Medical Clinic and Policlinic, University Medical Center Mainz, Mainz, Germany.
Clin Hemorheol Microcirc. 2011;49(1-4):261-9. doi: 10.3233/CH-2011-1476.
The slow coronary flow phenomenon (SCF), a condition described by the presence of inappropriate delay in the progression of intracoronary contrast during angiography in the absence of stenoses, has been shown in some patients presenting with chest pain. While several conditions leading to "secondary" slow flow are known, there are no definitive conclusions regarding the exact pathogenesis of "primary" SCF. The present paper outlines the mechanisms that may lead to SCF, emphasizing the role of hemorheological and vascular factors in the pathogenesis of this phenomenon. Small vessel dysfunction has been proposed in the pathogenesis of SCF since the first description of this syndrome in 1972. Abnormalities in coronary microvascular function result from increased microvascular resistances and impaired endothelial release of vasoactive substances, especially in production and bioavailability of endothelium derived NO. Inflammatory conditions (increased levels of C-reactive protein, interleukin-6 and adhesion molecules) and metabolic abnormalities such as impaired glycemic control, hyperuricemia and elevated serum gamma-glutamyltransferase were also found to contribute to microvascular dysfunction in patients with SCF. New studies have also indicated that increased blood viscosity and one of its major determinants, erythrocyte aggregation, is associated with the SCF. Rheological variables play a role in the control of shear stress and contribute to blood flow velocity changes. Although platelets do not have a significant influence on blood viscosity, it has been demonstrated that they are involved in the development of SCF. Increased mean platelet volume (MPV), an indicator of platelet activation and platelet aggregability is also significantly higher in patients with SCF compared with patients with normal coronary flow.
慢血流现象（SCF）是指在造影时存在不适当的延迟，而无明显狭窄的冠状动脉内对比剂的进展，这种现象在一些胸痛患者中有所体现。虽然导致“继发性”慢血流的情况有很多，但对于“原发性”SCF 的确切发病机制尚无明确结论。本文概述了可能导致 SCF 的机制，强调了血液流变学和血管因素在该现象发病机制中的作用。自 1972 年首次描述该综合征以来，小血管功能障碍一直被认为是 SCF 的发病机制之一。冠状动脉微血管功能异常是由于微血管阻力增加和内皮释放血管活性物质受损引起的，特别是内皮衍生的一氧化氮（NO）的产生和生物利用度受损。炎症状态（C 反应蛋白、白细胞介素-6 和黏附分子水平升高）和代谢异常（如血糖控制不佳、高尿酸血症和血清γ-谷氨酰转移酶升高）也被发现可导致 SCF 患者的微血管功能障碍。新的研究还表明，血液黏度增加及其主要决定因素之一——红细胞聚集与 SCF 有关。流变学变量在控制切应力方面发挥作用，并有助于血流速度的变化。尽管血小板对血液黏度没有显著影响，但已证明它们参与了 SCF 的发生。与正常冠状动脉血流患者相比，SCF 患者的平均血小板体积（MPV）升高，这是血小板活化和血小板聚集性的指标，也明显更高。
