Abstract 16918: A Transient Increase in Left Ventricular Load Leads to Cardiac Troponin I Release in the Absence of Myocardial Ischemia
Introduction: Although elevated serum cardiac troponin I (cTnI) concentrations are widely used as a biomarker for the detection of myocardial infarction, increased serum cTnI levels have been observed in the absence of ischemia in fluid overload states such as renal failure and advanced heart failure.
Hypothesis: Transient left ventricular (LV) stretch induced by a reversible elevation in preload without ischemia leads to significant transcardiac cTnI release.
Methods: Propofol-sedated swine (n=12) received intravenous phenylephrine (PE; 300 μg/min) for one hour to transiently raise LV end-diastolic pressure (EDP) to ∼30 mmHg. Hemodynamics were monitored throughout the experiment and myocardial perfusion was measured at baseline and during PE with fluorescent microspheres to exclude subendocardial ischemia. Serial blood sampling from the aorta and coronary sinus was performed to assess transcardiac cTnI release before, during, and after PE infusion.
Results: PE induced a significant rise in mean arterial pressure (MAP; from 99 ± 5 to 172 ± 5 mmHg, P<0.05) and LVEDP (from 16 ± 2 to 30 ± 3 mmHg, p<0.05) that normalized 15 minutes after the infusion was stopped (MAP: 94 ± 7 mmHg, LVEDP: 17 ± 2 mmHg). Subendocardial blood flow was unaffected by PE infusion (0.9 ± 0.1 mL/min/g vs. 0.8 ± 0.1 mL/min/g at baseline). Serial blood sampling revealed significant transcardiac cTnI release 60-minutes after cessation of PE (Table). The next day, circulating cTnI levels remained elevated but there was no longer a significant gradient between the aorta and coronary sinus.
Conclusions: These results demonstrate that a transient increase in LV preload produces measurable transcardiac cTnI release that results in sustained elevations in circulating cTnI. This response occurs without a change in subendocardial blood flow, indicating that elevations in hemodynamic load may provoke cardiomyocyte damage independently of ischemia-induced cell necrosis in the normal heart.
Author Disclosures: B.R. Weil: None. R.F. Young: None. V. Iyer: None. G. Suzuki: None. J.M. Canty: None.
- © 2015 by American Heart Association, Inc.