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.