Many studies suggest that patients who receive a ventricular pacemaker have
a higher incidence of systemic thromboembolism compared to patients receiv
ing a physiological pacemaker. However, the exact mechanism regarding the e
tiology of thromboembolism remains unclear. We evaluated the left atrial ap
pendage (LAA) functions, using multiplane transesophageal echocardiography
(TEE), in patients with different pacing modes. In order to evaluate the ej
ection fraction (EF), peak emptying (V-E) and filling (V-F) flow velocities
of the LAA by TEE, we studied 31 patients (mean age 63+/-18.5 years) who h
ad been paced for 5.0+/-2.9 years. Patients with atrial fibrillation, left
ventricular dysfunction and mitral valve disease were excluded. The pacing
indications were complete atrioventricular block (AVB) in 19 patients (9 VV
I, 10 VDD or DDD) and sick sinus syndrome (SSS) in 12 patients (5 VVI, 7 DD
D). Mean EF, V-E and V-F of the LAA were significantly lower in all patient
s with ventricular pacing (25.5+/-15.6%, 30.4+/-15.6 cm/s and 29.1+/-19.2 c
m/s, respectively) compared to those with physiologic pacing (48.5+/-16.9%,
59.6+/-16.3 cm/s, 57.9+/-18.5 cm/s, respectively) (P<0.01 in all). When pa
tients were further classified with respect to underlying heart disease whe
ther they had SSS or AVB, all measurements of the LAA (EF, V-E and V-F) in
both subgroup of patients with SSS and AVB were found significantly lower i
n those with ventricular pacing than in those with physiologic pacing (Tabl
es 3 and 4). This decrease, especially in LAA flow, was much greater in tho
se with SSS (Mean V-E and V-F <20 cm/s). In a patient paced with VVI for SS
S, a thrombus was detected within the LAA cavity. In conclusion, these resu
lts suggest that the pacing modality appeared to influence the LAA function
s in paced patients. Patients with asynchronous ventricular pacing modes ha
d a significantly higher incidence of depressed LAA functions than did pati
ents with physiological pacing, especially more marked in patients with sic
k sinus syndrome. This may be a factor responsible for increased risk of th
rombus formation and thromboembolic events in this patient population. (C)
2000 Elsevier Science Ireland Ltd. All rights reserved.