Intramural dyssynchrony from acute right ventricular apical pacing in human subjects with normal left ventricular function.
J Cardiovasc Transl Res
; 3(4): 321-9, 2010 Aug.
Article
em En
| MEDLINE
| ID: mdl-20559782
Ventricular pacing causes early myocardial shortening at the pacing site and pre-stretch at the opposing ventricular wall. This contraction pattern is energetically inefficient and may lead to decreased cardiac function. This study was designed to describe the acute effects of right ventricular apical (RV(a)) pacing on dyssynchrony and systolic function in human subjects with normal left ventricular (LV) function and compare these effects to pacing from alternate ventricular sites. Patients (n = 26) undergoing an electrophysiology evaluation were studied during atrial pacing (AAI) and dual chamber pacing from the RV(a), left ventricular free wall (LV(fw)), and the combination of RV(a) and LV(fw) (BiV). Tissue Doppler imaging was used to measure intramural dyssynchrony by utilizing an integrated cross-correlation synchrony index (CCSI) from the apical 4-chamber view. RV(a) and BiV pacing significantly reduced systolic function as measured by longitudinal systolic contraction amplitude (SCA(long)) (p < 0.05) and LV velocity time integral (VTI) (p < 0.05) compared to AAI and LV(fw) pacing. RV(a) (and to a lesser extent BiV) pacing resulted in septal and lateral intramural dyssynchrony as indicated by significantly (p < 0.05) lower CCSI values as compared to AAI. CCSI was significantly (p < 0.05) worse during RV(a) than LV(fw) pacing. In patients with normal LV function, acute ventricular pacing in the RV(a) alone, or in conjunction with LV(fw) pacing (BiV), results in impaired regional and global LV systolic function and intramural dyssynchrony as compared to LV(fw) pacing alone.
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Base de dados:
MEDLINE
Assunto principal:
Fibrilação Atrial
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Estimulação Cardíaca Artificial
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Função Ventricular Esquerda
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Ventrículos do Coração
Limite:
Adult
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Aged
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Ano de publicação:
2010
Tipo de documento:
Article