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| __NOTOC__
| | #Redirect[[No-reflow phenomenon]] |
| {{SI}}
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| {{CMG}}; Jennifer Giuseffi, M.D.; David M. Leder, M.D.; {{AO}}
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| {{SK}} Slow-flow, slow re-flow, low-flow
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| ==Overview==
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| Many definitions have been given to this phenomenon based on individual's area of specialty, but the definition that unites all fields was by Kloner et al in 1974 who described the condition as the inability to adequately perfuse myocardium after temporary occlusion
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| of an epicardial coronary artery without evidence of persistent mechanical obstruction, thus implying ongoing myocardial ischaemia. When defined angiographically, it is an acute reduction in coronary flow (TIMI grade 0-1) in the absence of dissection, [[thrombus]], spasm, or high-grade residual stenosis at the original target lesion. In other words, it is the failure of blood to reperfuse an ischemic area after the physical obstruction has been removed or bypassed.<ref name="urlMedscape & eMedicine Log In">{{cite web |url=http://www.medscape.com/viewarticle/543911_3 |title=Medscape |format= |work=|accessdate=}}</ref><ref name="pmid17592194">{{cite journal |author=Kishi T, Yamada A, Okamatsu S, Sunagawa K |title=Percutaneous coronary arterial thrombectomy for acute myocardial infarction reduces no-reflow phenomenon and protects against left ventricular remodeling related to the proximal left anterior descending and right coronary artery |journal=Int Heart J |volume=48 |issue=3 |pages=287–302 |year=2007|month=May |pmid=17592194 |doi= 10.1536/ihj.48.287|url=http://joi.jlc.jst.go.jp/JST.JSTAGE/ihj/48.287?from=PubMed |format={{dead link|date=April 2009}} – <sup>[http://scholar.google.co.uk/scholar?hl=en&lr=&q=intitle%3APercutaneous+coronary+arterial+thrombectomy+for+acute+myocardial+infarction+reduces+no-reflow+phenomenon+and+protects+against+left+ventricular+remodeling+related+to+the+proximal+left+anterior+descending+and+right+coronary+artery&as_publication=Int+Heart+J&as_ylo=2007&as_yhi=2007&btnG=SearchScholar search]</sup>}}</ref> A lesser degree of obstruction to coronary blood flow (TIMI grade 2) is sometimes referred to as slow-flow. No-reflow is an important predictor of [[mortality]] after PCI <ref name="pmid12514653">{{cite journal| author=Resnic FS, Wainstein M, Lee MK, Behrendt D, Wainstein RV, Ohno-Machado L et al.| title=No-reflow is an independent predictor of death and myocardial infarction after percutaneous coronary intervention. | journal=Am Heart J | year= 2003 | volume= 145|issue= 1 | pages= 42-6 | pmid=12514653 | doi=10.1067/mhj.2003.36 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12514653 }} </ref>.
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| ==Historical Perspective==
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| This phenomenon was first described by Krug et al <ref name="Krug-1966">{{Cite journal | last1 = Krug | first1 = A. | last2 = Du Mesnil de Rochemont | first2 = G. | last3 = Korb | first3 = . | title = Blood supply of the myocardium after temporary coronary occlusion. | journal = Circ Res | volume = 19 | issue = 1 | pages = 57-62 | month = Jul | year = 1966 | doi = | PMID = 5912914 }}</ref> during induced myocardial infarction in dog subjects in 1966, but the term 'no-reflow' was first used by Majno and colleagues in 1967 when they observed that brains of rabbits exposed to prolonged ischemia suffered significant changes in the microvasculature which impeded blood flow to the brain cells.
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| ==Pathophysiology==
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| ====Distal Embolization of Plaques and/or Thrombus====
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| 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).
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| 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.
