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Intensive Statin Therapy Useful in High-Risk Coronary Patients: Presented at ACC

By Jill Stein

ATLANTA, G.A. -- March 13, 2006 -- New data presented here at the 55^th Annual Scientific Session of the American College of Cardiology (ACC) show that very high-intensity statin therapy using rosuvastatin 40 mg/day induces regression of coronary atherosclerosis.

Rosuvastatin is the latest statin and typically leads to larger decreases in low-density lipoprotein cholesterol (LDL-C) and larger increases in high-density lipoprotein cholesterol (HDL-C) than previously available agents.

The results, from the Study to Evaluate the Effect of Rosuvastatin on Intravascular Ultrasound-Derived Coronary Atheroma Burden (ASTEROID), were also published on line on March 13^th in JAMA-Express (JAMA 2006:295).

Steven Nissen, MD, interim chairman, division of cardiovascular medicine, Cleveland Clinic Foundation, Cleveland, Ohio, and associates conducted a study to determine whether very intensive statin therapy could produce a regression of coronary atherosclerosis. He presented the results in a session on March 13^th.

While the most positive results from intravascular ultrasound (IVUS) trials thus far showed a postponement or halting of the progression of atherosclerosis during statin therapy, no major trial has provided convincing evidence of regression using rigorous IVUS measures of disease burden, Dr. Nissen pointed out. Percent atheroma volume (PAV) is considered the most rigorous IVUS measure of disease progression and regression, he said.

The 507 participants in the ASTEROID trial received intensive therapy with rosuvastatin at a dose of 40 mg/day. Two primary measures were prespecified: change in PAV and change in nominal atheroma volume in the 10-mm subsegment with the greatest disease severity at enrollment.

The trial also included a prespecified secondary efficacy variable: change in normalized total atheroma volume for the entire artery.

For secondary prevention patients with prior coronary disease, the study treatment decreased LDL-C to 60.8 mg/dL while increasing HDL-C by 14.7%, P <.001.

Mean change in PAV for the entire vessel was -0.98% (3.15%), with a median of -0.79%(P <.001 vs baseline). Mean change in atheroma volume in the most diseased 10-mm subsegment was -6.1 (10.1) mm³, with a median of -5.6 mm³ (P <.001 vs baseline).

The investigators also documented a 6.8% median reduction in total atheroma volume, with a mean reduction of -5.6 mm² (P <.001 versus baseline).

The statin regimen was well tolerated.

Dr. Nissen noted that the results should be interpreted with caution given the absence of a control group. "Because it was ethically unsound to administer low-intensity statin therapy to patients with advanced coronary disease, there was no control group who received placebo or a less active statin," he explained.

However, he was quick to emphasize that the study compensated for the lack of placebo controls by blinding date information on IVUS studies and resequencing the examinations to rule out possible observer bias in assessing the results.


[Presentation title: Effect of Very High-Intensity Statin Therapy on Regression of Coronary Atherosclerosis -- the ASTEROID Trial. Presented in a Late-Breaking Clinical Trials Session.]

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