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Table of Contents
REVIEW ARTICLE
Year : 2022  |  Volume : 12  |  Issue : 1  |  Page : 8-13

Coronary slow flow/no-reflow: Revisited


Department of Cardiology, Apollo Hospitals, Chennai, Tamil Nadu, India

Date of Submission06-Oct-2020
Date of Decision01-Nov-2020
Date of Acceptance21-Dec-2020
Date of Web Publication08-Feb-2022

Correspondence Address:
Dr. Immaneni Sathyamurthy
Department of Cardiology, Apollo Hospitals, Chennai - 600 006, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JICC.JICC_72_20

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  Abstract 


No-reflow is defined as failure to restore normal myocardial perfusion despite removal of mechanical obstruction in the epicardial coronary arteries. This phenomenon is associated with high risk of major adverse cardiac events, recurrent heart failure, arrhythmias, and death. The degree of reperfusion injury depends on the duration of preceding myocardial ischemia, infarct size, procedure variables, and patient characteristics. This complication predominantly occurs during percutaneous coronary intervention for acute coronary syndrome. Cardiac magnetic resonance imaging is the gold standard noninvasive method for assessing this phenomenon. Conditions such as flow-limiting dissection, in situ thrombosis, severe spasm, or high-grade residual stenosis should be excluded prior to making a diagnosis of no-reflow phenomenon. The management of no-reflow should be personalized according to the predominant mechanisms contributing to the microvascular obstruction.

Keywords: Acute coronary syndromes, primary percutaneous coronary angioplasty, slow flow


How to cite this article:
Kanthallu SN, Sathyamurthy I. Coronary slow flow/no-reflow: Revisited. J Indian coll cardiol 2022;12:8-13

How to cite this URL:
Kanthallu SN, Sathyamurthy I. Coronary slow flow/no-reflow: Revisited. J Indian coll cardiol [serial online] 2022 [cited 2022 May 27];12:8-13. Available from: https://www.joicc.org/text.asp?2022/12/1/8/337355




  Introduction Top


No-reflow is defined as failure to restore normal myocardial perfusion despite removal of anatomical obstruction in the epicardial coronary arteries. Angiographically, it is defined as acute reduction in coronary flow (thrombolysis in myocardial infarction (TIMI grade 0–1) in the absence of dissection, thrombus, spasm or high grade residual stenosis at the target lesion.[1]

This complication occurs mainly during percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS), PCI with rotational atherectomy, and PCI of saphenous vein grafts. This phenomenon is associated with high risk of major adverse cardiac events (MACE) secondary to poor infarct healing, negative myocardial remodeling, ventricular dilatation, recurrent heart failure, arrhythmias, and death. It results from obstruction of the myocardial microcirculation (vessels <200 μm in diameter) and was first described by Kloner et al.,[2] in a canine experimental model.


  Incidence Top


No reflow occurs in 5%–50% of patients during PCI (Niccoli et al., 2009).[3] In ST-elevation myocardial infarction (STEMI), the incidence of no-reflow varied between 11% and 41%, depending on patient's comorbidities, vessel, and lesion factors.[3] The incidence of no-reflow also varies according to the investigation used to diagnose it, like angiography (TIMI flow grade vs. TIMI frame count), myocardial contrast echocardiography (MCE), microvascular flow Doppler studies. It is a diagnosis of exclusion.

No reflow has been found to be an independent predictor of 1-year mortality with 3-fold increase in the adjusted risk of death in patients with STEMI undergoing primary PCI.[4] It also predicted an increased risk of death up to 5 years after primary PCI for STEMI (Kaplan–Meier estimates of 5-year mortality of 18.2% and 9.5% respectively; odds ratio 2.02, 95% confidence interval 1.44–2.82; P < 0.0001).[5]

[TAG:2]Predictors of No-Reflow[5][/TAG:2]

The degree of reperfusion injury depends on the duration of preceding myocardial ischemia, infarct size, procedure variables, and patient characteristics [Table 1].
Table 1: Predictors of no-reflow[5]

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  Pathophysiology Top


The potential mechanisms and the mediators responsible for no-reflow remain conjectural. However, the end result appears to be severe microvascular dysfunction. By addressing the possible mechanism in a given case, one can predict the success of restoration of flow in the micro circulation.