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| Other pathophysiologic mechanisms include:
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| * Release of active tissue factor from the dislodged plaque<ref name="Bonderman-2002">{{Cite journal | last1 = Bonderman | first1 = D. | last2 = Teml | first2 = A. | last3 = Jakowitsch | first3 = J. | last4 = Adlbrecht | first4 = C. | last5 = Gyöngyösi | first5 = M. | last6 = Sperker | first6 = W. | last7 = Lass | first7 = H. | last8 = Mosgoeller | first8 = W. | last9 = Glogar | first9 = DH. | title = Coronary no-reflow is caused by shedding of active tissue factor from dissected atherosclerotic plaque. | journal = Blood | volume = 99 | issue = 8 | pages = 2794-800 | month = Apr | year = 2002 | doi = | PMID = 11929768 }}</ref>
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| * Vasoconstriction secondary to [[serotonin]], [[adenosine diphosphate]], [[thromboxane A2]], released by the embolized [[platelet]]-rich [[atheromatous]] material<ref name="Gregorini-1999">{{Cite journal | last1 = Gregorini | first1 = L. | last2 = Marco | first2 = J. | last3 = Kozàkovà | first3 = M. | last4 = Palombo | first4 = C. | last5 = Anguissola | first5 = GB. | last6 = Marco | first6 = I. | last7 = Bernies | first7 = M. | last8 = Cassagneau | first8 = B. | last9 = Distante | first9 = A. | title = Alpha-adrenergic blockade improves recovery of myocardial perfusion and function after coronary stenting in patients with acute myocardial infarction. | journal = Circulation | volume = 99 | issue = 4 | pages = 482-90 | month = Feb | year = 1999 | doi = | PMID = 9927393 }}</ref>
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| * Reperfusion injury from the release of oxygen free radicals during inflammation
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| * Myocardial necrosis and stunning
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| * Microvascular damage<ref name="Kloner-1980">{{Cite journal | last1 = Kloner | first1 = RA. | last2 = Rude | first2 = RE. | last3 = Carlson | first3 = N. | last4 = Maroko | first4 = PR. | last5 = DeBoer | first5 = LW. | last6 = Braunwald | first6 = E. | title = Ultrastructural evidence of microvascular damage and myocardial cell injury after coronary artery occlusion: which comes first? | journal = Circulation | volume = 62 | issue = 5 | pages = 945-52 | month = Nov | year = 1980 | doi = | PMID = 7418179 }}</ref>
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| * Microvascular plugging with [[platelets]] or [[leukocytes]]
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| * Endothelial swelling and tissue edema compressing vasculature
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| ==Epidemiology and Demographics==
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| The reported incidence of no-flow ranges between 0.6-42% depending on the defining criteria and the clinical setting. It has been reported in anywhere from 11-30% of patients following [[thrombolysis]] or intervention in [[acute myocardial infarction]]. However, in routine, elective coronary intervention, the prevalence has been reported to be as low as 0.6-2%. This phenomenon appears to be more frequent during interventions on [[SVG|saphenous vein grafts (SVG)]] or thrombus containing lesions as well as during the use of rotational [[atherectomy]].
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| Gender does not appear to play a role in this phenomenon, but it seems to occur more frequently in older patients and in those who did not experience pre-infarct [[angina]]. Admission [[hyperglycemia]] has also been associated with higher incidence of [[no reflow]] as well as worse outcomes. Lesions at high-risk for [[no reflow]] include: diffuse atherosclerotic involvement, angiographic demonstrable [[thrombus]], irregular or ulcerative lesions, and long lesions with large plaque volume.
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| No reflow is a common (15%) finding during primary[[angioplasty]] for [[acute MI]].
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| ==Natural History, Complications and Prognosis==
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| In the cathetarization laboratory, no-reflow may be clinically silent or appear suddenly associated with severe chest pain, ischemic ([[EKG]]) changes, conduction abnormalities, and/or hemodynamic deterioration. This needs to be distinguished from slow-flow which can be caused by coronary dissection, macrothrombus formation, coronary vasospasm, or distal macroembolization.
