Ahmed Fozia Z, Khattar Rajdeep S, Zaidi Amir M, Neyses Ludwig, Oceandy Delvac, Mamas Mamas
Manchester Heart Centre, Manchester Royal Infirmary, Oxford Road, Manchester, M13 9WL, UK,
Heart Fail Rev. 2014 Sep;19(5):669-80. doi: 10.1007/s10741-013-9390-y.
Pacing-induced ventricular dysfunction and pacing-induced cardiomyopathy (PiCMP) are recognized complications of chronic right ventricular pacing. Alterations in myocardial perfusion and sympathetic innervation contribute to the development of pacing-induced heart disease. However, it is unlikely that these are the only processes involved. Matrix metalloproteinases (MMPs) are proteolytic enzymes that degrade the collagenous extracellular matrix and play a central role in left ventricular remodelling during the development of heart failure. While the pathophysiological mechanisms and altered MMP expression that occur in chronic pressure overload, ischaemic and non-ischaemic dilated cardiomyopathy have been defined, those that occur in the clinical setting of pacing-induced ventricular dysfunction and PiCMP have not been reported. Here we review the clinical epidemiology of pacing-induced ventricular dysfunction and discuss how data derived from animal models provide insight into how changes in MMP expression and function contribute to the development of PiCMP. The review concludes by exploring pacing strategies that may be used to prevent pacing-induced ventricular dysfunction.
起搏诱导的心室功能障碍和起搏诱导的心肌病（PiCMP）是慢性右心室起搏公认的并发症。心肌灌注和交感神经支配的改变促成了起搏诱导性心脏病的发展。然而，这些不太可能是唯一涉及的过程。基质金属蛋白酶（MMPs）是降解胶原细胞外基质的蛋白水解酶，在心力衰竭发展过程中的左心室重构中起核心作用。虽然慢性压力超负荷、缺血性和非缺血性扩张型心肌病中发生的病理生理机制及MMP表达改变已明确，但在起搏诱导的心室功能障碍和PiCMP临床背景下发生的情况尚未见报道。在此，我们综述起搏诱导的心室功能障碍的临床流行病学，并讨论来自动物模型的数据如何为MMP表达和功能变化如何促成PiCMP的发展提供见解。本文通过探索可用于预防起搏诱导的心室功能障碍的起搏策略来结束综述。
