Department of Anatomical Sciences, School of Medicine, St. George's University, Grenada, West Indies.
Clin Anat. 2011 Sep;24(6):675-83. doi: 10.1002/ca.21150. Epub 2011 Jul 12.
Much has been written regarding the potential clinical significance of myocardial bridges. As such bridging is often seen in normal individuals, it is clear that not all arteries bridged by myocardial segments produce clinical symptoms thereby suggesting that this feature may simply be an anatomical variant. However, some authors who have considered these bridges as the cause of cardiac ischemia have suggested two potential mechanisms for their pathophysiology. The first is a phasic systolic compression of the bridged segment with persistent mid-to-late diastolic reduction in arterial diameter and the second proposes a reduction in arterial flow. Both mechanisms may contribute to a reduced reserve in coronary blood flow. In this review, we discuss the evidence that exists regarding myocardial bridging and the potential for bridging to cause myocardial ischemia.
关于心肌桥的潜在临床意义已经有很多文献报道。由于心肌桥在正常个体中经常可见,因此很明显,并非所有由心肌段桥接的动脉都会产生临床症状,这表明这种特征可能仅仅是一种解剖变异。然而,一些将这些桥接视为心脏缺血原因的作者提出了两种潜在的病理生理学机制。第一种机制是桥接段的收缩期阶段性压缩,持续存在中晚期动脉直径减小,第二种机制则提出了动脉血流量减少。这两种机制都可能导致冠状动脉血流储备减少。在这篇综述中,我们讨论了关于心肌桥的证据以及心肌桥引起心肌缺血的可能性。