The Cardios haven't found a way to reduce CAD with any drug they are using. Might as well give up.
Annual coronary calcification questioned as end-point for CVD
Arch Intern Med 2009; 169: 2064–2070
MedWire News: Annual change in coronary artery calcification (CAC) does not appear to be a suitable surrogate end point for treatment trials in patients with cardiovascular disease (CVD) or chronic kidney disease, results of a systematic review published in the Archives of Internal Medicine suggest.
There was no consistent or reproducible treatment effect of any therapy intervention – including calcium-based phosphate binders, statins, and a low phosphorus diet – on change in CAC at 1 year. Study co-author Peter McCullough (Beaumont Health Center, Royal Oak, Michigan, USA) and colleagues comment: "How can our findings relate to the large body of work demonstrating that baseline and progressive CAC are risk predictors for cardiac events?
"It appears that CAC identified by computed tomography (CT) scanning is a proxy for the burden of atherosclerosis summed over all three coronary arteries.
"However, therapies aiming to reduce the overall CAC score have not been successful in the short term, and there appears to be no meaningful translation into hard clinical events."
The researchers performed a literature search for prospective randomized trials in which CAC was measured by CT at baseline and at 1 year of follow-up.
Of the 10 suitable trials found, five of them included 2135 patients with CVD (average age 64 years; 39% women), of whom 1370 were treated with statins, 564 with placebo, and 201 with antihypertensives.
The remaining five trials included 477 patients with chronic kidney disease (average age 55 years; 34% women), of whom 29 were treated with a low phosphorus diet, 229 with sevelamer hydrochloride, and 219 with or calcium-based phosphate binders.
The researchers then calculated the weighted mean annualized rate of CAC progression for all the therapies tested in these trials.
They found that CAC increased overall and in patients with CVD and chronic kidney disease by 17.2%, 16.9%, and 18.4%, respectively, while the rate among those assigned to receive placebo was 14.6% (two trials). None of the therapies showed a significant treatment effect on CAC measured at 1 year.
In an accompanying editorial, Patrick O'Malley (Uniformed Services University of the Health Sciences, Bethesda, Maryland, USA) urged caution before completely dismissing CAC as an endpoint.
"The short interval of follow-up between scans in this set of trials severely limits any inferences about differential effects of the interventions because it assumes that atherosclerosis progression is a linear phenomenon, when it is more likely an erratic, step-wise process that is dependent on the underlying instability of local plaques such that more follow-up time would be necessary to capture change," he said.
Annual coronary calcification questioned as end-point for CVD: Lipids Online (23 December 2009)
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