Discussion
Ventricular arrhythmias (VAs) are frequently seen after LVAD placement,
with ventricular fibrillation being the most common.6Ventricular fibrillation is a terminal cardiac arrhythmia characterized
by disorganized, high-frequency ventricular contractions that result in
diminished cardiac output and hemodynamic collapse. Risk factors of VF
include cardiomyopathies, electrolyte abnormalities, acidosis,
hypoxemia, and ischemia.8,9,10 Pre-LVAD ventricular
arrhythmias are also a known risk factor for ventricular arrhythmia
post-LVAD implantation, reflective of the fact that LVADs do not
necessarily reverse underlying arrhythmogenicity.13
Patients are typically equipped with an ICD in order to terminate
sustained VAs, but our patient’s ICD was at EOL and therefore was unable
to terminate VF. Patients with CF-LVAD may tolerate otherwise
life-threatening arrhythmias for certain period of time with no or
minimal symptoms as the device supports their native cardiac
function.11,12 However, as seen in our case, it is
very important to defibrillate even asymptomatic patients with ongoing
VAs to sinus (or paced) rhythm as soon as possible, since their ability
to maintain adequate hemodynamic stability remains tenuous and can lead
to right ventricular failure due to prolonged
dysrhythmia.17
Noteworthy
in our case was the presence of organized contractility and rhythmic
opening of the mitral valve on echocardiogram despite ventricular
fibrillation on ECG. While some cardiac motion and valve opening could
be explained by the negative pressure generated by the device,
ventricular fibrillation is generally thought to manifest as
asynchronous ventricular activity. The fact that organized activity
appeared on echocardiogram suggests that the echocardiographic findings
may appear incongruous with ECG findings of ventricular fibrillation.
Gray et al. described spatio-temporal patterns of electrical activity of
isolated blood-perfused dog, rabbit, and sheep hearts during ventricular
fibrillation and found that there was spatial and temporal patterning
rather than total chaotic electrical activity.15Furthermore, clinical and simulation data of human hearts suggest that
VF in humans is driven by fewer reentrant sources and organized by fewer
rotors compared to VF in animal models.16 It is
possible that these features of VF in human hearts contributed to the
seemingly discordant findings of VF on ECG yet organized contraction on
non-invasive imaging.