Cholesterol drug Lipitor, a top-selling medication from Pfizer, can halt, not just slow, the potentially fatal buildup of plaque in clogged arteries, researchers said Wednesday. Lipitor beat rival Pravachol in an 18-month trial of the two statin drugs, the study found.
THE STUDY is the first solid evidence that a prescription drug can stop the build-up of new plaque and even reverse it in some patients. A handful of drugs now available slow the buildup of new plaque, or atherosclerosis, in coronary arteries.
“We were excited we could find a regimen, although an intensive one, that could stop the disease in its tracks,” said the lead researcher, Dr. Steven Nissen of the Cleveland Clinic in Ohio.
The results of the 18-month clinical trial, presented at an annual meeting of the American Heart Association in Orlando, showed Lipitor halted the progression of plaque and cleared 0.4 percent of existing build-up among patients with clogged arteries.
That compared with a 2.7 percent increase in plaque for patients on a lower dose of Bristol-Myers Squibb Co.’s competing drug Pravachol.
Lipitor is the world’s top-selling drug with annual sales approaching $10 billion, and Pfizer will use the data on atherosclerosis to boost its marketing pitch for the drug.
The Pfizer drug is a more potent drug than Pravachol among the statin class of drugs that reduce low-density lipoproteins, or “bad” cholesterol, in the blood.
The 500-patient clinical trial, sponsored by Pfizer, set out to compare a more aggressive statin regimen of 80 milligrams of Lipitor daily with a moderate therapy of 40 milligrams of Pravachol, Nissen said.
Nissen said he was surprised to see that even when patients achieved low LDL levels on Pravachol, their disease still progressed more than it did for the Lipitor patients. This suggested to Nissen that massive LDL reduction, though important, is not the only factor at play, he said.
The trial also showed Lipitor reduced levels of a dangerous inflammatory protein called C-Reactive Protein by 36.4 percent, compared with a 5.2 percent reduction among Pravachol patients.
That may explain the disparity between the two drugs in halting plaque build-up, Nissen said.
Another factor in stopping plaque build-up may be raised levels of HDL or “good” cholesterol. An experimental HDL-raising drug from Esperion Therapeutics Inc. reduced fatty artery deposits by 4.2 percent in a small clinical trial reported earlier this month.
Nissen said it would still be up to individual physicians to decide whether to prescribe a high-dose therapy, such as 80 milligrams of Lipitor, for their patients with atherosclerosis, which is the leading cause of death from heart attack and stroke.
“I will let my colleagues look at the findings and make their own minds up,” he said. “I think there are some tough decisions that will have to be made.”
Deutsche Bank analyst Barbara Ryan said the findings “will force the market increasingly toward the most significant reduction that can be safely achieved for that patient.”
While Lipitor showed only “slight” plaque reductions, “it is reducing rather than just halting the progression. And what you’re seeing with Pravachol at 40 milligrams is they’re not even doing that,” Ryan said.
Bristol-Myers is sponsoring its own clinical trial comparing 40 milligrams of Pravachol with 80 milligrams of Lipitor in an attempt to prove that standard amounts of LDL reduction could be sufficient to prevent major heart problems.
The goal of the trial is to compare the two drugs in preventing secondary heart attacks, strokes and other problems among patients who have already been hospitalized for an acute heart incident and sent home, said Dr. Christopher Cannon of Brigham and Women’s Hospital of Boston.