Optimizing Temporal Waveform Analysis: A Novel Pipeline for Efficient Characterization of Left Coronary Artery Velocity Profiles.

Continuously measured arterial blood velocity can provide insight into physiological parameters and potential disease states. The efficient and effective description of the temporal profiles of arterial velocity is crucial for both clinical practice and research. We propose a pipeline to identify the minimum number of points of interest to adequately describe a velocity profile of the left coronary artery. This pipeline employs a novel operation that "stretches" a baseline waveform to quantify the utility of a point in fitting other waveforms. Our study introduces a comprehensive pipeline specifically designed to identify the minimal yet crucial number of points needed to accurately represent the velocity profile of the left coronary artery. Additionally, the only location-dependent portion of this pipeline is the first step, choosing all of the possible points of interest. Hence, this work is broadly applicable to other waveforms. This versatility paves the way for a novel non-frequency domain method that can enhance the analysis of physiological waveforms. Such advancements have potential implications in both research and clinical treatment of various diseases, underscoring the broader applicability and impact.

Postural orthostatic tachycardia syndrome explained using a baroreflex response model.

Patients with postural orthostatic tachycardia syndrome (POTS) experience an excessive increase in heart rate (HR) and low-frequency (∼0.1 Hz) blood pressure (BP) and HR oscillations upon head-up tilt (HUT). These responses are attributed to increased baroreflex (BR) responses modulating sympathetic and parasympathetic signalling. This study uses a closed-loop cardiovascular compartment model controlled by the BR to predict BP and HR dynamics in response to HUT. The cardiovascular model predicts these quantities in the left ventricle, upper and lower body arteries and veins. HUT is simulated by letting gravity shift blood volume (BV) from the upper to the lower body compartments, and the BR control is modelled using set-point functions modulating peripheral vascular resistance, compliance, and cardiac contractility in response to changes in mean carotid BP. We demonstrate that modulation of parameters characterizing BR sensitivity allows us to predict the persistent increase in HR and the low-frequency BP and HR oscillations observed in POTS patients. Moreover, by increasing BR sensitivity, inhibiting BR control of the lower body vasculature, and decreasing central BV, we demonstrate that it is possible to simulate patients with neuropathic and hyperadrenergic POTS.