Pathophysiology is shown in [Figure 1] which involves:
Figure 1: Possible mechanisms in the genesis of no-reflow phenomenon

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  1. Ischemic injury
  2. Reperfusion injury
  3. Distal atherothrombotic embolization.



  Endothelial Injury Top


After prolonged ischemia, there is endothelial swelling secondary to alteration of Na+-H+ exchange that compromises the capillary lumen resulting in endothelial necrosis and extravasation of blood cells (vascular rhexis). There is release of vascular endothelial growth factor (VEGF), which binds with VEGF-2 receptor and dissociates the VEGF-2-VE-Cadherin complex at intercellular adherens and increases the permeability by destabilizing it.[6] VEGF is also released by shear stress following reperfusion. Endothelial nitric oxide production is also altered. There is reactive oxygen species (ROS) mediated endothelial cell adhesion. Extravasation of fluid into the interstitial space leads to edema, resulting in compression of microvasculature. Muscle cells also get swollen following ischemia, which compress the intramural micro vessel. Anti-bodies directed against intercellular adhesion molecule-1 or P-select in on endothelium has shown to reduce reflow.


  Leukocyte Intravascular Plugging Top


Activated neutrophil plays an important role in no-reflow phenomenon and depleting neutrophils resulted in abolition of no-reflow. Oxidants produced during ischemia/reperfusion cause CD-11, CD-18 mediated neutrophil adhesion[7] and anti-bodies directed against them have shown to prevent no-reflow. Leukocytes accumulation in micro capillaries cause mechanical plugging,[8] as these cells are stiff, viscoelastic and need lot of deformation to traverse these vessels. There is cellular acidosis secondary to ischemia, that makes leukocytes stiffer, and resulting low perfusion pressure further worsens the forward flow and aggravates the no-reflow. It also releases ROS, which further injure the capillary endothelium. There is calcium overload and increase in mitochondrial permeability transmission pore (MPTP) function.


  Platelets Top


Platelets will cause mechanical plugging and release platelet-derived vasoactive and chemotactic mediators thereby cause no-reflow.


  Vasospasm Top


Spasm of microvasculature occurs because of effect of various chemicals released, and autonomic dysfunction with resultant increased alpha-adrenergic receptor mediated vasoconstriction.

There is systemic inflammation as evidenced by raised C-reactive protein (CRP). There is elevation in serum endothelin-1 level, which might aggravate reperfusion injury. There is increase in microvascular hematocrit with resultant increased viscosity in the capillaries and increased resistance to forward flow and worsening of no-reflow.


  Diagnosis of No-Reflow Top


Clinical features of no-reflow

Clinically, there is sudden increase in the intensity of chest pain, with hemodynamic compromise. It can be associated with malignant ventricular arrhythmias, refractory heart failure, even cardiac rupture, and death.

Electro cardiogram

There will be persistent or increase in ST segment elevation, newonset Q waves following successful primary PCI or failure of ST elevation resolution following thrombolysis,[9] indicating no reflow phenomenon. A distortion of terminal portion of QRS complex was significantly associated with infarct size, impaired myocardial salvage, and reperfusion injury as assessed by cardiac magnetic resonance (CMR) imaging in STEMI patients.

Echocardiography

MCE is a useful tool to identify no-reflow phenomenon following revascularization. Micro bubbles of inert gases are injected intravenously or intra coronary route. Failure of uptake or paradoxical persistence of micro bubbles in the myocardium indicates no-reflow phenomenon. Limitations with this procedure are long learning curve, limited spatial resolution, detects only 1/3 of patients with micro vascular obstruction (MVO) after ACS. It also predicts prognosis following PCI. The acute myocardial infarction contrast imaging[10] trial compared MCE done 1 day after PCI with TIMI flow grade, myocardial blush grade, peak creatine kinase, ST-segment resolution, and echocardiographic wall motion score. This study revealed only the endocardial length of the myocardial perfusion defect on MCE and a TIMI score <3 in the angiogram predicted left ventricular (LV) remodeling and outcomes.


  Biomarkers Top


C-reactive protein

There are a conflicting data about elevated serum levels of CRP[11] as a predictor of no-reflow.

