Loukas Marios, Bhatnagar Amit, Arumugam Shreya, Smith Kyle, Matusz Petru, Gielecki Jerzy, Tubbs R Shane
Department of Anatomical Sciences, St. George's University, Grenada, West Indies; Department of Anatomy, Varmia and Mazuria University School of Medicine, Olsztyn, Poland.
Department of Anatomical Sciences, St. George's University, Grenada, West Indies; Department of Internal Medicine, Carney Hospital, Boston, MA.
Cardiovasc Pathol. 2014 Jul-Aug;23(4):198-203. doi: 10.1016/j.carpath.2014.03.002. Epub 2014 Mar 19.
Myocardial bridging is a common anatomic variation of the human heart in which an epicardial coronary artery takes an intramural course within the myocardium. Studies have proposed that myocardial bridges offer a "protective effect" from atherosclerosis within the involved coronary artery.
We examined 250 formalin-fixed human hearts with gross dissection and histologic and immunohistochemical techniques. The bridged arteries were divided into premyocardial, myocardial, and postmyocardial segments. Atherogenic activity was assessed by comparing proliferative activity (Ki-67), smooth muscle α-actin, and macrophages. In addition, atherosclerotic lesions were carefully categorized according to the Stary classification.
The presence of myocardial bridges was confirmed in 92 hearts (36.8%). The most common location of a myocardial bridge was over the anterior interventricular artery in 38 (41.3%) hearts. Overall, the bridged segments demonstrated weaker Ki-67 activity, a decreased number of smooth muscle cells and macrophages, and lower modal Stary classifications for atherosclerosis severity as compared to pre- and postbridge segments of the same coronary artery.
Atherosclerotic lesions in vessel sections deep to the myocardial bridges were found to be less developed in contrast to the pre- and postbridge segments of the same coronary arteries. Although the precise mechanism of atherogenic protection is unknown, it has been proposed that compression by the contracting myocardium stimulates the release of anticoagulant and growth factors, which could have a synergistic effect in protecting the endothelium from denudation, inflammation, and resultant atherosclerosis.
心肌桥是人类心脏常见的一种解剖变异,表现为心外膜冠状动脉走行于心肌内。研究表明,心肌桥对其所累及的冠状动脉具有“保护作用”,可防止动脉粥样硬化。
我们采用大体解剖、组织学及免疫组化技术对250例福尔马林固定的人体心脏进行了检查。将有桥血管分为心肌前、心肌内和心肌后段。通过比较增殖活性(Ki-67)、平滑肌α-肌动蛋白和巨噬细胞来评估致动脉粥样硬化活性。此外,根据Stary分类法对动脉粥样硬化病变进行仔细分类。
92例心脏(36.8%)证实存在心肌桥。心肌桥最常见的位置是前室间动脉,共38例(41.3%)。总体而言,与同一冠状动脉的心肌桥前段和后段相比,心肌桥段的Ki-67活性较弱,平滑肌细胞和巨噬细胞数量减少,动脉粥样硬化严重程度的Stary分级较低。
与同一冠状动脉的心肌桥前段和后段相比,心肌桥深部血管段的动脉粥样硬化病变发展程度较低。虽然致动脉粥样硬化保护的确切机制尚不清楚,但有人提出,收缩的心肌产生的压迫会刺激抗凝因子和生长因子的释放,这可能对保护内皮免受剥脱、炎症及由此导致的动脉粥样硬化具有协同作用。