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| The presence of no-reflow is clinically important as its presence has been associated with a five to ten fold increase in mortality,<ref name="Resnic-2003">{{Cite journal | last1 = Resnic | first1 = FS. | last2 = Wainstein | first2 = M. | last3 = Lee | first3 = MK. | last4 = Behrendt | first4 = D. | last5 = Wainstein | first5 = RV. | last6 = Ohno-Machado | first6 = L. | last7 = Kirshenbaum | first7 = JM. | last8 = Rogers | first8 = CD. | last9 = Popma | first9 = JJ. | title = No-reflow is an independent predictor of death and myocardial infarction after percutaneous coronary intervention. | journal = Am Heart J | volume = 145 | issue = 1 | pages = 42-6 | month = Jan | year = 2003 | doi = 10.1067/mhj.2003.36 | PMID = 12514653 }}</ref> as well as a high incidence of myocardial infarction (MI), left ventricular dysfunction, ventricular arrhythmias, early congestive heart failure and cardiogenic shock. Predictors of outcome include:
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| * Duration of coronary occlusion
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| * Extent of myocardium supplied by the occluded artery
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| * Patency of infarct-related artery
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| * Quality of collateral circulation
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| * Presence of pre-infarction angina which produces a preconditioning-like effect and might correlate with preservation of collateral circulation.
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| Hyperglycemia in acute myocardial infarction is associated with an increased risk of in-hospital mortality, as well as no-reflow phenomenon.
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| ==Diagnosis==
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| ====Coronary Angiography====
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| The method that provides the most definite diagnosis is coronary intervention. This involves the use of Thrombolysis in Myocardial Infarction (TIMI) blood flow grades (TFG) to evaluate the quality of coronary blood flow. This method measures the coronary artery clearance of the injected radiographic dye.
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| * Grade 0 - No perfusion. No antegrade flow beyond the point of occlusion.
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| * Grade 1 - Penetration without perfusion. Contrast material passes beyond the area of obstruction but fails to opacify the entire coronary bed distal to the obstruction for the duration of the cineangiographic filming sequence.
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| * Grade 2 - Partial perfusion. Contrast material passes across the obstruction and opacifies the coronary bed distal to the obstruction. However, the rate of entry of contrast material into the vessel distal to the obstruction or its rate of clearance from the distal bed (or both) are perceptibly slower than its flow into or clearance from comparable areas not perfused by the previously occluded vessel (i.e. opposite coronary artery or the coronary bed proximal to the obstruction).
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| * Grade 3 - Complete perfusion. Antegrade flow into the bed distal to the obstruction occurs as promptly as antegrade flow into the bed proximal to the obstruction, and clearance of contrast material from the involved bed is as rapid as clearance from an uninvolved bed in the same vessel or the opposite artery
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| A more accurate technique to evaluate no-reflow is by using the number of angiographic frames required for a dye to reach a specified distal segment in the coronary artery, this was referred to as the corrected TIMI frame count (TFC) by Gibson et al in 1999.
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| ====Myocardial Contrast Echocardiography====
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| This is the gold standard technique for investigating no-reflow phenomenon. This involves the use of intravascular contrast agents that contain tracers. This modality can be used to assess microvascular perfusion. It has the advantage of defining the extent of myocardium affected and also producing a good prognostic value which correllates with the TIMI flow grade.
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| ====Myocardial Blush====
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| This involves the use of TIMI myocardial perfusion grade (TMPG) which serves as a measure of the filling and clearance of radiocontrast in the myocardium. More information on the TMPG grading system can be found [[TIMI myocardial perfusion grade|here]].
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| ====Coronary Doppler Imaging====
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| This involves the study of the coronary blood flow velocity patterns. No-reflow has a pathognomonic features which is the presence of:
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| * Systolic flow reversal
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| * Reduced antegrade systolic flow
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| * Forward diastolic flow with a rapid deceleration slope
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| This method also helps in distinguishing those with microthrombi from those without.
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| ====Other Modalities====
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| * Nuclear imaging single-photon emission computed tomography using thallium or technetium-99m.
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| * Positron emission tomography
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| * Contrast-enhanced MRI
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| ==Treatment==
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| When no-reflow phenomenon is diagnosed, the mainstay of treatment is pharmacologic. The optimal management of no-reflow after restoration of coronary blood flow is unknown. More emphases are laid on prevention rather than the treatment.
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| ====Supportive Care====
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| Most patients experience chest pain, hypotension and cardiac arrhythmias, therefore, attention to supportive measures is highly recommended. This involves [[analgesia]], intravenous fluids, intravenous inotropic agents, temporary cardiac pacing, and the use of intraaortic balloon pump support if necessary.