Index of microcirculatory resistance

Index of microcirculatory resistance (IMR) is calculated as the product of distal coronary pressure and hyperemic transit time (derived by thermodilution during intracoronary papaverine or intravenous adenosine). An IMR <32 U was found to be a good predictor of long term improvement in wall motion score at the end of 3 months.[12]

Cardiac magnetic resonance imaging

Cardiac magnetic resonance imaging is the gold standard noninvasive method for assessing no reflow phenomenon. It has highest spatial resolution with good reproducibility.[13] Precontrast T2-weighted sequences provide information regarding myocardial edema [Figure 2]a, and intra-myocardial hemorrhage.[14] There are two approaches for diagnosing MVO by contrast enhanced CMR.
Figure 2: (a) Pre-contrast T2 weighted sequences provide information regarding myocardial edema (b) Hypo-intense areas on first pass perfusion images (c) At 3 minutes - early contrast enhancement (d) At 10 minutes interval - late contrast enhancement

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  1. Perfusional approach
  2. Delayed enhancement approach.


Perfusional approach

Following intravenous injection of gadolinium, there will be either absent or significant delay in the appearance of contrast within the infarcted area with no-reflow. As high as 50% of STEMI patients show hypointense areas on first pass perfusion images [Figure 2]b.[15] This could be secondary to no-reflow due to myocardial edema. On 10-min contrast-enhanced sequence, the hypointense area disappears with edema of reperfused myocardium, which proves that the first pass perfusion CMR carry more sensitivity but less specificity.[15]

Delayed enhancement approach

After intravenous gadolinium injection, images were taken at 3 min (early contrast enhancement) [Figure 2]c and 10 min interval [Figure 2]d (late contrast enhancement).

Late contrast enhancement late gadolinium enhancement (LGE) at 10 min appeared to be the most reliable method to assess the MVO. It has been shown that 10 min LGE images predict MACE[16] better. The hypointense areas on these images correspond to severe MVO, where even-after 10 min of passive diffusion, the contrast has not reached the media. MVO extent >2.6% of LV by CMR was the strongest independent predictor of death after heart failure hospitalization.


  Nuclear Imaging Top


Both single-photon emission computed tomography and positron emission tomography have demonstrated no-reflow phenomenon in humans. It detects MVO, even when there is no angiographic no-reflow. These tests are underutilized in daily practice.


  Coronary Angiography Top


TIMI group has described two indices namely TIMI scale[17] and TIMI frame count. TIMI flow grade <1 and high TIMI frame[18],[19] count indicate no-reflow. However, this method lacks sensitivity and specificity in assessing no-reflow as significant proportion of patients with TIMI Grade-3 flow,[20] actually have no-reflow.

Densitometric method called myocardial blush grading[21] is a useful technique in assessing no-reflow by angiography. Myocardial tissue opacification intensity (myocardial blush) is graded into four grades (0–3) (0-no myocardial blush, 1-minimal myocardial blush, 2-moderate myocardial blush but less than that obtained during the angiography of a contralateral noninfarct related coronary artery, and 3-normal myocardial blush or contrast density similar to that obtained during angiography of a contralateral noninfarct related artery).

It is important to note that no-reflow phenomenon develops over hours to days following reperfusion. Hence, it is not possible to diagnose no-reflow by coronary angiogram in all cases.


  Management: Top


Conditions such as flow-limiting dissection, in situ thrombosis, severe coronary spasm, distal athero thromboembolism, high grade residual stenosis or coronary air embolism should be excluded prior to making a diagnosis of no-reflow phenomenon [Figure 3].[22]
Figure 3: Management of no-reflow[39]

Click here to view



  Mechanical Therapy Top


The risk of no-reflow can be reduced by direct stenting instead of predilatation in primary PCI and one should avoid high pressure inflation. Ischemic preconditioning with intravenous (IV) nicorandil, IV Glycoprotein (GP) II–bIIIa inhibitors (upstream) and loading with high intensity statin (Kim and Choi)[23] have shown to reduce the occurrence of no-reflow. A forceful injection of intra coronary saline[24] or contrast may help to clear micro vascular plugging. Caution should be taken while stenting the lesions with no-reflow as poor distal run-off might lead to acute stent thrombosis. When injecting vasodilators through guiding catheters, the medication does not reach the target of interest with TIMI-0 flow and get into the nontarget coronary vessel. Hence, delivery of these agents at the site of interest by distal infusion catheters[25] or the over the wire balloon catheters found to have better results in no-reflow.

