Kp. Anderson et al., MYOCARDIAL ELECTRICAL PROPAGATION IN PATIENTS WITH IDIOPATHIC DILATEDCARDIOMYOPATHY, The Journal of clinical investigation, 92(1), 1993, pp. 122-140
Myocardial propagation may contribute to fatal arrhythmias in patients
with idiopathic dilated cardiomyopathy (IDC). We examined this proper
ty in 15 patients with IDC undergoing cardiac transplantation and in 1
4 control subjects. An 8 X 8 array with electrodes 2 mm apart was used
to determine the electrical activation sequence over a small region o
f the left ventricular surface. Tissue from the area beneath the elect
rode array was examined in the patients with IDC. The patients with ID
C could be divided into three groups. Group I (n = 7) had activation p
atterns and estimates of longitudinal (theta(L) = 0.84+/-0.09 m/s) and
transverse (theta(T) = 0.23+/-0.05 m/s) conduction velocities that we
re no different from controls (theta(L) = 0.80+/-0.08 m/s, theta(L) 0.
23+/-0.03 m/s). Group II (n= 4) had fractionated electrograms and dist
urbed transverse conduction with normal longitudinal activation, featu
res characteristic of nonuniform anisotropic properties. Two of the co
ntrol patients also had this pattern. Group III (n = 4) had fractionat
ed potentials and severely disturbed transverse and longitudinal propa
gation. The amount of myocardial fibrosis correlated with the severity
of abnormal propagation. We conclude that (a) severe contractile dysf
unction is not necessarily accompanied by changes in propagation, and
(b) nonuniform anisotropic propagation is present in a large proportio
n of patients with IDC and could underlie ventricular arrhythmias in t
his disorder.