Department of Cardiology, Beijing AnZhen Hospital, Capital Medical University, Chaoyang District, Beijing 100029, China.
Med Hypotheses. 2010 Sep;75(3):334-7. doi: 10.1016/j.mehy.2010.03.016. Epub 2010 Apr 10.
Coronary slow flow phenomenon (CSFP) is an important, angiographic entity characterized by delayed progression of the contrast medium injected into the coronary tree. Since definition of this phenomenon in 1972, there has not been any clear-cut etiology. Original data often focused on histological or pathological changes in coronary artery itself. It was confirmed that small vessel structural defect as well as an underlying residual microvascular resistance abnormality coexists in the coronary microcirculation. Early atherosclerosis was also detected in epicardial coronary arteries by intravascular ultrasound (IVUS). Taken together, it can be suggested that a combination of morphological and functional abnormalities in small vessels and epicardial coronary arteries contributes to the pathogenesis of CSFP. CSFP may be defined as a local disease confined to coronary arteries. However, another feature of CSFP is its frequent occurrence in association with more widespread vascular abnormalities. Reduced endothelial function is implicated in CSFP as measured by flow-mediated dilatation (FMD) of the brachial artery, suggesting that endothelial dysfunction appears to be a generalized process affecting both coronary and peripheral vasculature. In addition, several studies have now demonstrated that carotid intima-media thickness (IMT) is significantly increased in patients with CSFP and there was a significant correlation between coronary intima-media thickness and carotid IMT. Therefore, we hypothesize that CSFP is not an isolated finding but may be part of a systemic vascular disturbance. CSFP is not an infrequently detected finding typically observed in patients presenting with an acute coronary syndrome, usually unstable angina. The subsequent clinical course is characterized by high frequency of relapsing chest pain resulting in considerable impairment in quality of life. Accordingly, further experimental investigations and clinical studies are warranted to shed light into the pathogenesis as well as therapeutics of CSFP.
冠状动脉慢血流现象（CSFP）是一种重要的血管造影实体，其特征为注入冠状动脉树的造影剂进展缓慢。自 1972 年定义该现象以来，其病因尚无明确结论。原始数据通常侧重于冠状动脉本身的组织学或病理学变化。现已证实，冠状动脉微循环中存在小血管结构缺陷以及潜在的残余微血管阻力异常。血管内超声（IVUS）也证实了心外膜冠状动脉的早期动脉粥样硬化。总之，这表明小血管和心外膜冠状动脉的形态和功能异常的结合有助于 CSFP 的发病机制。CSFP 可定义为局限于冠状动脉的局部疾病。然而，CSFP 的另一个特征是其常与更广泛的血管异常同时发生。血流介导的扩张（FMD）测量的肱动脉内皮功能受损与 CSFP 有关，这表明内皮功能障碍似乎是一种影响冠状动脉和外周血管的全身性过程。此外，几项研究现已表明，CSFP 患者的颈动脉内膜中层厚度（IMT）显著增加，且冠状动脉内膜中层厚度与颈动脉 IMT 之间存在显著相关性。因此，我们假设 CSFP 不是孤立的发现，而是全身性血管紊乱的一部分。CSFP 是一种常见的发现，通常见于急性冠状动脉综合征患者，尤其是不稳定型心绞痛患者。随后的临床过程表现为胸痛反复发作的高频率，导致生活质量明显受损。因此，需要进一步的实验研究和临床研究来阐明 CSFP 的发病机制和治疗方法。