During the rotational atherectomy, there is microembolization of calcified plaque particles and the heat generated causes platelet activation. Predictors of slow flow following rotational atherectomy are lesion length, recent unstable angina, and use of beta blockers within 24 h prior to the procedure.[26] To reduce this, cocktail[27] of nitrate, heparin, with calcium channel blockers was used as flush solution. The runs should be short (<15 s) with burr speed of >140000 rpm, with deceleration <5000 rpm to reduce this complication.[28]


  Thrombus Aspiration Top


Routine thrombus aspiration before PCI versus stenting alone has not shown reduction in 30-day mortality in STEMI patients. Recent meta-analyses have shown increased risk of stroke with thrombus aspiration in these patients.

Embolic protection devices are used to protect the micro vasculature from getting choked with embolic debris while performing PCI. The challenges that we encounter while using these devices are deliverability of device in severe stenosis or tortuous vessel, getting a good landing zone, embolization of debris while crossing the lesion, side branches getting the debris if present proximal to the device and minimal debris escaping the filter to the distal bed.


  Pharmacological Therapy: Top


Adenosine

Adenosine is an endogenous purine nucleoside when administered IV/intra-coronary (IC) route, causes arteriolar vasodilatation with inhibition of neutrophil migration, prevention of super-oxide generation, blockade of endothelin release through opening of ATP-sensitive potassium channels (KATP). It prevents mitochondrial calcium overload and release of cytochrome C release, thereby negates opening of MPTP, which precludes cellular apoptosis [Table 2].[22]
Table 2: Pharmacological therapy

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Acute Myocardial Infarction Studyof Adenosine II (AMISTAD II) trail[29] found no benefit with respect to clinical outcomes, including congestive heart failure, rehospitalization for congestive heart failure (CHF), death from any cause at 6 months. In a post hoc analysis, patients who achieved early reperfusion (<3 h) had better clinical outcomes and 1-month and 6-month mortality rates.

The IC nitroprusside versus adenosine in Acute Myocardial Infarction (REOPEN) trail[30] evaluated efficacy of IV nitroprusside versus adenosine following IC thrombus aspiration in patients with STEMI undergoing PCI. Even though ST resolution was better with adenosine compared to nitroprusside, the 30-day clinical outcomes were not statistically significant. However, at 1-year follow-up, adenosine group scored over the nitroprusside group in reducing the incidence of composite events of MI, heart failure, and death.

Sodium nitroprusside

Nitroprusside causes coronary vasodilatation of both epicardial and micro circulation through activating guanylate cyclase in the vascular smooth muscle. Its effect on no-reflow is sustained comparing to other pharmacological agents. It produces additive effect when administered after adenosine injection. It was found to produce more rapid ST resolution, fewer MACE and higher left ventricular ejection fraction (LVEF), when administered along with tirofiban compared to tirofiban alone (Zhao et al).[31] It was compared against nicorandil, found to be more effective, when TIMI frame count was measured and found to be statistically significant.

Calcium channel blockers

Calcium channel blockers such as verapamil, diltiazem, and nicardipine have shown to improve no-re flow, when administered IC route. In a meta-analysis involving 7 trails with 539 patients with IC verapamil at a dosage of 200 μg to 2 mg, there was significant reduction in incidence of no-reflow, a better TIMI grade and TIMI frame count and a reduction in MACE at the end of 2 months after PCI.[32] Nicardipine was found to be more potent and the effect is more sustained with minimal myocardial depression comparing to IC verapamil. It was found to be beneficial in preventing no-reflow in patients undergoing PCI with rotational atherectomy and in saphenous vein graft angioplasty.[33]

Nicorandil

Nicorandil is a direct KATP channel opener and is a nitric oxide donor. It was found to improve microvascular flow and the functional recovery in a randomized study in patients with acute MI.[34]

Glycoprotein IIb–IIIa inhibitor

In INFUSE anterior myocardial infarction trail, 452 anterior STEMI patients undergoing PCI received abxicimab IC route and found to have significant reduction in infarct size at 30 days, as confirmed by CMR.[35] However, because of their bleeding risk, routine use of GP IIb–IIIa inhibitor is not recommended during PCI.

