Microscope-based near-infrared stereo-imaging system for quantifying the motion of the murine epicardial coronary arteriesin vivo

David S Long,Hui Zhu,Morton H Friedman

doi:10.1117/1.jbo.18.9.096013

Abstract

Atherosclerosis is a leading cause of mortality in industrialized countries. In addition to "traditional" systemic risk factors for atherosclerosis, the geometry and motion of coronary arteries may contribute to individual susceptibility to the development and progression of disease in these vessels. To be able to test this, we have developed a high-speed (∼40 frames per second) microscope-based stereo-imaging system to quantify the motion of epicardial coronary arteries of mice. Using near-infrared nontargeted quantum dots as an imaging contrast agent, we synchronously acquired paired images of a surgically exposed murine heart, from which the three-dimensional geometry of the coronary arteries was reconstructed. The reconstructed geometry was tracked frame by frame through the cardiac cycle to quantify the in vivo motion of the vessel, from which displacements, curvature, and torsion parameters were derived. Illustrative results for a C57BL/6J mouse are presented.

Highlights

Coronary artery atherosclerosis is a leading cause of morbidity and mortality in Western societies
The imaging system was used to quantify the motion of a left epicardial coronary artery segment of a 29.2-g male C57BL/6J mouse
The mouse was intravenously injected with ∼8.5 pmol∕g of nontargeted, near-infrared quantum dots (Qdots) and imaged at a frame rate of 40 fps

Summary

Introduction

Coronary artery atherosclerosis is a leading cause of morbidity and mortality in Western societies. Atherosclerosis is a progressive fibroinflammatory disease identified by intimal thickening, the focal accumulation of lipids, fibrous elements, and cellular elements within the walls of large arteries, known as atherosclerotic lesions.[1] Lesions preferentially develop at arterial branches, the outer walls of bifurcations, and the inner wall of curved sections; the cause of this focal vasculopathy is not fully understood. It is, understood from epidemiological and clinical studies that individual susceptibility to the development and localization of atherosclerotic lesions is influenced by systemic risk factors, including smoking, diabetes mellitus, obesity, hypertension, and high cholesterol. One prevalent explanation of the focal nature of the disease is that the local fluid mechanical stresses at the walls of coronary arteries,[4] as well as mechanical stresses within the vessel wall, may mediate the phenotype of endothelial cells, thereby producing atherosusceptible sites.[5,6,7,8,9] it has been speculated that certain aspects of arterial geometry and motion, which vary substantially among individuals, may increase an individual’s

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