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Review
. 2002 Feb;87(2):162-8.
doi: 10.1136/heart.87.2.162.

The "no-reflow" phenomenon: basic science and clinical correlates

Thorsten Reffelmann  1 , Robert A Kloner
Affiliations
Review

The "no-reflow" phenomenon: basic science and clinical correlates

Thorsten Reffelmann et al. Heart. 2002 Feb.
No abstract available

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Figures

Figure 1
Figure 1
Anatomical no-reflow, visualised in a rabbit model of coronary occlusion and reperfusion. Monastral blue (A) and thioflavin S (B, photography under ultraviolet light, Minolta Y48 barrier filter) were injected into the left atrium after 120 minutes of coronary artery occlusion and 120 minutes of reperfusion. Both dyes leave a substantial part of the left ventricle unstained, indicating areas of no or low perfusion. A close look at the slices demonstrates that (although closely correlating) the area not stained by monastral blue is slightly larger than the non-fluorescent area, reflecting the ability of the two dyes to penetrate into areas of hypoperfusion.
Figure 2
Figure 2
Schematic figure, summarising different mechanisms, involved in the development of no-reflow, and accompanying ultrastructural alterations of the microvascular bed (RBC, red blood cell).
See this image and copyright information in PMC

References

    1. Kloner RA, Ganote CE, Jennings RB. The “no-reflow” phenomenon after temporary coronary occlusion in dogs. J Clin Invest 1974;54:1496–508. ▸ This is the first article describing anatomical no-reflow after experimental myocardial infarction in the canine model, using thioflavin S as a marker of anatomical no-reflow. The corresponding ultrastructural changes of the microvasculature are evaluated by electron microscopy. - PubMed
    1. Kloner RA, Rude RE, Carlson N, et al. Ultrastructural evidence of microvascular damage and myocardial cell injury after coronary artery occlusion: which comes first? Circulation 1980;62:945–52. ▸ The spatial and temporal distribution of ultrastructural alterations of the microvascular bed is evaluated in comparison to myocyte fine structure. Microvascular changes lagged behind myocyte changes of irreversible ischaemic damage. - PubMed
    1. Ambrosio G, Weisman HF, Mannisi JA, et al. Progressive impairment of regional myocardial perfusion after initial restoration of postischemic blood flow. Circulation 1989;80:1846–61. ▸ This landmark article provides evidence of reperfusion injury at the microvascular level, demonstrating a substantial increase of anatomical no-reflow with ongoing reperfusion and a progressive decrease of tissue perfusion. - PubMed
    1. Piana RN, Paik GY, Moscucci M, et al. Incidence and treatment of `no-reflow' after percutaneous coronary intervention. Circulation 1994;89:2514–18. ▸ In a retrospective analysis, the incidence of angiographical no-reflow in elective PTCA procedures as well as in primary PTCA for acute myocardial infarction is evaluated. - PubMed
    1. Morishima I, Sone T, Okumura K, et al. Angiographic no-reflow phenomenon as a predictor of adverse long-term outcome in patients treated with percutaneous transluminal coronary angioplasty for first acute myocardial infarction. J Am Coll Cardiol 2000;36:1202–9. - PubMed