Highlights
- •The effect of the metabolic syndrome (MS) on prognosis in the catheterization laboratory is controversial.
- •Patients with MS had more CAD, ACS, and elevated atherogenic biomarkers.
- •MS had a significant effect on mortality in stable patients and not in patients with ACS.
Past studies examining the effects of the metabolic syndrome (MS) on prognosis in
postangiography patients were limited in size or were controversial in results. The
aim of the study was to examine the association of the MS and the risk for long-term
mortality in a large cohort of patients undergoing coronary angiography for various
clinical indications. Medical history, physical examination, and laboratory values
were used to diagnose patients with the MS. Cox regression models were used to analyze
the effect of MS on long-term all-cause mortality. We prospectively recruited 3,525
consecutive patients with a mean age of 66 ± 22 years (range 24 to 97) and 72% men.
Thirty percent of the cohort had MS. Patients with MS were more likely to have advanced
coronary artery disease and acute coronary syndrome (p <0.001). Patients with MS had
more abnormalities in their metabolic and inflammatory biomarkers regardless of their
clinical presentation. A total of 495 deaths occurred during a mean follow-up period
of 1,614 ± 709 days (median 1,780, interquartile range 1,030 to 2,178). MS was associated
with an increased risk of death in the general cohort (hazard ratio [HR] 1.27, 95%
confidence interval [CI] 1.01 to 1.56, p = 0.02). MS had a significant effect on mortality
in stable patients (HR 1.55, 95% CI 1.1 to 2.18, p = 0.01), whereas it did not have
a significant effect on mortality in patients with acute coronary syndrome (HR 1.11,
95% CI 0.86 to 1.44, p = 0.42). In conclusion, MS is associated with increased mortality
in postangiography patients. Its adverse outcome is mainly seen in patients with stable
angina.
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Article Info
Publication History
Published online: November 14, 2014
Accepted:
October 28,
2014
Received in revised form:
October 28,
2014
Received:
September 11,
2014
Footnotes
This study was supported by internal departmental resources.
See page 286 for disclosure information.
Identification
Copyright
© 2015 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