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| ====Exclude All Mechanical Causes====
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| Restore normal blood flow through epicardial coronary arteries and microvasculature to prevent persistence of myocardial ischemia. No-reflow needs to be distinguished from slow-flow resulting from coronary artery dissection, thrombus, coronary vasospasm, or residual stenosis. These etiologies must be excluded as part of the treatment of no-reflow. Ultimately, the goals are to improve outcomes, relieve chest pain and alleviate myocardial ischemia.
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| ====Administration of Vasodilators====
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| Medications such as [[verapamil]],<ref name="Werner-2002">{{Cite journal | last1 = Werner | first1 = GS. | last2 = Lang | first2 = K. | last3 = Kuehnert | first3 = H. | last4 = Figulla | first4 = HR. | title = Intracoronary verapamil for reversal of no-reflow during coronary angioplasty for acute myocardial infarction. | journal = Catheter Cardiovasc Interv | volume = 57 | issue = 4 | pages = 444-51 | month = Dec | year = 2002 | doi = 10.1002/ccd.10375 | PMID = 12455077 }}</ref> [[adenosine]] and [[nitroprusside]]<ref name="Hillegass-2001">{{Cite journal | last1 = Hillegass | first1 = WB. | last2 = Dean | first2 = NA. | last3 = Liao | first3 = L. | last4 = Rhinehart | first4 = RG. | last5 = Myers | first5 = PR. | title = Treatment of no-reflow and impaired flow with the nitric oxide donor nitroprusside following percutaneous coronary interventions: initial human clinical experience. | journal = J Am Coll Cardiol | volume = 37 | issue = 5 | pages = 1335-43 | month = Apr | year = 2001 | doi = | PMID = 11300444 }}</ref> through the intracoronary route have been used with results.
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| ==Prevention==
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| ====Thrombectomy====
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| This procedure is usually done to improve perfusion in STEMI patients before they undergo PCI. It can be done using either a manual thrombus aspiration device or a mechanical thrombectomy device, with the manual device having an edge over the mechanical device in some studies. A meta-analysis study proved that among patients with AMI treated with PCI, the use of manual thrombectomy device is associated with better epicardial and myocardial perfusion, less distal embolization and significant reduction in 30-day mortality.<ref name="De Luca-2008">{{Cite journal | last1 = De Luca | first1 = G. | last2 = Dudek | first2 = D. | last3 = Sardella | first3 = G. | last4 = Marino | first4 = P. | last5 = Chevalier | first5 = B. | last6 = Zijlstra | first6 = F. | title = Adjunctive manual thrombectomy improves myocardial perfusion and mortality in patients undergoing primary percutaneous coronary intervention for ST-elevation myocardial infarction: a meta-analysis of randomized trials. | journal = Eur Heart J | volume = 29 | issue = 24 | pages = 3002-10 | month = Dec | year = 2008 | doi = 10.1093/eurheartj/ehn389 | PMID = 18775918 }}</ref> Care should be exercised when aspirating in the proximal [[LAD]] or proximal [[circumflex]] locations so that clot does not go down the other adjacent artery.
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| ====Distal Embolic Protection Devices====
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| Distal protection devices may be used in SVGs to prevent distal [[embolization]] of clot, debris, and vasoactive mediators. However, the Enhanced Myocardial Efficacy and Recovery by Aspiration of Liberated Debris (EMERALD) and the Protection Devices in PCI Treatment of Myocardial Infarction for Salvage of Endangered Myocardium (PROMISE) trials showed inconsistent results with regards to embolic protection devices in use for primary PCI of native vessels.
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| ====Direct stenting====
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| When intervening on high-risk lesions, limit the amount of instrumentation within the target vessel, which includes minimizing overaggressive balloon or [[stent]] expansion. In patients undergoing rotational [[atherectomy]], shorter runs, slower speeds and smaller initial burr size with small stepwise increases in burr size should be employed to help prevent [[no reflow]].
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| ====Systemic GP IIb/IIIa inhibitors====
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| Systemic [[glycoprotein IIb/IIIa]] receptor antagonists are recommended as pre-treatment in patients presenting with unstable coronary syndromes undergoing PCI. The TITAN-TIMI 34 trial showed early initiation of [[eptifibatide]] in the emergency room prior to primary PCI improved myocardial perfusion without an increased risk of bleeding.
