Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
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

PubMed Disclaimer

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

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

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