Effect Of Exercise On Seismocardiographic Signals

• Published in: Journal of cardiac failure Vol. 29; no. 4; p. 598
• Main Authors: Sandler, Richard H, Dhar, Rajkumar, Raval, Nirav, Mentz, Robert, Darwish, Sara, Darwish, Seena, Assi, May, Mansy, Hansen
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 01.04.2023
• ISSN: 1071-9164; 1532-8414
• DOI: 10.1016/j.cardfail.2022.10.131

Seismocardiography (SCG) measures the vibration of the chest wall surface due to cardiac events such as valve closure, blood flow momentum changes and myocardial muscle contraction. Pilot studies suggest that features extracted from SCG may be predictive of heart failure readmission, which, if confirmed, suggests potential utility of SCG as a non-invasive diagnostic tool in patients with heart failure (HF). Initial understanding of exercise effects on SCG signals in healthy subjects may improve SCG diagnostic value in the later study of HF subjects. To obtain pilot data on the SCG response to exercise-induced stress in health. Five healthy subjects participated after obtaining IRB approval and informed consent. SCG was acquired using a tri-axial accelerometer placed at the left lower sternal border 4th intercostal space. SCG and ECG signals were acquired simultaneously with subjects resting in the sitting position for 8 minutes followed by 120 sec of continuous pre-exercise data capture. Then subjects pedaled a bike for 1 minute after reaching 70% of their maximum heart rate (HR =0.7*(220-subject age)), after which post-exercise ECG and SCG data was captured for 50 seconds. The SCG events (each event corresponds to one cardiac cycle) were identified using the ECG R-wave [3]. The magnitudes of SCG1 and SCG2 (similar to the auscultated S1 and S2) were calculated for each SCG beat pre- and post-exercise. Results are shown in Table 1. SCG1 magnitude increased significantly with exercise, whereas SCG2 magnitude did not show notable changes. Exercise-induced stress caused significant SCG1 amplitude changes while SCG2 amplitudes were largely unchanged. The ratio between SCG1 and SCG2 amplitudes may provide a dimensionless parameter that correlates with exercise tolerance. While the exact mechanism is not known, the increased SCG1 magnitude may be indicative of more vigorous ventricular contractility. The small changes in SCG2 may be reflective of smaller pressure gradient alterations from aortic rebound. More investigations are needed to confirm the study results in both healthy subjects and those with heart diseases.