Adrenaline

In patients with refractory no-reflow phenomenon following primary PCI for STEMI, IC adrenaline injection results in improvement in coronary flow, LVEF, ST resolution in addition to lowering clinical events at 30 days (RESTORE Study).[36]

Future directions

Glucagon like peptide-1 analog, liraglutide have been studied in a small randomized controlled trails and found to reduce no-reflow.[37] Possible mechanisms are glucose modulation, reduced inflammation and improved endothelial function. Early ischemia induced, VEGF mediated endothelial disruption is a novel target and angiopoietin-like 4 (ANGPTL-4) is found to counteract this process.[38] Lower level of serum ANGPTL-4 on admission was found to be associated with higher no-reflow in CMR following reperfusion.


  Conclusion Top


The optimal treatment of no-reflow is by trial and error. The management of no-reflow should be tailor-made according to the mechanisms contributing to the MVO. It is associated with 10-fold higher incidence of death and myocardial infarction[39] compared to patients without no reflow. Patient characteristics and lesion characteristics should be taken into account while individualizing the treatment strategies (anti-platelets therapy, vasodilators, embolic protection device, thrombus aspiration, pharmacologic pre- and post-conditioning strategies), so that, the occurrence of this complication following revascularization can be minimized.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Kloner RA. No reflow revisited. J Am Coll Cardiol 1989;14:1814-5.  Back to cited text no. 1
    
2.
Kloner RA, Ganote CE, Jennings RB. The “no-reflow” phenomenon after temporary coronary occlusion in the dog. J Clin Invest 1974;54:1496-508.  Back to cited text no. 2
    
3.
Niccoli G, Burzotta F, Galiuto L, Crea F. Myocardial no-reflow in humans J Am Coll Cardiol: 2009:54(4):281-92.  Back to cited text no. 3
    
4.
Ndrepepa G, Tiroch K, Fusaro M, Keta D, Seyfarth M, Byrne RA, et al. 5-year prognostic value of no-reflow phenomenon after percutaneous coronary intervention in patients with acute myocardial infarction. J Am Coll Cardiol 2010;55:2383-9.  Back to cited text no. 4
    
5.
Ndrepepa G, Tiroch K, Keta D, Fusaro M, Seyfarth M, Pache J, et al. Predictive factors and impact of no reflow after primary percutaneous coronary intervention in patients with acute myocardial infarction. Circ Cardiovasc Interv 2010;3:27-33.  Back to cited text no. 5
    
6.
Weis SM, Cheresh DA. Pathophysiological consequences of VEGF-induced vascular permeability. Nature 2005;437:497-504.  Back to cited text no. 6
    
7.
Jerome SN, Smith CW, Korthuis RJ. CD18-dependent adherence reactions play an important role in the development of the no-reflow phenomenon. Am J Physiol 1993;264:H479-83.  Back to cited text no. 7
    
8.
Engler RL, Schmid-Schönbein GW, Pavelec RS. Leukocyte capillary plugging in myocardial ischemia and reperfusion in the dog. Am J Pathol 1983;111:98-111.  Back to cited text no. 8
    
9.
Claeys MJ, Bosmans J, Veenstra L, Jorens P, De RaedtH, Vrints CJ. Determinants and prognostic implications of persistent ST-segment elevation after primary angioplasty for acute myocardial infarction: Importance of microvascular reperfusion injury on clinical outcome. Circulation 1999;99:1972-7.  Back to cited text no. 9
    
10.
Galiuto L, Garramone B, Scara A, Rebuzzi AG, Crea F, Torre GL, et al. On behalf of the AMICI investigators. “The extent of microvascular damage at myocardial contrast echocardiography is superior to other known indexes of post-infarct reperfusion in predicting left ventricular remodeling: results of the AMICI study.” J Am Coll Cardiol 2008;51:552-9.  Back to cited text no. 10
    
11.
Tomai F, Ribichini F, Ghini AS, Ferrero V, Andò G, Vassanelli C, et al. Elevated C-reactive protein levels and coronary microvascular dysfunction in patients with coronary artery disease. Eur Heart J 2005;26:2099-105.  Back to cited text no. 11
    
12.
Fearon WF, Shah M, Ng M, Brinton T, Wilson A, Tremmel JA, et al. Predictive value of the index of microcirculatory resistance in patients with ST-segment elevation myocardial infarction. J Am Coll Cardiol 2008;51:560-5.  Back to cited text no. 12
    
