Use of MIBG Scan Images in PVC Ablations

Premature ventricular contractions (PVC) are the most common arrhythmia to be observed in the
absence of structural heart disease, and 'frequent' PVCs are estimated to occur in 1-4% of
the general population.1 Idiopathic PVCs are usually associated with a benign course from the
standpoint of arrhythmic death, but often result in significant symptoms for the patient such
as palpitations, dizziness, pre-syncope and rarely syncope. More recently, a new concept of
PVC- mediated cardiomyopathy has emerged that is reversible with suppression of the PVCs.2
Both of those patient populations are currently targeted with PVC suppressive therapy which
often involves as the first step using medical therapy such as a beta blocker, calcium
channel blocker or an antiarrhythmic. If those fail or if the patients wants to avoid medical
therapy an ablation to eliminate the abnormal myocardial tissue that is the origin of the
PVCs is often performed.

Radiofrequency ablation (RFA) for PVCs has been performed for several decades and has a
well-defined safety and effectiveness profile in patients with symptomatic frequent
ventricular ectopic beats and PVC-induced cardiomyopathy. Successful PVC suppression ≥80% of
RV and LV PVCs has been reported to be as high as ~80% using an ablation approach.9 Studies
found improvements in patient symptoms with elimination of PVCs. In LV dysfunction following
ablation demonstrated a significant inverse correlation between EF and PVC burden before
ablation, and a significant post procedural improvement in ejection fraction (EF) in 82% of
patients who had abnormal systolic function before ablation.8 Improvement of the overall LV
EF ranged from 13%-23% after PVC ablation.5,8,10

Autonomic innervation of the heart plays a major role in the normal regulation of myocardial
function, heart rate, and coronary blood flow. Abnormal sympathetic cardiac innervation has
been shown to have prognostic value for different heart diseases, e.g. heart transplant,
coronary artery disease, heart failure, arrhythmias, etc. Importantly, there is a clear
association with an increased cardiac morbidity and mortality in heart diseases. Patients
with myocardial infarction as well as patients with heart failure exhibit well recognized
abnormalities in autonomic tone. PVCs especially in the setting of preserved EF (normal heart
patients) have frequently an automatic/triggered mechanism, which is influenced by the
cardiac innervation.

Decreased reuptake by impaired myocardial presynaptic nerve terminals results in a buildup of
these catecholamines in the synaptic cleft. This leads to a downregulation of postsynaptic
beta-adrenergic receptors, with resultant worsening cardiomyopathy and increased
arrhythmogenesis.

Cardiac sympathetic innervation can be directly imaged with commonly used nuclear
radioisotope, 123I-meta-iodobenzylguanidine (123I-mIBG). As a norepinephrine analogue,
123I-mIBG is similarly released into the synaptic cleft in response to sympathetic input by
presynaptic nerve terminals 123I-metaiodobenzylguanidine (123I-MIBG) allows visualization of
the cardiac innervation, which could provide additional information to understand the origin,
prognosis and pathophysiology of PVCs and guide potential ablation procedures.

Inclusion Criteria:

- Scheduled for PVC ablation

Exclusion Criteria:

- pregnancy