Abstract 11841: Enzymatic Infarct Size Determination Using Heart Specific Fatty Acid Binding Protein is Fast and Accurate
Purpose: In clinical practice, myocardial necrosis is assessed with the early plasma marker high sensitivity Troponin I (Trop). However, it takes several hours of ischemia before plasma levels are elevated. While myoglobin elevates faster upon necrosis, it is not tissue specific. In search for a comparably accurate, yet faster detectable marker of myocardial necrosis, we evaluated heart specific fatty acid binding protein (hFABP), a small cytosolic, cardiac specific marker. We determined hFABP release patterns during acute myocardial infarction (AMI) ± reperfusion (Rep) in comparison to Trop release and morphometric infarct size (IS) determination using triphenyl tetrazolium chloride (TTC).
Methods: In 8 swine (37±3 kg), AMI was induced by 8 hr sustained balloon occlusion (chronic) or 2 hr occlusion followed by 6 hr reperfusion. Blood samples were taken at predetermined intervals and analyzed for hFABP and Trop with ELISA.
Results: hFABP increased significantly faster than Trop upon occlusion (90±35 vs. 188±62 min, mean ± SD, p<0.04) with peak values at 5±1 hr followed by decline. Trop did not reach peak levels within 8 hr. Area under Curve (AUC) for hFABP and Trop did not correlate strongly with IS (R²=0.57 vs. 0.34). In contrast, at Rep, hFABP increased immediately whereas Trop release was delayed 20±15 min. (p=0.03). hFABP peak values were reached in 38±15 min after Rep., Trop in 145±15min. (p<0.001). IS by TTC correlated well with 8 hr AUC both for both markers (R²=0.90). However, hFABP reperfusion peak values (Fig.) showed the highest correlation (R²=0.98 vs. 0.87) with the intercept coinciding with mean baseline hFABP values (6.9±2.1).
Conclusions: hFABP release rises significantly faster and correlates better with IS than Trop in a large animal AMI-Rep model. Maximal hFABP release can be measured within 1 hr upon reperfusion or 5 hr in chronic MI. hFABP provides an accurate and fast marker for the longitudinal in vivo measurement of infarct size.
- © 2011 by American Heart Association, Inc.