13.
Albert TS, Kim RJ, Judd RM. Assessment of no-reflow regions using cardiac MRI. Basic Res Cardiol 2006;101:383-90.  Back to cited text no. 13
    
14.
García-Dorado D, Oliveras J, Gili J, Sanz E, Pérez-Villa F, Barrabés J, et al. Analysis of myocardial oedema by magnetic resonance imaging early after coronary artery occlusion with or without reperfusion. Cardiovasc Res 1993;27:1462-9.  Back to cited text no. 14
    
15.
Bouleti C, Mewton N, Germain S. The no-reflow phenomenon: State of the art. Arch Cardiovasc Dis 2015;108:661-74.  Back to cited text no. 15
    
16.
Nijveldt R, Hofman MB, Hirsch A, Beek AM, Umans VA, Algra PR, et al. Assessment of microvascular obstruction and prediction of short-term remodeling after acute myocardial infarction: Cardiac MR imaging study. Radiology 2009;250:363-70.  Back to cited text no. 16
    
17.
TIMI Study Group. The thrombolysis in myocardial infarction (TIMI) trial. Phase I findings. N Engl J Med 1985;312:932-6.  Back to cited text no. 17
    
18.
Gibson CM, Murphy SA, Rizzo MJ, Ryan KA, Marble SJ, McCabe CH, et al. Relationship between TIMI frame count and clinical outcomes after thrombolytic administration. Thrombolysis in myocardial infarction (TIMI) study group. Circulation 1999;99:1945-50.  Back to cited text no. 18
    
19.
Gibson CM, Murphy SA, Rizzo MJ, Ryan KA, Marble SJ, McCabe CH, et al. Thrombolysis in myocardial infarction (TIMI) study group. Relationship between TIMI frame count and clinical outcomes after thrombolytic administration. Circulation 1999;99:1945-50.  Back to cited text no. 19
    
20.
Hamada S, Nishiue T, Nakamura S, Sugiura T, Kamihata H, Miyoshi H, et al. TIMI frame count immediately after primary coronary angioplasty as a predictor of functional recovery in patients with TIMI 3 reperfused acute myocardial infarction. J Am Coll Cardiol 2001;38:666-71.  Back to cited text no. 20
    
21.
Henriques JP, Zijlstra F, van 't Hof AW, de Boer MJ, Dambrink JH, Gosselink M, et al. Angiographic assessment of reperfusion in acute myocardial infarction by myocardial blush grade. Circulation 2003;107:2115-9.  Back to cited text no. 21
    
22.
Safian RD. No-Reflow. In: Safian RD, Freed M, editors. The manual of interventional cardiology, 3rd ed. Royal Oak, MI: Physicians Press; 2001;413-21. [Last accessed on 2020 Oct 06]  Back to cited text no. 22
    
23.
Kim C, Choi D. Timing of high intensity statin for acute coronary syndrome: how earlier initiation makes better? J Thorac Dis 2018;10:S2149-52.  Back to cited text no. 23
    
24.
Calhoun KH, Tan L, Seikaly H. An integrated theory of the no-reflow phenomenon and the beneficial effect of vascular washout on no-reflow. Laryngoscope 1999;109:528-35.  Back to cited text no. 24
    
25.
Wilson W, Eccleston D. How to manage no reflow phenomenon with local drug delivery via a rapid exchange catheter. Catheter Cardiovasc Interv 2011;77:217-9.  Back to cited text no. 25
    
26.
Sharma SK, Dangas G, Mehran R, Duvvuri S, Kini A, Cocke TP, et al. Risk factors for the development of slow flow during rotational coronary atherectomy. Am J Cardiol 1997;80:219-22.  Back to cited text no. 26
    
27.
Fischell TA, Haller S, Pulukurthy S, Virk IS. Nicardipine and adenosine “flush cocktail” to prevent no-reflow during rotational atherectomy. Cardiovasc Revasc Med 2008;9:224-8.  Back to cited text no. 27
    
28.
Tomey MI, Kini AS, Sharma SK. Current status of rotational atherectomy. JACC Cardiovasc Interv 2014;7:345-53.  Back to cited text no. 28
    
