No-reflow phenomenon pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Jennifer Giuseffi, M.D.; David M. Leder, M.D.; Ayokunle Olubaniyi, M.B,B.S [2]
Overview
Pathophysiology
Distal Embolization of Plaques and/or Thrombus
The primary mechanism of no-reflow is likely due to distal embolization of atheromatous and thrombotic debris dislodged by balloon inflation or stent implantation.[1][2] During PCI, microthrombi and small particles of plaques are thought to be showered downstream, occluding small arteries, arterioles, and collateral microvasculature. Analysis of the aspirate obtained from patients without no-reflow revealed a greater amount of atheromatous plaques and significantly more platelet and fibrin complex, macrophages, and cholesterolcrystals than those who experienced no-reflow. The 30-day mortality was significantly higher (27.5%) in patients with no-reflow phenomenon than in patients with normal coronary blood flow after PCI (5.3%, P < 0.001). Predictors of no-reflow include a higher plaque burden, thrombus, lipid pools by IVUS, higher lesion elastic membrane cross-sectional area, pre-infarction angina, and TIMI flow grade 0 on the initial coronary angiogram, among other factors.
Other pathophysiologic mechanisms include:
- Release of active tissue factor from the dislodged plaque[3]
- Vasoconstriction secondary to serotonin, adenosine diphosphate, thromboxane A2, released by the embolized platelet-rich atheromatous material[4]
- Reperfusion injury from the release of oxygen free radicals during inflammation
- Myocardial necrosis and stunning
- Microvascular damage[5]
- Microvascular plugging with platelets or leukocytes
- Endothelial swelling and tissue edema compressing vasculature
References
- ↑ Henriques, JP.; Zijlstra, F.; Ottervanger, JP.; de Boer, MJ.; van 't Hof, AW.; Hoorntje, JC.; Suryapranata, H. (2002). "Incidence and clinical significance of distal embolization during primary angioplasty for acute myocardial infarction". Eur Heart J. 23 (14): 1112–7. doi:10.1053/euhj.2001.3035. PMID 12090749. Unknown parameter
|month=ignored (help) - ↑ Kawaguchi, R.; Oshima, S.; Jingu, M.; Tsurugaya, H.; Toyama, T.; Hoshizaki, H.; Taniguchi, K. (2007). "Usefulness of virtual histology intravascular ultrasound to predict distal embolization for ST-segment elevation myocardial infarction". J Am Coll Cardiol. 50 (17): 1641–6. doi:10.1016/j.jacc.2007.06.051. PMID 17950144. Unknown parameter
|month=ignored (help) - ↑ Bonderman, D.; Teml, A.; Jakowitsch, J.; Adlbrecht, C.; Gyöngyösi, M.; Sperker, W.; Lass, H.; Mosgoeller, W.; Glogar, DH. (2002). "Coronary no-reflow is caused by shedding of active tissue factor from dissected atherosclerotic plaque". Blood. 99 (8): 2794–800. PMID 11929768. Unknown parameter
|month=ignored (help) - ↑ Gregorini, L.; Marco, J.; Kozàkovà, M.; Palombo, C.; Anguissola, GB.; Marco, I.; Bernies, M.; Cassagneau, B.; Distante, A. (1999). "Alpha-adrenergic blockade improves recovery of myocardial perfusion and function after coronary stenting in patients with acute myocardial infarction". Circulation. 99 (4): 482–90. PMID 9927393. Unknown parameter
|month=ignored (help) - ↑ Kloner, RA.; Rude, RE.; Carlson, N.; Maroko, PR.; DeBoer, LW.; Braunwald, E. (1980). "Ultrastructural evidence of microvascular damage and myocardial cell injury after coronary artery occlusion: which comes first?". Circulation. 62 (5): 945–52. PMID 7418179. Unknown parameter
|month=ignored (help)