Usefulness of serum unbound free fatty acid levels to predict death early in patients with ST-segment elevation myocardial infarction (from the Thrombolysis In Myocardial Infarction [TIMI] II trial).
Pubmed ID: 24176067
Pubmed Central ID: PMC3893002
Journal: The American journal of cardiology
Publication Date: 01/15/2014
Affiliation: FFA Sciences LLC, San Diego, California; Torrey Pines Institute for Molecular Studies, San Diego, California. Electronic address: email@example.com.
MeSH Terms: Humans, Male, Female, Risk Factors, United States, Middle Aged, Cause of Death, Prognosis, Follow-Up Studies, Survival Rate, Myocardial Infarction, Time Factors, Drug Therapy, Combination, Electrocardiography, Injections, Intravenous, Fatty Acids, Nonesterified, Fibrinolytic Agents, Heparin, Thrombolytic Therapy, Tissue Plasminogen Activator, Biomarkers
Grants: DK058762, DK070314, R33 DK070314, R01 DK058762
Authors: Huber AH, Kampf JP, Kwan T, Zhu B, Adams J, Kleinfeld AM
Cite As: Huber AH, Kampf JP, Kwan T, Zhu B, Adams J 3rd, Kleinfeld AM. Usefulness of serum unbound free fatty acid levels to predict death early in patients with ST-segment elevation myocardial infarction (from the Thrombolysis In Myocardial Infarction [TIMI] II trial). Am J Cardiol 2014 Jan 15;113(2):279-84. Epub 2013 Oct 5.
Circulating total free fatty acid (FFA) levels are elevated early in myocardial infarction (MI) and have been associated with an increase in mortality. We investigated the association of serum unbound FFA (FFAu) levels with mortality in patients presenting with ST-segment elevation MI in the Thrombolysis In Myocardial Infarction II trial. The Thrombolysis In Myocardial Infarction II trial enrolled patients within 4 hours of chest pain onset. The patients were treated with a recombinant tissue plasminogen activator within 1 hour of enrollment. The FFAu concentration was evaluated in serum samples from 1,834 patients obtained at baseline, before therapy. The FFAu level was an independent risk factor for death as early as at 1 day of hospitalization and continued to be an independent risk factor for the >3.8 years of follow-up. When adjusted for other cardiovascular risk factors, the FFAu levels in the fourth versus the first quartile remained an independent risk factor for death from MI (hazard ratio 5.0, 95% confidence interval 1.9 to 13.0), all cardiac death (hazard ratio 2.4, 95% confidence interval 1.3 to 4.4), and all-cause death (hazard ratio 1.9, 95% confidence interval 1.2 to 3.1). Women were twice as likely to be in the upper 2 FFAu quartiles and had approximately twice the rate of death as men. In conclusion, FFAu elevation is 1 of the earliest molecular biomarkers of mortality in patients with ST-segment elevation MI and was independent of other risk factors known to affect the outcomes after ST-segment elevation MI.