Accelerometer-based evaluation of left ventricular diastolic function

Background Miniaturised accelerometers are increasingly integrated into pacing leads, which enables extraction of functional parameters for cardiac monitoring. To date, research has focused primarily on systolic function, while diastolic function has received limited attention. Purpose We investigated the feasibility of defining an accelerometer-derived index sensitive to changes in diastolic function, with the isovolumic relaxation time constant τ of left ventricular (LV) pressure serving as reference. Our hypothesis was that faster LV relaxation would generate stronger wall-mounted acceleration signals, driven by more rapid release of restoring forces and enhanced mitral inflow. Methods In 14 anaesthetized, open-chest pigs, an accelerometer was sutured to the LV anterior epicardium and a calibrated microtip pressure catheter inserted into the LV (Figure 1A). Measurements were performed at baseline and during different interventions including esmolol infusion, adrenaline infusion and induction of myocardial ischaemia. Electrocardiogram (ECG), left ventricular pressure (LVP), and acceleration signals were recorded simultaneously and segmented into cardiac cycles using R peaks on ECG (Figure 1B). τ was estimated by fitting a monoexponential model with zero asymptote to the LVP decay phase. The LV impulse (ILV) in each cycle was defined as the cumulative sum of the absolute Z-axis acceleration over a diastolic interval of 100 ms (Figure 1C). Pearson correlation coefficients were used to quantify the association between ILV and τ. Paired two-tailed t-tests were used to compare each intervention with baseline. Results Across 14 experiments, 225 heartbeats were included in the analysis. Esmolol infusion significantly impaired LV relaxation as shown in prolonging τ (40.93±9.71 ms vs. 52.54±11.32 ms, P<0.001), accompanied by a decreasing ILV (4.04±1.26 m/s vs. 3.36±1.19 m/s, P<0.001). In contrast, adrenaline infusion significantly improved LV relaxation (τ: 43.93±12.61 ms vs. 36.66±8.37 ms, P<0.001) and increased ILV (4.30±1.16 m/s vs. 5.24±1.04 m/s, P<0.001). During ischaemia, τ was significantly prolonged (42.33±10.58 ms vs. 50.53±16.37 ms, P=0.002) and ILV reduced (4.18±1.22 m/s vs. 3.06±1.04 m/s, P<0.001). There was a statistically significant negative correlation between τ and ILV in 12 of the 14 animals, with a mean correlation coefficient of R²=0.78±0.21 (Figure 2). Conclusion Accelerometer-derived LV impulse during early filling correlates closely with the invasive gold standard of ventricular diastolic function across different interventions. This technique offers a novel approach for continuous diastolic function monitoring using accelerometers in implantable devices, with potential extension to wearable devices for non-invasive, long-term assessment.