Cardiovascular Medicine Division, Cardio Thoracic and Vascular Department, University of Pisa, Via Paradisa 2, 56124 Pisa, Italy.
Curr Pharm Des. 2013;19(13):2366-74. doi: 10.2174/1381612811319130004.
For decades coronary macrovascular atherosclerosis has been considered the principal manifestation of coronary heart disease, with most of our effort dedicated to identifying and removal of coronary stenosis. However, growing body of literature indicates that coronary microcirculation also contributes substantially to the pathophysiology of cardiovascular disease. An understanding of mechanisms regulating microvascular function is of critical importance in understanding its role in disease, especially because these regulatory mechanisms vary substantially across species, vascular bed and due to comorbidities. Indeed, the most obvious consequence of coronary stenosis is that it may limit blood supply to the dependent myocardium to the point of causing ischaemia during exercise or even at rest. However, this flow limiting effect is not only due to the passive hydraulic effect of a narrowed conduit, but also to active responses in the coronary microcirculation triggered by the presence of an epicardial stenosis. To understand this problem it is important to review the inter-related mechanisms that regulate flow to the left ventricular wall and modulate transmural distribution of flow. These regulatory mechanisms operate hierarchically and are heterogeneously distributed along the coronary vascular tree. It is also important to discuss the effect of myocardial performance in modulating both blood flow demands and coronary resistance. Some of the interactions between coronary stenosis and microcirculation are transient, like those documented in acute coronary syndromes or during percutaneous interventions. However, microcirculatory remodeling may be triggered by a chronic coronary stenosis, leading to a sustained impairment of blood supply even after successful removal of the epicardial stenosis. A deeper understanding of these phenomena may explain paradoxical findings in patients undergoing coronary revascularization, particularly when functional tests are used in their assessment. These aspects are discussed in detail in this review.
几十年来，冠状动脉大血管粥样硬化一直被认为是冠心病的主要表现，我们的大部分努力都致力于识别和消除冠状动脉狭窄。然而，越来越多的文献表明，冠状动脉微循环也对心血管疾病的病理生理学有重要贡献。了解调节微血管功能的机制对于理解其在疾病中的作用至关重要，特别是因为这些调节机制在不同物种、血管床和由于合并症而有很大差异。事实上，冠状动脉狭窄最明显的后果是，它可能会限制依赖心肌的血液供应，导致在运动甚至休息时发生缺血。然而，这种限制血流的效应不仅是由于狭窄管腔的被动水力效应，还与存在心外膜狭窄时冠状动脉微循环中的主动反应有关。为了理解这个问题，重要的是要回顾调节流向左心室壁的相互关联的机制，并调节血流的跨壁分布。这些调节机制是分层运作的，并且在冠状动脉树中呈异质性分布。讨论心肌功能在调节血流需求和冠状动脉阻力方面的作用也很重要。一些冠状动脉狭窄和微循环之间的相互作用是短暂的，例如在急性冠状动脉综合征或经皮介入治疗期间记录到的那些。然而，慢性冠状动脉狭窄可能会引发微循环重构，导致即使成功消除心外膜狭窄后，血液供应仍持续受损。对这些现象的更深入了解可能会解释接受冠状动脉血运重建的患者中出现的矛盾发现，特别是在使用功能测试评估时。这方面在本综述中进行了详细讨论。
