DALLAS, Aug. 6 – Cholesterol-lowering drugs may also slow the progression of calcium build-up in arteries, according to a report in today’s rapid access issue of Circulation: Journal of the American Heart Association.
In the development of atherosclerosis fatty plaques forming in artery walls can become calcified. Scientists speculate that studying calcium deposits inside patients’ coronary arteries with computed tomography techniques, such as electron beam tomography (EBCT), can track the progression of atherosclerosis. That would allow doctors to monitor whether lipid-lowering therapies slow the progression of coronary artery calcification, says Stephan Achenbach, M.D., lead author of the study and a staff cardiologist at the University of Erlangen-Nurnberg, Germany.
This is the first prospective study to exam how lipid levels affect the progression of calcium build-up. Researchers found that calcium in the coronary arteries progresses if left untreated. They also found that lipid-lowering therapy (in this case cerivastatin) can slow that progression. On average, coronary calcium increased only 8.8 percent during statin treatment, compared to a 25 percent increase without treatment.
Progression of calcification was completely stopped in a group of patients in whom the drug reduced low-density lipoprotein (LDL – the “bad” cholesterol) to an extremely low level (below 100 milligrams per deciliter).
Achenbach and co-authors studied 66 patients who had calcium in their coronary arteries. These patients had undergone EBCT, a scanning technique that takes 40 images of the heart in one breathhold. All patients had elevated lipid levels (LDL above 130 mg/dl). For the first year of the study, participants did not take lipid-lowering medication. At the end of that year, they had an EBCT to see how much the calcification had progressed.
The patients then took cerivastatin for one year and underwent a scan at the end of their treatment to see how the medicine affected calcium progression. In all scans, the amount of coronary calcification was quantified and compared.
“These values were averages and there is variability to the test,” says Achenbach, who’s not certain if the findings will change practices. “We need further research to find methods that permit us to assess the efficacy of treatment in one single, individual patient.”
The study was supported by a grant from Bayer Vital, AG, Leverkusen.
Co-authors of the study include Dieter Ropers, M.D.; Karsten Pohle, M.D.; Alexander Leber, M.D.; Christian Thilo, M.D.; Andreas Knez, M.D.; Theresa Menendez, M.D.; Ralph Maeffert, M.D.; Magda Kusus, M.D.; Matthias Regenfus, M.D.; Andrea Bickel; Ralph Haberl, M.D.; Gerhard Steinbeck, M.D.; Werner Moshage, M.D.; and Werner G. Daniel, M.D.
Contact: Carole Bullock; email: firstname.lastname@example.org; phone: 214-706-1279, of the American Heart Association.