennsylvania in Philadelphia.
"These were very high doses. Physicians don’t like to prescribe the highest doses, and patients don’t like to take them, because they don’t think they’re safe and that they don’t have added benefit. [This study] was a good opportunity to show, in more than 1,000 patients, that if you treat patients for 24 months, [these drugs] are actually very well tolerated, the safety profile looks very good, [and] you can regress disease and get very good lipid changes," said Dr. Nicholls, clinical director of the Cleveland Clinic Center for Clinical Research.
Dr. Nicholls also highlighted the "unprecedented" regression of coronary atheroma (the study’s primary efficacy measure) that was achieved in most study patients after 2 years of treatment with maximum dosages of either of the two statins. "It’s quite profound, the ability of the high doses of these therapies to remove lipid and reduce inflammation," he said at the annual scientific sessions of the American Heart Association. "It’s not a clinical marker," he acknowledged, "but it’s a reasonable surrogate, in that [coronary atheroma] is the pathology that ultimately causes events."
Until now, rosuvastatin was known to hold a modest but consistent edge over atorvastatin in its ability to lower blood levels of LDL cholesterol and also to produce a higher rise in HDL cholesterol, but the clinical meaning of these differences had not been established. Dr. Nicholls and his associates ran SATURN (Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin vs. Atorvastatin) to "compare the effect of maximal dosages of the most efficacious statin regimens on progression of coronary atherosclerosis," a 40-mg/day dosage or rosuvastatin and an 80-mg/day dosage of atorvastatin.
Simultaneously with Dr. Nicholls’ report at the meeting, the results appeared in an article online (N. Engl. J. Med. 2011 Nov. 15 [doi:10.1056/NEJMoa1110874]).
From January 2008 through June 2009, the researchers enrolled 1,578 patients with coronary disease at 208 centers. After randomization, patients underwent a 2-week run-in phase of treatment, receiving their assigned drug at half the study dose. This phase eliminated nearly 200 patients, although Dr. Nicholls said that most did not continue because of investigators’ inability to obtain a usable, baseline intravascular ultrasound (IVUS) image of the patient’s target artery, and not because of adverse effects of treatment. The 1,385 patients who remained in the study (691 on atorvastatin and 694 on rosuvastatin) had their dosage scaled up to the full study level and then remained on treatment for 104 weeks, after which they underwent follow-up IVUS imaging of their index coronary artery. The study’s primary end point was the change in percent atheroma volume from baseline to follow-up IVUS.
The results showed that this primary end point decreased by an average of 0.99% in the atorvastatin-treated patients, and by an average of 1.22% in those on rosuvastatin. Although each group had statistically significant atheroma shrinkage, compared with baseline, the two groups did not significantly differ from each other. The percentage of patients with atheroma shrinkage was 69% in the rosuvastatin group and 63% in the atorvastatin group, a difference that neared – but did not reach – statistical significance.
After 2 years of treatment, average LDL cholesterol levels were 70.2 mg/dL on atorvastatin and 62.6 mg/dL on rosuvastatin, a statistically significant difference. By the end of the study, the mean HDL cholesterol levels in the two groups stood at 48.6 mg/dL for those on atorvastatin and 50.4 mg/dL for those on rosuvastatin. Although this difference in HDL also was statistically significant, "we were somewhat surprised [that] the difference in HDL was not quite as large as we suspected," Dr. Nicholls said. "At the highest doses, the difference in HDL effect appears to dissipate."
Based on the primary end point results, "the study provides no basis to infer differential clinical benefit between atorvastatin and rosuvastatin," commented Dr. Darwin R. Labarthe, professor of preventive medicine at Northwestern University in Chicago and the designated discussant for the report at the meeting.
The study showed "a low number of clinical and biochemical adverse events in both groups," said Dr. Nicholls. An elevated ALT level occurred in 2.0% of the atorvastatin patients and in 0.7% of the rosuvastatin patients, a statistically significant difference. Proteinuria occurred in 3.8% of the rosuvastatin patients and in 1.7% of those on atorvastatin, also a statistically significant difference. No patient had rhabdomyolysis, and the two groups did not differ significantly in their rates of major adverse cardiovascular events, which occurred in 7.1% of the atorvastatin patients and in 7.5% of those on rosuvastatin.
Although Dr. Nicholls highlighted the high level of coronary-atheroma regression seen among most patients in both study arms, some experts dismissed the immediate importance of this finding without evidence for the association of this regression with clinical end points.
"The question is whether plaque stability is any different," commented Dr. Robert H. Eckel, professor of medicine and an atherosclerosis specialist at the University of Colorado at Denver, Aurora. "It is possible that with regression the plaque is more stable, but it is a surrogate marker. We don’t know whether that will translate into a clinical benefit." The U.S. cholesterol-treatment goals set by the National Heart, Lung, and Blood Institute, which are now in late stages of revision, "are directed by evidence-based outcomes," and hence the findings from SATURN "will not influence" goal revisions, he said in an interview.
