A coupled atrioventricular-aortic setup for in-vitro hemodynamic study of the systemic circulation: Design, fabrication, and physiological relevancy

PLoS One. 2022 Nov 4;17(11):e0267765. doi: 10.1371/journal.pone.0267765. eCollection 2022.

Abstract

In-vitro models of the systemic circulation have gained a lot of interest for fundamental understanding of cardiovascular dynamics and for applied hemodynamic research. In this study, we introduce a physiologically accurate in-vitro hydraulic setup that models the hemodynamics of the coupled atrioventricular-aortic system. This unique experimental simulator has three major components: 1) an arterial system consisting of a human-scale artificial aorta along with the main branches, 2) an artificial left ventricle (LV) sac connected to a programmable piston-in-cylinder pump for simulating cardiac contraction and relaxation, and 3) an artificial left atrium (LA). The setup is designed in such a way that the basal LV is directly connected to the aortic root via an aortic valve, and to the LA via an artificial mitral valve. As a result, two-way hemodynamic couplings can be achieved for studying the effects that the LV, aorta, and LA have on each other. The collected pressure and flow measurements from this setup demonstrate a remarkable correspondence to clinical hemodynamics. We also investigate the physiological relevancies of isolated effects on cardiovascular hemodynamics of various major global parameters found in the circulatory system, including LV contractility, LV preload, heart rate, aortic compliance, and peripheral resistance. Subsequent control over such parameters ultimately captures physiological hemodynamic effects of LV systolic dysfunction, preload (cardiac) diseases, and afterload (arterial) diseases. The detailed design and fabrication of the proposed setup is also provided.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, N.I.H., Extramural

MeSH terms

  • Aorta / physiology
  • Aortic Valve
  • Hemodynamics* / physiology
  • Humans
  • Myocardial Contraction
  • Ventricular Dysfunction, Left*
  • Ventricular Function, Left

Associated data

  • Dryad/10.5061/dryad.x0k6djhmt

Grants and funding

This study was partially funded by the National Institutes of Health (NIH; No. 1_R56AG068630_01). NP is supported by the American Heart Association (AHA) Career Development Award No. 20CDA35260167. The funders of this study had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.