Hemodynamic assessment of diastolic function for experimental models

Abstract

Traditionally, the evaluation of cardiac function has focused on systolic function; however, there is a growing appreciation for the contribution of diastolic function to overall cardiac health. Given the emerging interest in evaluating diastolic function in all models of heart failure, there is a need for sensitivity, accuracy, and precision in the hemodynamic assessment of diastolic function. Hemodynamics measure cardiac pressures in vivo, offering a direct assessment of diastolic function. In this review, we summarize the underlying principles of diastolic function, dividing diastole into two phases: 1) relaxation and 2) filling. We identify parameters used to comprehensively evaluate diastolic function by hemodynamics, clarify how each parameter is obtained, and consider the advantages and limitations associated with each measure. We provide a summary of the sensitivity of each diastolic parameter to loading conditions. Furthermore, we discuss differences that can occur in the accuracy of diastolic and systolic indices when generated by automated software compared with custom software analysis and the magnitude each parameter is influenced during inspiration with healthy breathing and a mild breathing load, commonly expected in heart failure. Finally, we identify key variables to control (e.g., body temperature, anesthetic, sampling rate) when collecting hemodynamic data. This review provides fundamental knowledge for users to succeed in troubleshooting and guidelines for evaluating diastolic function by hemodynamics in experimental models of heart failure.

A new approach to improve the hemodynamic assessment of cardiac function independent of respiratory influence

“…In cases where a cardiac cycle fell across two respiratory phases, the cycle was placed into the respiratory phase with the majority (> 50%) of data points for that given cardiac cycle. Tau Weiss, Tau Glantz, and Tau Logistic were calculated as described previously 38 .…”

Neuronatin regulates whole‐body metabolism: is thermogenesis involved?

“…Overexpression of PLN and increases in the ratio of PLN relative to SERCA has been implicated in dilated cardiomyopathy, heart failure, and skeletal muscle myopathies. 11,[47][48][49] Thus, finding ways to reduce the amount of PLN relative to SERCA is an active field of research. 50,51 Long considered to be the functional homolog of PLN, sarcolipin (SLN) is a small 31 amino acid protein that binds to and regulates the SERCA pump.…”

“…In muscle, PLN inhibition of SERCA prolongs relaxation and reduces contractility via a reduction in SR Ca 2+ stores. Overexpression of PLN and increases in the ratio of PLN relative to SERCA has been implicated in dilated cardiomyopathy, heart failure, and skeletal muscle myopathies 11,47–49 . Thus, finding ways to reduce the amount of PLN relative to SERCA is an active field of research 50,51 …”

Effects of enriched-potassium diet on cardiorespiratory outcomes in experimental non-ischemic chronic heart failure

“…Indeed, we found a significant increase in LV-end diastolic pressure (LVEDP) in CHF rats compared to Sham rats and this was not significantly reduced by enriched-K + diet in CHF (Additional file 1 : Table S6). Since cardiac diastolic function is influenced by ventilation, we determined ventilation-dependent modulation of cardiac function during each inspiratory and expiratory cycles [ 40 ]. Intraventricular pressures at the end of diastole (nEDV) during inspiration (ins) were similar between Sham and CHF groups (Fig.…”