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| ====Intracoronary Treatment====
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| * Intracoronary administration of [[adenosine]], [[verapamil]], [[streptokinase]], or [[abciximab]] have been used during PCI to reduce reperfusion injury and improve myocardial perfusion, but none have been associated with good prognostic outcomes.
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| ====Vasodilators====
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| In addition, a cocktail of [[heparin]], [[nitroglycerin]] and [[calcium channel blockers|calcium channel blockers (CCB)]] should be infused simultaneously. Adding two [[arteriolar vasodilators]], i.e. [[nicardipine]] and [[adenosine]], to the flush "cocktail" may be helpful in further reducing incidence of no reflow, however traditionally the CCB used is [[verapamil]]. A recent study found no evidence that the administration of [[adenosine]] and [[verapamil]] can reduce all-cause mortality and improve outcomes, but there was an increase incidence of adenosine-induced hypotension and bradycardia.
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| ====Chronic statin therapy====
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| A recent study by Zhao JL et al in 2009 showed patients presenting with acute MI and hyperglycemia had lower incidence of [[no reflow]] if they were pretreated with [[HMG-CoA reductase]] inhibitors prior to angiography.
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| ==ACCF/AHA/SCAI 2011 Guidelines for Percutaneous Coronary Intervention (DO NOT EDIT)<ref name="pmid22070837">{{cite journal |author=Levine GN, Bates ER, Blankenship JC, Bailey SR, Bittl JA, Cercek B, Chambers CE, Ellis SG, Guyton RA, Hollenberg SM, Khot UN, Lange RA, Mauri L, Mehran R, Moussa ID, Mukherjee D, Nallamothu BK, Ting HH |title=2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention: Executive Summary A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions |journal=[[Journal of the American College of Cardiology]] |volume=58|issue=24|pages=2550–83|year=2011|month=December|pmid=22070837|doi=10.1016/j.jacc.2011.08.006|url=http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(11)02875-0|accessdate=2011-12-08|url=http://content.onlinejacc.org/cgi/reprint/58/24/2550.pdf|PDF}}</ref>==
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| ===No-Reflow Pharmacological Therapies (DO NOT EDIT)<ref name="pmid22070837">{{cite journal |author=Levine GN, Bates ER, Blankenship JC, Bailey SR, Bittl JA, Cercek B, Chambers CE, Ellis SG, Guyton RA, Hollenberg SM, Khot UN, Lange RA, Mauri L, Mehran R, Moussa ID, Mukherjee D, Nallamothu BK, Ting HH |title=2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention: Executive Summary A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions |journal=[[Journal of the American College of Cardiology]]|volume=58 |issue=24|pages=2550–83|year=2011|month=December|pmid=22070837|doi=10.1016/j.jacc.2011.08.006|url=http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(11)02875-0|accessdate=2011-12-08|url=http://content.onlinejacc.org/cgi/reprint/58/24/2550.pdf|PDF}}</ref>===
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| {|class="wikitable"
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| | colspan="1" style="text-align:center; background:LemonChiffon"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class IIa]]
