Left atrial strain: a sensitive whistleblower lost in translation

Abstract

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): This work was supported by the Netherlands Organisation for Scientific Research (NWO- ZonMw, VIDI grant 016.176.340 to J.L.) and the Dutch Heart Foundation (ERA-CVD JTC2018 grant 2018T094; Dr. Dekker Program grant 2015T082 to J.L.) Background Left atrial (LA) function measured by peak/reservoir strain (PLAS) has been shown to be of prognostic value in various cardiac pathologies, including heart failure (HF). However, the underlying mechanisms leading to reduced PLAS remain poorly understood. Purpose To investigate how various combinations of left ventricular (LV) systolic-, diastolic, and LA failure affect PLAS. Method The CircAdapt computational model of the human heart and circulation is used to simulate the abovementioned LV and LA substrates, starting from a healthy reference simulation. LV systolic failure was simulated by a 25% decrease of LV contractility and LV eccentric hypertrophy (simultaneous increase of LV wall mass and area by 30%). LV diastolic failure was simulated by increasing LV myocardial stiffness by 100%, impairing LV relaxation function (increasing relaxation time constant from 35ms to 60ms, and LV concentric remodeling (increasing LV wall mass by 30%). LA failure was simulated by a fully non-contractile LA myocardium. Results LV systolic failure was characterized by reduced LV GLS (21 to 12%) and LVEF (54 to 34%), with marginal increase in PLAS (42 to 46%; Figure top row, first vs second column). LV diastolic failure was characterized by reduced PLAS (42 to 23%; Figure first vs third and fourth columns) with LA dilation (i.e. peak LA volume: 50 to 80 ml). Furthermore, LV concentric remodeling increased LVEF (54 to 64%). LA failure led to LA dilation and reduction of PLAS, regardless of LV substrate. Lastly, LV diastolic dysfunction and LA failure did not affect LV GLS (Figure bottom row). Conclusion Simulations showed that acute LV systolic failure hardly affected PLAS, but predominantly decreased LV GLS and LVEF. On the contrary, both LV diastolic dysfunction and LA failure reduced PLAS, rather than LV GLS and LVEF. Hence, LA strain can be considered as a whistleblower sensitive to various LV and/or LA abnormalities, which may explain why it is a rather nonspecific diagnostic marker. Abstract Figure. LA and LV strain in various substrates