29.
Ross AM, Gibbons RJ, Stone GW, Kloner RA, Alexander RW, AMISTAD-II Investigators. A randomized, double-blinded, placebo-controlled multicenter trial of adenosine as an adjunct to reperfusion in the treatment of acute myocardial infarction (AMISTAD-II). J Am Coll Cardiol 2005;45:1775-80.  Back to cited text no. 29
    
30.
Niccoli G, Rigattieri S, De Vita MR, Valgimigli M, Corvo P, Fabbiocchi F, et al. Open label, randomized, placebo-controlled evaluation of intracoronary adenosine or nitroprusside after thrombus aspiration during primary percutaneous coronary intervention for the intervention of microvascular obstruction in acute myocardial infarction: the REOPEN-AMI study (Intracoronary Nitroprusside Versus Adenosine in Acute Myocardial Infarction). J Am Coll Cardiol Intv 2013;6:580-9.  Back to cited text no. 30
    
31.
Zhao YJ, Fu XH, Ma XX, Wang DY, Dong QL, Wang YB, et al. Intracoronary fixed dose of nitroprusside via thrombus aspiration catheter for the prevention of the no-reflow phenomenon following primary percutaneous coronary intervention in acute myocardial infarction. Exp Ther Med 2013;6:479-84.  Back to cited text no. 31
    
32.
Wang L, Cheng Z, Gu Y, Peng D. Short-term effects of verapamil and diltiazem in the treatment of no reflow phenomenon: A meta-analysis of randomized controlled trials. Biomed Res Int 2015;2015:382086.  Back to cited text no. 32
    
33.
Michaels AD, Appleby M, Otten MH, Dauterman K, Ports TA, Chou TM, et al. Pretreatment with intracoronary verapamil prior to percutaneous coronary intervention in saphenous vein graft lesions: Results of the randomized, controlled vasodilator prevention of no-reflow (VAPOR) trail. J Invas Cardiol 2002;14:299-302.  Back to cited text no. 33
    
34.
Ito H, Taniyama Y, Iwakura K, Nishikawa N, Masuyama T, Kuzuya T, et al. Intravenous nicorandil can preserve microvascular integrity and myocardial viability in patients with reperfused anterior wall myocardial infarction. J Am Coll Cardiol 1999;33:654-60.  Back to cited text no. 34
    
35.
Stone GW, Maehara A, Witzenbichler B, Godlewski J, Parise H, Dambrink JH, et al. Intracoronary abciximab and aspiration thrombectomy in patients with large anterior myocardial infarction: The INFUSE-AMI randomized trial. JAMA 2012;307:1817-26.  Back to cited text no. 35
    
36.
Navarese EP, Frediani L, Kandzari DE, Caiazzo G , Cenname A M, Cortese B,et al. Efficacy and safety of intracoronary epinephrine versus conventional treatments alone in STEMI patients with refractory coronary no-reflow during primary PCI: The RESTORE observational study. Catheter Cardiovasc Interv.2020; 1-10.  Back to cited text no. 36
    
37.
Chen WR, Tian F, Chen YD, Wang J, Yang JJ, Wang ZF, et al. Effects of liraglutide on no-reflow in patients with acute ST-segment elevation myocardial infarction. Int J Cardiol 2016;208:109-14.  Back to cited text no. 37
    
38.
Galaup A, Gomez E, Souktani R, Durand M, Cazes A, Monnot C, et al. Protection against myocardial infarction and no-reflow through preservation of vascular integrity by angiopoietin-like 4. Circulation 2012;125:140-9.  Back to cited text no. 38
    
39.
Abbo KM, Dooris M, Glazier S, O'Neill WW, Byrd D, Grines CL, et al. No-reflow after percutaneous coronary intervention: Clinical and angiographic characteristics, treatment and outcome. Am J Cardiol 1995;75:778-82.  Back to cited text no. 39
    


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  In this article
Abstract
Introduction
Incidence
Predictors of No...
Pathophysiology
Endothelial Injury
Leukocyte Intrav...
Platelets
Vasospasm
Diagnosis of No-...
Biomarkers
Nuclear Imaging
Coronary Angiography
Management:
Mechanical Therapy
Thrombus Aspiration
Pharmacological ...
Conclusion
References
Article Figures
Article Tables

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