Dr. Eckel and other experts also said they believe that the results would prod insurers and patients to focus more on treatment with generic atorvastatin and less on treatment with a pricier, proprietary rosuvastatin. "Price will drive treatment decisions," Dr. Eckel said. "In many cases, third-party payers and patients won’t pay for Crestor."
The SATURN study was sponsored by AstraZeneca, which markets rosuvastatin (Crestor). Dr. Nicholls said that he has been a consultant to and has received honoraria from AstraZeneca, Eli Lilly, Anthera, Omthera, Merck, Takeda, Resverlogix, Sanofi-Aventis, CSL Behring, Esperion, and Boehringer Ingelheim. He said he has received research support from AstraZeneca, Anthera, Eli Lilly, Novartis, Resverlogix, Roche, and LipoScience. Dr. Rader has been a consultant or advisor to Genentech, Merck, and Roche, and he has spoken on behalf of and has received research grants from Merck. Dr. Labarthe, Dr. Eckel, and Dr. Lloyd-Jones said that they had no relevant disclosures.
ORLANDO – Results from a head-to-head comparison of the two top statins on the U.S. market, rosuvastatin and atorvastatin, in more than 1,000 patients with coronary disease – a study apparently designed to more definitively prove rosuvastatin’s superiority – instead showed that atorvastatin was statistically indistinguishable from its somewhat more potent rival for the study’s primary end point.
With this finding coming just 2 weeks before atorvastatin’s expected availability as a substantially cheaper generic drug, the study – funded by AstraZeneca, the company that markets rosuvastatin (Crestor) – appeared to have the ironic consequence of convincing experts, as well as likely payers and patients, that generic atorvastatin will do just fine for most clinical situations.
And by testing maximum dosages of both drugs for 2 years of therapy and showing that both were "amazingly well tolerated" by patients, in the words of the study’s leader, Dr. Stephen J. Nicholls, the trial also added to existing evidence that intensive therapy using either agent was safe and should be accepted more readily by physicians and patients.
The results "add to the body of evidence that these two statins are safe and quite effective for reducing risk," commented Dr. Daniel J. Rader, professor of medicine and director of the preventive cardiology program at the University of Pennsylvania in Philadelphia.
"These were very high doses. Physicians don’t like to prescribe the highest doses, and patients don’t like to take them, because they don’t think they’re safe and that they don’t have added benefit. [This study] was a good opportunity to show, in more than 1,000 patients, that if you treat patients for 24 months, [these drugs] are actually very well tolerated, the safety profile looks very good, [and] you can regress disease and get very good lipid changes," said Dr. Nicholls, clinical director of the Cleveland Clinic Center for Clinical Research.
Dr. Nicholls also highlighted the "unprecedented" regression of coronary atheroma (the study’s primary efficacy measure) that was achieved in most study patients after 2 years of treatment with maximum dosages of either of the two statins. "It’s quite profound, the ability of the high doses of these therapies to remove lipid and reduce inflammation," he said at the annual scientific sessions of the American Heart Association. "It’s not a clinical marker," he acknowledged, "but it’s a reasonable surrogate, in that [coronary atheroma] is the pathology that ultimately causes events."
Until now, rosuvastatin was known to hold a modest but consistent edge over atorvastatin in its ability to lower blood levels of LDL cholesterol and also to produce a higher rise in HDL cholesterol, but the clinical meaning of these differences had not been established. Dr. Nicholls and his associates ran SATURN (Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin vs. Atorvastatin) to "compare the effect of maximal dosages of the most efficacious statin regimens on progression of coronary atherosclerosis," a 40-mg/day dosage or rosuvastatin and an 80-mg/day dosage of atorvastatin.
Simultaneously with Dr. Nicholls’ report at the meeting, the results appeared in an article online (N. Engl. J. Med. 2011 Nov. 15 [doi:10.1056/NEJMoa1110874]).
From January 2008 through June 2009, the researchers enrolled 1,578 patients with coronary disease at 208 centers. After randomization, patients underwent a 2-week run-in phase of treatment, receiving their assigned drug at half the study dose. This phase eliminated nearly 200 patients, although Dr. Nicholls said that most did not continue because of investigators’ inability to obtain a usable, baseline intravascular ultrasound (IVUS) image of the patient’s target artery, and not because of adverse effects of treatment. The 1,385 patients who remained in the study (691 on atorvastatin and 694 on rosuvastatin) had their dosage scaled up to the full study level and then remained on treatment for 104 weeks, after which they underwent follow-up IVUS imaging of their index coronary artery. The study’s primary end point was the change in percent atheroma volume from baseline to follow-up IVUS.
