Statins Tame Plaque Inflammation

I'm sure  they followed the high-dose guidelines for 80 mg and didn't put anyone new on the drug.
And they decided against testing watermelon juice on plaque reduction.
Find out from your doctor if this was a well-run trial.
http://www.medpagetoday.com/Cardiology/Atherosclerosis/39499?

More intense statin therapy is associated with greater reductions in atherosclerotic plaque inflammation, which may or may not explain the drugs' effects on cardiovascular events, an imaging study showed.
Both 10-mg and 80-mg doses of atorvastatin reduced a marker of plaque inflammation on fluorodeoxyglucose-positron emission tomography/computed tomography (FDG-PET/CT) imaging, but the reduction was 10.6% greater through 12 weeks with the higher dose (P=0.01), according to Ahmed Tawakol, MD, of Massachusetts General Hospital in Boston, and colleagues.
The reductions in inflammation were seen as early as 4 weeks into the study, the researchers reported online in the Journal of the American College of Cardiology.
"Taken together, these findings provide evidence of a rapid reduction in vascular inflammation with statin therapy and provide new insights regarding the graded reductions in vascular plaque activity as it relates to increases in statin doses," the authors wrote. "The results also confirm the ability of PET imaging as a tool to detect changes in vascular inflammation early in the course of treatment, something not as well validated with other non-invasive imaging methods."
In addition, "these data support the hypothesis that statin therapy may result in a reduction in cardiovascular benefit in part due to a rapid reduction in arterial inflammation," they wrote, noting, however, that it is not clear whether there is a clinical benefit to such a reduction.
The 10-center study recruited 83 adults who either had cardiovascular risk factors or established atherosclerosis and who were not taking high doses of statins (they could be taking low doses). The patients were randomized to atorvastatin 10 mg or 80 mg for 12 weeks.
Imaging of the ascending thoracic aorta and carotid arteries was performed at baseline, 4 weeks, and 12 weeks to assess the target-to-background ratio (TBR) of FDG uptake with the artery wall, a marker of plaque inflammation.
At 12 weeks, the patients receiving the higher dose had a significant 14.4% reduction in TBR (P <0.001), whereas those receiving the lower dose had a nonsignificant 4.2% reduction (P=0.2).
The changes in inflammation were not related to changes in the patients' lipid profiles -- which included dose-dependent reductions in total and LDL cholesterol and triglycerides -- or to changes in C-reactive protein.
"Besides demonstrating that atorvastatin has anti-inflammatory effects in a dose-dependent response in atherosclerotic patients, the present study nicely illustrates the usefulness of FDG-PET to study plaque inflammation and its inflection by drug treatment in vivo," according to Bernhard Gerber, MD, PhD, of the Université Catholique de Louvain in Belgium.
"Because of its high costs, it is unlikely that FDG-PET will be widely used to identify high-risk plaques and to monitor treatment response on targeted vessels in individual patients clinically," he continued in an accompanying editorial. "However, as shown by the present study, PET is attractive to study anti-inflammatory effects of various drugs in experimental trials."
The researchers acknowledged some limitations of their study, including the lack of a placebo group, of an assessment of drug effects beyond 12 weeks, and of complete information for 16 of the patients who were initially randomized.