Quantifying and Reducing Motion Artifacts in Wearable Seismocardiogram Measurements During Walking to Assess Left Ventricular Health.

GOAL: Our objective is to provide a framework for extracting signals of interest from the wearable seismocardiogram (SCG) measured during walking at normal (subject's preferred pace) and moderately fast (1.34-1.45 m/s) speeds. METHODS: We demonstrate, using empirical mode decomposition (EMD) and feature tracking algorithms, that the pre-ejection period (PEP) can be accurately estimated from a wearable patch that simultaneously measures electrocardiogram and sternal acceleration signals. We also provide a method to determine the minimum number of heartbeats required for an accurate estimate to be obtained for the PEP from the accelerometer signals during walking. RESULTS: The EMD-based denoising approach provides a statistically significant increase in the signal-to-noise ratio of wearable SCG signals and also improves estimation of PEP during walking. CONCLUSION: The algorithms described in this paper can be used to provide hemodynamic assessment from wearable SCG during walking. SIGNIFICANCE: A major limitation in the use of the SCG, a measure of local chest vibrations caused by cardiac ejection of blood in the vasculature, is that a user must remain completely still for high-quality measurements. The motion can create artifacts and practically render the signal unreadable. Addressing this limitation could allow, for the first time, SCG measurements to be obtained reliably during movement-aside from increasing the coverage throughout the day of cardiovascular monitoring, analyzing SCG signals during movement would quantify the cardiovascular system's response to stress (exercise), and thus provide a more holistic assessment of overall health.

Antenatal maternally-administered phosphodiesterase type 5 inhibitors normalize eNOS expression in the fetal lamb model of congenital diaphragmatic hernia.

PURPOSE: Pulmonary hypertension (pHTN), a main determinant of survival in congenital diaphragmatic hernia (CDH), results from in utero vascular remodeling. Phosphodiesterase type 5 (PDE5) inhibitors have never been used antenatally to treat pHTN. The purpose of this study is to determine if antenatal PDE5 inhibitors can prevent pHTN in the fetal lamb model of CDH. METHODS: CDH was created in pregnant ewes. Postoperatively, pregnant ewes received oral placebo or tadalafil, a PDE5 inhibitor, until delivery. Near term gestation, lambs underwent resuscitations, and lung tissue was snap frozen for protein analysis. RESULTS: Mean cGMP levels were 0.53±0.11 in placebo-treated fetal lambs and 1.73±0.21 in tadalafil-treated fetal lambs (p=0.002). Normalized expression of eNOS was 82%±12% in Normal-Placebo, 61%±5% in CDH-Placebo, 116%±6% in Normal-Tadalafil, and 86%±8% in CDH-Tadalafil lambs. Normalized expression of ß-sGC was 105%±15% in Normal-Placebo, 82%±3% in CDH-Placebo, 158%±16% in Normal-Tadalafil, and 86%±8% in CDH-Tadalafil lambs. Endothelial NOS and ß-sGC were significantly decreased in CDH (p=0.0007 and 0.01 for eNOS and ß-sGC, respectively), and tadalafil significantly increased eNOS expression (p=0.0002). CONCLUSIONS: PDE5 inhibitors can cross the placental barrier. ß-sGC and eNOS are downregulated in fetal lambs with CDH. Antenatal PDE5 inhibitors normalize eNOS and may prevent in utero vascular remodeling in CDH.