Abstract 16153: Exercise Stress Testing Triggers Immediate Changes in Cardiac Troponin I Levels in Patients With Advanced Heart Failure
Background: Recent studies have shown that cardiac troponin (cTn) has prognostic implications throughout its range in patients with and without CAD. Elevations of cTn occur in heart failure and correlate with adverse outcomes but it is unclear whether this relationship stems from chronic myocardial fibrotic changes or acute increases in wall stress.
Methods: Using a highly sensitive assay (LOD < 0.0001 ng/ml) for cTn (Singulex, Alameda, CA), we studied cardiac troponin I (cTnI) in 108 HF patients and 25 healthy controls undergoing exercise stress testing. Blood samples were collected before and immediately after exercise for all subjects. In controls, a mid-exercise sample was collected at the median time when HF patients stopped exercising.
Results: We were able to quantify cTnI levels in all study subjects (LOQ = 0.0003 ng/ml). Median cTnI at baseline was 0.0018 ng/ml in controls (interquartile range [IQR] 0.0010-0.0034) and 0.0164 (IQR 0.0089-0.0368) in HF patients (p<0.001) (Figure 1a). Post-exercise median cTnI was 0.0017 ng/ml (IQR 0.0010-0.0048) in controls and 0.0178 (IQR 0.0090-0.0401) in HF patients (p<0.001). Immediate exercise-induced cTnI elevations were higher in all HF patients (median increase 0.0009 ng/ml, IQR -0.0003 to +0.0033) than in controls mid-exercise (median decrease 0.0002, IQR -0.0004 to +0.0004, p=0.009) and at exhaustion (median increase 0.0002, IQR -0.0002 to +0.0007, p=0.029). HF patients with exercise-induced ischemia during stress testing had similar cTnI elevations (median increase 0.0010 ng/ml, IQR -0.0004 to +0.0033) as the non-ischemic HF patients (median increase 0.0009, IQR 0.0000-0.0032), p=0.259 (Figure 1b).
Conclusion: Baseline cTnI levels prior to exercise are elevated in HF patients. However, exercise induces a rise in cTn detectable with an ultrasensitive assay, suggesting that acute changes in wall stress and subendocardial ischemia may contribute to the elevation of cTn in patients with heart failure.
- © 2011 by American Heart Association, Inc.