“Direct observation of a stable spiral wave reentry in ventricles of a whole human heart using optical mapping for Voltage and Calcium”

From the studies of Gordon Moe in the 1960s, functional reentry has been investigated as a mechanism for tachycardia and fibrillation; however, it was not until 1990 that optical mapping (OM) experiments verified the existence of reentrant spiral-waves using sheep hearts.¹ Eventually, it was shown that electromechanical 3-D vortex filaments drive cardiac fibrillation.² To date, only multiple complex and short lived reentrant waves have been recorded using OM on human ventricles.³ So far, The presence of single spiral-waves in human ventricles has only been demonstrated using low-resolution intracardiac electrocardiograms.⁴ We report the first high resolution visualization of a stable spiral-wave in human ventricles using OM (voltage and calcium, Fig 1A) of the posterior epicardial surface (~7×7cm²) of an explanted heart from a 38 years old female transplant-recipient, who presented with cardiogenic shock secondary to viral cardiomyopathy.

Figure 1.

A: Movie frame showing an instant in time of the clockwise functional reentrant waves for voltage and calcium. Below are the voltage and calcium signals in time from one pixel in the center of the tissue. B: Image of the heart identifying the RV and LV; lower image shows contour lines during one rotation of the voltage signal. LV = left ventricle; RV = right ventricle.

The video shows two episodes of transiently stable scar-free ventricular tachycardia produced by a functional reentrant wave. The first is a spiral-wave (cyclelength of 325ms) that rotates clockwise across the interventricular septum, followed by another spiral-wave rotating counter-clockwise (360ms). Reentries were initiated with rapid pacing during a down pacing protocol used to calculate action potential duration restitution (at pacing periods of 330ms and 390ms, respectively, stimulus site shown in Fig 1B). The clockwise example lasted for over 50 rotations, producing monomorphic ECG, before degenerating into VF that self-terminated after 19sec. The induction of reentries was reproducible, and we observed other episodes. No drugs affecting electrophysiology were used.

The spiral-waves were not anatomical but functional reentries, following functional and dynamic lines of block that moved continuously across the tissue. Furthermore, no anatomical or anchoring regions of block were observed before spiral-wave initiation or after termination, such that pacing waves propagated smoothly across the tissue without regional slowing. The isochronous and conduction velocity maps are consistent with a spiral-wave propagating over the anisotropic cardiac tissue (Fig 1B). These results suggest that stable functional reentry can be responsible for a subset of monomorphic ventricular tachycardia in human hearts.