Objective: To assess the effects of VVI (ventricular demand) and DDD (dual-chamber) pacing models on cardiac remodeling and the long-term clinical outcome of patients with symptomatic bradycardia.

Methods: All patients with DDD and VVI pacing models at our hospital from January 1991 to January 2003 were retrospectively analyzed.

Results: After a follow-up period of over 8 years in DDD and VVI groups (97 ± 27, 107 ± 44 months), left atrial diameter [(45 ± 12) mm vs (39 ± 12) mm, P < 0.01] and left ventricular end-diastolic diameter [(53 ± 11) mm vs (50 ± 9) mm, P = 0.01] in 57 patients with VVI pacing model were markedly enlarged than those at pre-implantation. And tricuspid regurgitation increased (42.4% vs 16.9%, P < 0.05). But in 59 patients with DDD pacing model, except for increased tricuspid regurgitation (42.1% vs 10.5%, P < 0.01), left atrial diameter [(37 ± 5) mm vs. (35 ± 5) mm, P = 0.07] and left ventricular end-diastolic diameter [(47 ± 7) mm vs (47 ± 5) mm, P = 0.32] were not significantly different. Mitral regurgitation significantly increased only in the VVI group (P < 0.01). The increases of left ventricular end-diastolic diameter (P = 0.04), mitral valve (P = 0.02) and tricuspid regurgitation (P < 0.01) were much more pronounced in the VVI group than those in the DDD group. Left ventricular ejection fraction (LVEF) showed no difference with that at pre-implantation (P = 0.11 in DDD group, P = 0.05 in VVI group). But the LVEF value was lower (P = 0.04) while the incidence of thrombosis was higher (P = 0.03) in the VVI group than those in the DDD group at post-implantation. However, the incidence of atrial fibrillation (P = 0.14), hospitalization (P = 0.08) and survival (P = 0.77) showed no significant difference between two groups.

Conclusion: DDD pacing offers more benefits over VVI pacing through improving cardiac functions and arresting left ventricular remodeling. However, neither groups showed any difference in decreasing mortality rate and hospitalization. Moreover, both pacing modes fail to reverse cardiac electrical and anatomical remodeling. It is imperative to explore more physiological pacing site and rational atrioventricular (AV) interval to improve the prognosis of patients.

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