No-reflow phenomenon pathophysiology: Difference between revisions
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Created page with "__NOTOC__ {{No-reflow phenomenon}} {{SI}} {{CMG}}; Jennifer Giuseffi, M.D.; David M. Leder, M.D.; {{AO}} ==Overview== ==Pathophysiology== ====Distal Embolization of Plaques..." |
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====Distal Embolization of Plaques and/or Thrombus==== | ====Distal Embolization of Plaques and/or Thrombus==== | ||
The primary mechanism of no-reflow is likely due to distal embolization of [[Atheromatous plaque|atheromatous]] and thrombotic debris dislodged by balloon inflation or [[stent]] implantation.<ref name="Henriques-2002">{{Cite journal | last1 = Henriques | first1 = JP. |last2 = Zijlstra | first2 = F. | last3 = Ottervanger | first3 = JP. | last4 = de Boer | first4 = MJ. | last5 = van 't Hof | first5 = AW. |last6 = Hoorntje | first6 = JC. | last7 = Suryapranata |first7 = H. | title = Incidence and clinical significance of distal embolization during primary angioplasty for acute myocardial infarction. | journal = Eur Heart J | volume = 23 | issue = 14 | pages = 1112-7 | month = Jul| year = 2002 | doi = 10.1053/euhj.2001.3035 | PMID = 12090749 }}</ref><ref name="Kawaguchi-2007">{{Cite journal | last1 = Kawaguchi |first1 = R. | last2 = Oshima | first2 = S. | last3 = Jingu | first3 = M. | last4 = Tsurugaya | first4 = H. | last5 = Toyama | first5 = T. |last6 = Hoshizaki | first6 = H. | last7 = Taniguchi | first7 = K. | title = Usefulness of virtual histology intravascular ultrasound to predict distal embolization for ST-segment elevation myocardial infarction. | journal = J Am Coll Cardiol | volume = 50 | issue = 17 | pages = 1641-6 | month = Oct | year = 2007 | doi = 10.1016/j.jacc.2007.06.051 | PMID = 17950144 }}</ref> 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 plaque]]s and significantly more [[platelet]] and [[fibrin]] complex, [[macrophage]]s, and [[cholesterol]]crystals 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). | The primary mechanism of no-reflow is likely due to distal embolization of [[Atheromatous plaque|atheromatous]] and thrombotic debris dislodged by balloon inflation or [[stent]] implantation.<ref name="Henriques-2002">{{Cite journal | last1 = Henriques | first1 = JP. |last2 = Zijlstra | first2 = F. | last3 = Ottervanger | first3 = JP. | last4 = de Boer | first4 = MJ. | last5 = van 't Hof | first5 = AW. |last6 = Hoorntje | first6 = JC. | last7 = Suryapranata |first7 = H. | title = Incidence and clinical significance of distal embolization during primary angioplasty for acute myocardial infarction. | journal = Eur Heart J | volume = 23 | issue = 14 | pages = 1112-7 | month = Jul| year = 2002 | doi = 10.1053/euhj.2001.3035 | PMID = 12090749 }}</ref><ref name="Kawaguchi-2007">{{Cite journal | last1 = Kawaguchi |first1 = R. | last2 = Oshima | first2 = S. | last3 = Jingu | first3 = M. | last4 = Tsurugaya | first4 = H. | last5 = Toyama | first5 = T. |last6 = Hoshizaki | first6 = H. | last7 = Taniguchi | first7 = K. | title = Usefulness of virtual histology intravascular ultrasound to predict distal embolization for ST-segment elevation myocardial infarction. | journal = J Am Coll Cardiol | volume = 50 | issue = 17 | pages = 1641-6 | month = Oct | year = 2007 | doi = 10.1016/j.jacc.2007.06.051 | PMID = 17950144 }}</ref> 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 plaque]]s and significantly more [[platelet]] and [[fibrin]] complex, [[macrophage]]s, and [[cholesterol]]crystals 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,[[Angina|pre-infarction angina]], and [[TIMI flow grade]] 0 on the initial [[coronary angiogram]], among other factors. | Predictors of no-reflow include a higher [[plaque]] burden, [[thrombus]], [[lipid]] pools by [[IVUS]], higher lesion elastic membrane cross-sectional area, [[Angina|pre-infarction angina]], and [[TIMI flow grade]] 0 on the initial [[coronary angiogram]], among other factors. | ||
Other pathophysiologic mechanisms include: | Other pathophysiologic mechanisms include: | ||
Latest revision as of 17:56, 15 September 2013
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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)