Troponin Release and Reversible Left Ventricular Dysfunction After Transient Pressure Overload

The authors previously demonstrated that brief ischemia elicits cardiac troponin I (cTnI) release and myocyte apoptosis in the absence of necrosis. It remains uncertain whether other pathophysiological stresses can produce apoptosis and transient cTnI release without ischemia. This study sought to d...

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Bibliographic Details
Published in:Journal of the American College of Cardiology 2018-06, Vol.71 (25), p.2906-2916
Main Authors: Weil, Brian R., Suzuki, Gen, Young, Rebeccah F., Iyer, Vijay, Canty, John M.
Format: Article
Language:English
Subjects:
Acute coronary syndromes
Animals
Apoptosis
Blood pressure
Calcium-binding protein
cardiac troponin I
Cardiology
cardiomyocyte apoptosis
Carotid arteries
Catheters
Coronary vessels
Data collection
Diastolic pressure
Embolisms
Heart
Heart attacks
Heart failure
Hemodynamics
Intravenous administration
Ischemia
Laboratory animals
left ventricular preload
Livestock
Myocardial ischemia
myocardial stretch
myocardial stunning
Myocardium - metabolism
Myocardium - pathology
Myocytes
Necrosis
Phenylephrine
pressure overload
Propofol
Swine
Troponin
Troponin I
Troponin I - blood
Ventricle
Ventricular Dysfunction, Left - blood
Ventricular Dysfunction, Left - pathology
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Summary:The authors previously demonstrated that brief ischemia elicits cardiac troponin I (cTnI) release and myocyte apoptosis in the absence of necrosis. It remains uncertain whether other pathophysiological stresses can produce apoptosis and transient cTnI release without ischemia. This study sought to determine whether a transient increase in left ventricular (LV) preload elicits cTnI release in the absence of ischemia. Propofol-anesthetized swine (N = 13) received intravenous phenylephrine (PE) (300 μg/min) for 1 h to increase left ventricular end-diastolic pressure (LVEDP) to ∼30 mm Hg. Serial cTnI and echocardiographic function were assessed for 24 h, and myocardial tissue was analyzed for apoptosis and necrosis. PE infusion increased systolic blood pressure from 137 ± 14 mm Hg to 192 ± 11 mm Hg (mean ± SD; p 
ISSN:0735-1097
1558-3597
DOI:10.1016/j.jacc.2018.04.029