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长期右心室心尖部起搏患者心尖部壁运动异常的发生率。

The prevalence of apical wall motion abnormalities in patients with long-term right ventricular apical pacing.

机构信息

Department of Cardiovascular Medicine, Akita University Graduate School of Medicine, Akita, Japan.

出版信息

J Am Soc Echocardiogr. 2011 May;24(5):556-564.e1. doi: 10.1016/j.echo.2010.12.025. Epub 2011 Feb 24.

DOI:10.1016/j.echo.2010.12.025
PMID:21353472
Abstract

BACKGROUND

Long-term right ventricular apical pacing (RVAP) can lead to adverse clinical outcomes. Although left ventricular (LV) dyssynchrony is the major causative factor, other potential mechanisms are not fully understood. We sought to clarify whether RVAP elicits apical wall motion abnormalities that contribute to LV contractile dysfunction.

METHODS

We studied annual echocardiographic data over a 5-year period after pacemaker implantation (PMI) for 74 patients who underwent RVAP. The patients were divided into two groups according to the percentage of ventricular pacing: right ventricular (RV) pacing < 50% and RV pacing ≥ 50%. We assessed LV ejection fraction, LV end-diastolic volume, and left atrial dimension. To assess regional wall motion abnormalities, the wall motion score index was calculated.

RESULTS

LV wall motion abnormality was observed in 64% of the subjects and was more pronounced in apical segments than in other segments. At 2 years after PMI, brain natriuretic peptide levels were significantly higher in the group with RV pacing ≥ 50% than in the group with RV pacing < 50%. The subjects with RV pacing ≥ 50% had higher LV end-diastolic dimension and lower ejection fraction at 3 years after PMI.

CONCLUSION

Long-term RVAP elicits apical wall motion abnormalities that could in part contribute to LV contractile dysfunction.

摘要

背景

长期右心室心尖部起搏(RVAP)可导致不良的临床结局。虽然左心室(LV)不同步是主要的致病因素,但其他潜在的机制尚不完全清楚。我们试图阐明 RVAP 是否引起心尖壁运动异常,从而导致 LV 收缩功能障碍。

方法

我们研究了 74 例因 RVAP 行起搏器植入(PMI)后 5 年的年度超声心动图数据。根据心室起搏的百分比将患者分为两组:右心室(RV)起搏<50%和 RV 起搏≥50%。我们评估了 LV 射血分数、LV 舒张末期容积和左心房内径。为了评估节段性壁运动异常,计算了壁运动评分指数。

结果

64%的患者存在 LV 壁运动异常,心尖段比其他节段更明显。在 PMI 后 2 年,RV 起搏≥50%组的脑利钠肽水平明显高于 RV 起搏<50%组。在 PMI 后 3 年,RV 起搏≥50%组的 LV 舒张末期内径较高,射血分数较低。

结论

长期 RVAP 引起心尖壁运动异常,这可能部分导致 LV 收缩功能障碍。

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