Troponin Release and Reversible Left Ventricular Dysfunction After Transient Pressure Overload

Abstract

Transient elevations of LVEDP lead to cTnI release, apoptosis, and reversible stretch-induced stunning in the absence of ischemia. Thus, preload-induced myocyte injury may explain many cTnI elevations seen in the absence of clinical signs or symptoms of myocardial ischemia.

Fourth Universal Definition of Myocardial Infarction (2018)

“…Although elevated cTn values reflect injury to myocardial cells, they do not indicate the underlying pathophysiologic mechanisms, and can arise following preload-induced mechanical stretch or physiological stresses in otherwise normal hearts. [32][33][34] Various causes have been suggested for the release of structural proteins from the myocardium, including normal turnover of myocardial cells, apoptosis, cellular release of cTn degradation products, increased cellular wall permeability, formation and release of membranous blebs, and myocyte necrosis. 27,35 Yet, it is not possible clinically to distinguish which increases of cTn levels are due to which mechanisms.…”

Race duration and blood pressure are major predictors of exercise-induced cardiac troponin elevation

“…It has been hypothesized that cTn can be released due to reversible myocyte injury and stretch-induced apoptosis, or increased membrane permeability with leakage of loosely bound cTn (2,6). Exercise-induced troponin increase has also been thought to be due to increased wall tension and ventricular strain caused by volume overload, neurohormonal stimulation and/or reversible ischaemia due to increased myocardial energy demands (2,7). Several studies have attempted to identify predictors of the exercise-induced cTn release; however, most of these studies are small, sampled cTn only immediately after exercise or used older cTn assays.…”

Effect of Improving Volume Overload on Home Blood Pressure Variability in Hemodialysis Patients

“…Fluctuation in BP is a hemodynamic phenomenon that is influenced by interactions among extracellular fluid volume, humoral, sympathetic, and cardiovascular factors . Although it was not detected in the present study, several researches in vivo and in vitro have demonstrated that excessive fluid volume would cause cardiomyocyte injury and apoptosis, which could induce a series of cardiovascular dysfunctions by impairing biochemical signal transduction, vascular tone adaptation, and baroreflex control of circulation . When HD patients are fluid overloaded, the sustained preload‐induced cardiomyocyte injury might lead to abnormal expression and production of bioactive substances that could disrupt BP regulation .…”