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Acta Physiologica Congress

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Acta Physiologica 2011; Volume 201, Supplement 682
The 90th Annual Meeting of The German Physiological Society
3/26/2011-3/29/2011
Regensburg, Germany


PACING- INDUCED VENTRICULAR DYSSYNCHRONY:A CHRONIC ANIMAL STUDY WITH MINIPIGS
Abstract number: P015

*Blanke1 K., Salameh1 A., Rastan2 A., Hiyasat3 B., Dhein2 S., Dahnert1 I., Janousek4 J.

Question: 

Previous studies have demonstrated that conventional right ventricular pacing is detrimental to left ventricular function in animals and humans. Therefore the interest in alternate pacing sites has increased recently. In regard to this the aim of this study was to investigate if left ventricular apex pacing is the more superior pacing site which improves cardiac function.

Methods: 

Therefore 14 minipigs underwent ventricular pacing at 120 beats/min for one year. 7 minipigs were stimulated from the right ventricular free wall (RVFW) and 7 minipigs from the left ventricular apex (LVA), respectively. The pacing was performed in a DDD mode. 7 Minipigs paced from the right atrium (AAI) served as control group. 2- dimensional strain echocardiography and pressure- volume- loops were carried out to assess left ventricular performance. The size of cardiomyocytes as well as the distribution of the gap junction protein Cx43 were studied by immunohistology. Furthermore real time PCR- experiments were performed to investigate the Cx43- mRNA expression.

Results: 

RVFW pacing significantly impaired stroke work, ejection fraction, cardiac index, dp/dt max, dp/dt min and contractility as compared to the control group. In contrast LVA- stimulated minipigs showed an improvement in stroke work, ejection fraction, dp/dt max, dp/dt min in comparison with RVFW- paced minipigs. 2- dimensional strain analysis revealed that RVFW- pacing significantly increased mechanical dyssynchrony of the left ventricle compared to LVA- pacing. RVFW- and LVA- pacing showed a significant decrease in length and an increase in width of cardiomyocytes of the left ventricle compared to the control group. There were no differences in size of cardiomyocytes as well as in distribution of Cx43 between RVFW- and LVA- pacing, respectively. Furthermore the Cx43 mRNA expression of cardiomyocytes was significantly decreased after RVFW pacing in relation to LVA- paced minipigs.

Conclusion: 

Ventricular pacing leads to heart failure in the chronic minipig model. Pacing at the RVFW results in a crucial impairment of the left ventricular function in contrast to LVA- pacing which results in better left ventricular performance. Such insights into alternate pacing sites may further help to answer the question which pacing site is the best one for pacemaker therapy in humans.

Figure 1 

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 201, Supplement 682 :P015

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