This article is more than 5 years old. Information may no longer be current.
Key biomarkers may predict CV events, mortality
Velagaleti RS. Arterioscler Thromb Vasc Biol. 2010; doi:10.1161/ATVBAHA.110.208462.
Click Here to Manage Email Alerts
High concentrations of tissue inhibitor of matrix metalloproteinase-1 and procollagen type III aminoterminal peptide were found to significantly increase the risk of mortality, with the latter also associated with incident CVD.
The study consisted of 922 participants from the Framingham Study (mean age, 58 years). Researchers related incident CVD and death to circulating concentrations of matrix metalloproteinase-9, log of tissue inhibitor of matrix metalloproteinase-1, and log of procollagen type III aminoterminal peptide (PIIINP).
During follow-up (mean, 9.9 years), 51 deaths and 81 CVD events were recorded. For mortality risk, each standard deviation increment of log of tissue inhibitor of matrix metalloproteinase-1 was associated with a multivariable-adjusted HR of 1.72 (95% CI, 1.30-2.27), with the same increment generating a HR of 1.47 (95% CI, 1.11-1.96) in log-PIIINP. Log-PIIINP concentrations were also associated with CVD risk with a HR per standard deviation of 1.35 (95% CI, 1.05-1.74).
For participants with both biomarkers higher than the median, there was a roughly two-fold higher incidence rate of death (HR=2.78; 95% CI, 1.43-5.40) and CVD (HR=1.77; 95% CI, 1.04-3.03) vs. those with either or both less than the median. Researchers found no relationship between matrix metalloproteinase-9 and either CVD or mortality.
Limitations of the study were that only three biomarkers were measured, and that all members of the cohort were middle-aged, white and of European descent. Results of the study should not be generalized across other age groups and ethnicities.
“[These] patients with both markers higher than the median are at markedly higher risk of death and CVD,” the researchers wrote. “Our findings confirm and extend previous research that demonstrated that ventricular and vascular remodeling antedates clinical CVD. Additional research is needed to delineate the utility of these measures for screening, to estimate the risk of individual CVD events, and to use the measures in clinical settings.”