Metabolic syndrome does not impact on risk prediction in CAD
Medwire News: Diagnosing the metabolic syndrome (MetS) does not improve risk prediction in patients with coronary artery disease (CAD) compared with the assessment of total risk based on its components, researchers report.
CAD patients with diabetes who also have MetS are at particularly increased risk for death or MI. However, the US researchers report that detecting Mets in CAD patients does not help identify those at increased risk of these outcomes, after adjusting for its individual components.
As reported in Journal of The American College of Cardiology, David Maron (Vanderbilt University School of Medicine, Tennessee) and colleagues performed a post hoc analysis of 2248 stable CAD patients who participated in the COURAGE trial. They found that risk for death or MI increased across four risk groups comprising patients with: neither MetS nor diabetes (14%); MetS alone (16%); diabetes alone (17%); or both diabetes and MetS (25%).
After examining the distribution of the number of components of MetS and their relationship to endpoint events, the authors found that for each endpoint, there was a significant trend for increasing risk as the number of MetS components increased.
Further analysis showed that hypertension, low high-density lipoprotein cholesterol, and elevated glucose were the strongest independent predictors among Met S components of death or MI, at hazard ratios (HRs) of 1.30, 1.26, and 1.17, respectively.
MetS was associated with a 1.41-fold increased risk for death or MI, but after adjusting for its individual components, the association was no longer statistically significant (HR=1.15; 95% confidence interval: 0.79-1.68).
Further analysis revealed that allocation to initial percutaneous coronary intervention did not affect the incidence of death or MI within any group, the authors note.
They conclude that the increased risk for MI and death in CAD patients with MetS is accounted for by the syndrome's component risk factors, with no additional independent risk imparted by the MetS itself, therefore undermining the clinical utility of identifying the syndrome in patients with CAD.
The authors suggest that the underlying risk factors should be the principal targets of therapy and say their research underscores the need to identify more effective methods to prevent and treat the individual components of the syndrome.
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By Sally Robertson