The results showed that this primary end point decreased by an average of 0.99% in the atorvastatin-treated patients, and by an average of 1.22% in those on rosuvastatin. Although each group had statistically significant atheroma shrinkage, compared with baseline, the two groups did not significantly differ from each other. The percentage of patients with atheroma shrinkage was 69% in the rosuvastatin group and 63% in the atorvastatin group, a difference that neared – but did not reach – statistical significance.
After 2 years of treatment, average LDL cholesterol levels were 70.2 mg/dL on atorvastatin and 62.6 mg/dL on rosuvastatin, a statistically significant difference. By the end of the study, the mean HDL cholesterol levels in the two groups stood at 48.6 mg/dL for those on atorvastatin and 50.4 mg/dL for those on rosuvastatin. Although this difference in HDL also was statistically significant, "we were somewhat surprised [that] the difference in HDL was not quite as large as we suspected," Dr. Nicholls said. "At the highest doses, the difference in HDL effect appears to dissipate."
Based on the primary end point results, "the study provides no basis to infer differential clinical benefit between atorvastatin and rosuvastatin," commented Dr. Darwin R. Labarthe, professor of preventive medicine at Northwestern University in Chicago and the designated discussant for the report at the meeting.
The study showed "a low number of clinical and biochemical adverse events in both groups," said Dr. Nicholls. An elevated ALT level occurred in 2.0% of the atorvastatin patients and in 0.7% of the rosuvastatin patients, a statistically significant difference. Proteinuria occurred in 3.8% of the rosuvastatin patients and in 1.7% of those on atorvastatin, also a statistically significant difference. No patient had rhabdomyolysis, and the two groups did not differ significantly in their rates of major adverse cardiovascular events, which occurred in 7.1% of the atorvastatin patients and in 7.5% of those on rosuvastatin.
Although Dr. Nicholls highlighted the high level of coronary-atheroma regression seen among most patients in both study arms, some experts dismissed the immediate importance of this finding without evidence for the association of this regression with clinical end points.
"The question is whether plaque stability is any different," commented Dr. Robert H. Eckel, professor of medicine and an atherosclerosis specialist at the University of Colorado at Denver, Aurora. "It is possible that with regression the plaque is more stable, but it is a surrogate marker. We don’t know whether that will translate into a clinical benefit." The U.S. cholesterol-treatment goals set by the National Heart, Lung, and Blood Institute, which are now in late stages of revision, "are directed by evidence-based outcomes," and hence the findings from SATURN "will not influence" goal revisions, he said in an interview.
Dr. Eckel and other experts also said they believe that the results would prod insurers and patients to focus more on treatment with generic atorvastatin and less on treatment with a pricier, proprietary rosuvastatin. "Price will drive treatment decisions," Dr. Eckel said. "In many cases, third-party payers and patients won’t pay for Crestor."
The SATURN study was sponsored by AstraZeneca, which markets rosuvastatin (Crestor). Dr. Nicholls said that he has been a consultant to and has received honoraria from AstraZeneca, Eli Lilly, Anthera, Omthera, Merck, Takeda, Resverlogix, Sanofi-Aventis, CSL Behring, Esperion, and Boehringer Ingelheim. He said he has received research support from AstraZeneca, Anthera, Eli Lilly, Novartis, Resverlogix, Roche, and LipoScience. Dr. Rader has been a consultant or advisor to Genentech, Merck, and Roche, and he has spoken on behalf of and has received research grants from Merck. Dr. Labarthe, Dr. Eckel, and Dr. Lloyd-Jones said that they had no relevant disclosures.
FROM THE ANNUAL SCIENTIFIC SESSIONS OF THE AMERICAN HEART ASSOCIATION
Major Finding: At their maximal labeled dosages, 2 years of treatment with rosuvastatin or atorvastatin led to similar average levels of coronary atheroma volume shrinkage (1.22% and 0.99%, respectively), and were both safe and well tolerated.
Data Source: The SATURN study, which randomized 1,385 patients with coronary artery disease to 2 years of treatment with 40-mg/day rosuvastatin or 80-mg/day atorvastatin.
Disclosures: The SATURN study was sponsored by AstraZeneca, which markets rosuvastatin (Crestor). Dr. Nicholls said that he has been a consultant to and has received honoraria from AstraZeneca, Eli Lilly, Anthera, Omthera, Merck, Takeda, Resverlogix, Sanofi-Aventis, CSL Behring, Esperion, and Boehringer Ingelheim. He said he has received research support from AstraZeneca, Anthera, Eli Lilly, Novartis, Resverlogix, Roche, and LipoScience. Dr. Rader has been a consultant or advisor to Genentech, Merck, and Roche, and he has spoken on behalf of and has received research grants from Merck. Dr. Labarthe and Dr. Eckel said that they had no relevant disclosures.