The factors that contribute to the occurrence of sudden cardiac death (SCD)
in patients with chronic myocardial infarction (MI) are not entirely clear
. The present study tests the hypothesis that augmented sympathetic nerve r
egeneration (nerve sprouting) increases the probability of ventricular tach
ycardia (VT), ventricular fibrillation (VF), and SCD in chronic MI. In dogs
with MI and complete atrioventricular (AV) block, we induced cardiac sympa
thetic nerve sprouting by infusing nerve growth factor (NGF) to the left st
ellate ganglion (experimental group, n=9). Another 6 dogs with MI and compl
ete AV block but without NGF infusion served as controls (n=6). Immunocytoc
hemical staining revealed a greater magnitude of sympathetic nerve sproutin
g in the experimental group than in the control group. After MI, all dogs s
howed spontaneous VT that persisted for 5.8+/-2.0 days (phase 1 VT). Sponta
neous VT reappeared 13.1+/-6.0 days after surgery (phase 2 VT). The frequen
cy of phase 2 VT was 10-fold higher in the experimental group (2.0+/-2.0/d)
than in the control group (0.2+/-0.2/d, P<0.05). Four dogs in the experime
ntal group but none in the control group died suddenly of spontaneous VF. W
e conclude that MI results in sympathetic nerve sprouting. NGF infusion to
the left stellate ganglion in dogs with chronic MI and AV block augments sy
mpathetic nerve sprouting and creates a high-yield model of spontaneous VT,
VF, and SCD. The magnitude of sympathetic nerve sprouting may be an import
ant determinant of SCD in chronic MI.