Abstract
Optical mapping (OM) of cardiac electrical activity conventionally collects information from a three-dimensional (3-D) surface as a two-dimensional (2-D) projection map. When applied to measurements of the embryonic heart, this method ignores the substantial and complex curvature of the heart surface, resulting in significant errors when calculating conduction velocity, an important electrophysiological parameter. Optical coherence tomography (OCT) is capable of imaging the 3-D structure of the embryonic heart and accurately characterizing the surface topology. We demonstrate an integrated OCT/OM imaging system capable of simultaneous conduction mapping and 3-D structural imaging. From these multimodal data, we obtained 3-D activation maps and corrected conduction velocity maps of early embryonic quail hearts. 3-D correction eliminates underestimation bias in 2-D conduction velocity measurements, therefore enabling more accurate measurements with less experimental variability. The integrated system will also open the door to correlate the structure and electrophysiology, thereby improving our understanding of heart development.
Highlights
The developmental status of the heterogeneous conduction system in the embryonic heart can be characterized by parameters such as action potential (AP) morphology, activation sequence, and conduction velocity
An AP trace was recorded at each pixel in an Optical mapping (OM) image
The geometrically correct activation map can be visualized in the context of 3-D features, such as the surface curvature and the looping of the heart
Summary
Coordinated electrical activation and propagation play an important role as a heart develops from a linear tube to a complicated four-chambered form, for initiating rhythmic contractions of cardiac myocytes for efficient blood pumping, and for maintaining normal cardiac development.[1,2,3] The developmental status of the heterogeneous conduction system in the embryonic heart can be characterized by parameters such as action potential (AP) morphology, activation sequence, and conduction velocity. Due to technology limitations, there has been a very limited number of studies of embryonic heart development that directly measure these electrophysiological parameters.[4,5,6,7,8,9,10,11,12,13,14] Among the reported studies, the more quantitative parameter, conduction velocity, has seldom been reported.[7,8,9,10,11] Studies of murine and zebrafish knockout models have shown that the absence of or reduced protein expression of certain connexins in the developing heart can both modify conduction velocity and lead to congenital heart defects (CHDs), such as ventricular septal defects and conotruncal heart defects.[3,15,16] These types of CHDs are relatively common and are sometimes life-threatening in humans. As a result of limitations in technology to accurately measure conduction velocity, the mechanisms and the interplay between electrophysiology and heart structure are still poorly understood
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