A novel wireless implant for central venous pressure measurement: First animal experience

Tejaswini Manavi,Patricia Vazquez,Helen O’Grady,Jerson Martina,Michael Rose,Douglas Nielsen,David Fitzpatrick,Omid Forouzan,Michael Nagy,Faisal Sharif,Haroon Zafar

doi:10.1016/j.cvdhj.2020.10.004

Abstract

Background/ObjectiveCentral venous pressure (CVP) serves as a surrogate for right atrial pressure, and thus could potentially predict a wider range of heart failure conditions. The purpose of this work is to assess CVP, through an implantable sensor incorporated with a novel anchor design, in the inferior and superior vena cava of an animal model.MethodsTwo animals (Dorset sheep) were implanted with sensors at 3 different locations: inferior vena cava (IVC), superior vena cava (SVC), and pulmonary artery (PA). Two sensors with distinct anchor designs considering anatomical requirements were used. A standard PA sensor (trade name Cordella) was deployed in the PA and SVC, whereas a sensor with a modified cylindrical anchor with various struts was designed to reside in the IVC. Each implant was calibrated against a Millar catheter reference sensor. The ability of the central venous sensors to detect changes in pressure was evaluated by modifying the fluid volume of the animal.ResultsThe sensors implanted in both sheep were successful, which provided an opportunity to understand the relationship between PA and CVP via simultaneous readings. The mapping and implantation in the IVC took less than 15 minutes. Multiple readings were taken at each implant location using a hand-held reader device under various conditions. CVP recorded in the IVC (6.49 mm Hg) and SVC (6.14 mm Hg) were nearly the same. PA pressure (13–14 mm Hg) measured was higher than CVP, as expected. The SVC waveforms showed clear beats and respiration. Respiration could be seen in the IVC waveforms, but not all beats were easily distinguishable. Both SVC and IVC readings showed increases in pressure (3.7 and 2.7 mm Hg for SVC and IVC, respectively) after fluid overload was induced via extra saline administration.ConclusionIn this work, the feasibility of measuring CVP noninvasively was demonstrated. The established ability of wireless PA pressure sensors to enable prevention of decompensation events weeks ahead can now be explored using central venous versions of such sensors.

Highlights

Heart failure (HF) is a widespread disease affecting more than 37.7 million people worldwide[1] and is a main cause of hospitalization in the United States and Europe, with more than 1 million per year in both regions.[2]
The sensors implanted in both sheep were successful, which provided an opportunity to understand the relationship between pulmonary artery (PA) and Central venous pressure (CVP) via simultaneous readings
CVP recorded in the inferior vena cava (IVC) (6.49 mm Hg) and superior vena cava (SVC) (6.14 mm Hg) were nearly the same

Summary

Introduction

Heart failure (HF) is a widespread disease affecting more than 37.7 million people worldwide[1] and is a main cause of hospitalization in the United States and Europe, with more than 1 million per year in both regions.[2]. Most advanced and decompensated HF patients develop congestive HF,[5] when heart overload leads to accumulation of fluid and pressure around itself and its periphery. In the presence of impaired myocardial pumping, lower perfusion of arterial blood volume activates several neurohormonal mechanisms, which increase heart filling pressures and promote retention of fluids. The presence of congestion exacerbates the progressive deterioration of HF syndrome, significantly shortening life expectancy,[6,7] and represents the leading cause of hospitalization in these patients, even ahead of low cardiac output.[4,5,8,9,10,11]

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