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| |bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''1.''' Administration of an [[vasodilator|intracoronary vasodilator]] ([[adenosine]], [[calcium channel blocker]], or [[nitroprusside]]) is reasonable to treat PCI-related [[No reflow phenomenon|no-reflow]] that occurs during primary or elective PCI.<ref name="pmid17070151">{{cite journal |author=Amit G, Cafri C, Yaroslavtsev S, Fuchs S, Paltiel O, Abu-Ful A, Weinstein JM, Wolak A, Ilia R, Zahger D |title=Intracoronary nitroprusside for the prevention of the no-reflow phenomenon after primary percutaneous coronary intervention in acute myocardial infarction. A randomized, double-blind, placebo-controlled clinical trial|journal=[[American Heart Journal]] |volume=152 |issue=5 |pages=887.e9–14 |year=2006|month=November|pmid=17070151|doi=10.1016/j.ahj.2006.05.010|url=http://linkinghub.elsevier.com/retrieve/pii/S0002-8703(06)00458-3|accessdate=2011-12-15}}</ref><ref name="pmid10973014">{{cite journal |author=Assali AR, Sdringola S, Ghani M, Denkats AE, Yepes A, Hanna GP, Schroth G, Fujise K, Anderson HV, Smalling RW, Rosales OR|title=Intracoronary adenosine administered during percutaneous intervention in acute myocardial infarction and reduction in the incidence of "no reflow" phenomenon |journal=[[Catheterization and Cardiovascular Interventions : Official Journal of the Society for Cardiac Angiography & Interventions]] |volume=51 |issue=1 |pages=27–31; discussion 32|year=2000 |month=September|pmid=10973014|doi= |url=http://dx.doi.org/10.1002/1522-726X(200009)51:1<27::AID-CCD7>3.0.CO;2-0|accessdate=2011-12-15}}</ref><ref name="pmid15065143">{{cite journal |author=Barcin C, Denktas AE, Lennon RJ, Hammes L, Higano ST, Holmes DR, Garratt KN, Lerman A|title=Comparison of combination therapy of adenosine and nitroprusside with adenosine alone in the treatment of angiographic no-reflow phenomenon |journal=[[Catheterization and Cardiovascular Interventions : Official Journal of the Society for Cardiac Angiography & Interventions]] |volume=61 |issue=4 |pages=484–91|year=2004 |month=April|pmid=15065143|doi=10.1002/ccd.20010|url=http://dx.doi.org/10.1002/ccd.20010 |accessdate=2011-12-15}}</ref><ref name="pmid18928946">{{cite journal|author=Fischell TA, Haller S, Pulukurthy S, Virk IS|title=Nicardipine and adenosine "flush cocktail" to prevent no-reflow during rotational atherectomy|journal=[[Cardiovascular Revascularization Medicine : Including Molecular Interventions]] |volume=9|issue=4|pages=224–8|year=2008 |pmid=18928946|doi=10.1016/j.carrev.2008.03.002|url=http://linkinghub.elsevier.com/retrieve/pii/S1553-8389(08)00118-8|accessdate=2011-12-15}}</ref><ref name="pmid11300444">{{cite journal |author=Hillegass WB, Dean NA, Liao L, Rhinehart RG, Myers PR|title=Treatment of no-reflow and impaired flow with the nitric oxide donor nitroprusside following percutaneous coronary interventions: initial human clinical experience|journal=[[Journal of the American College of Cardiology]] |volume=37 |issue=5 |pages=1335–43|year=2001|month=April |pmid=11300444|doi=|url=http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(01)01138-X|accessdate=2011-12-15}}</ref><ref name="pmid17034064">{{cite journal |author=Huang RI, Patel P, Walinsky P, Fischman DL, Ogilby JD, Awar M, Frankil C, Savage MP|title=Efficacy of intracoronary nicardipine in the treatment of no-reflow during percutaneous coronary intervention|journal=[[Catheterization and Cardiovascular Interventions : Official Journal of the Society for Cardiac Angiography & Interventions]] |volume=68|issue=5 |pages=671–6 |year=2006|month=November|pmid=17034064 |doi=10.1002/ccd.20885|url=http://dx.doi.org/10.1002/ccd.20885|accessdate=2011-12-15}}</ref><ref name="pmid10080465">{{cite journal |author=Ito H, Taniyama Y, Iwakura K, Nishikawa N, Masuyama T, Kuzuya T, Hori M, Higashino Y, Fujii K, Minamino T|title=Intravenous nicorandil can preserve microvascular integrity and myocardial viability in patients with reperfused anterior wall myocardial infarction |journal=[[Journal of the American College of Cardiology]] |volume=33 |issue=3 |pages=654–60 |year=1999|month=March |pmid=10080465|doi=|url=http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(98)00604-4|accessdate=2011-12-15}}</ref><ref name="pmid8922307">{{cite journal|author=Kaplan BM, Benzuly KH, Kinn JW, Bowers TR, Tilli FV, Grines CL, O'Neill WW, Safian RD|title=Treatment of no-reflow in degenerated saphenous vein graft interventions: comparison of intracoronary verapamil and 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