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Table of Contents
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
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JICC.JICC_72_20

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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.


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]

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  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 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 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.


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


Conflicts of interest

There are no conflicts of interest.

  References Top

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  [Figure 1], [Figure 2], [Figure 3]

  [Table 1], [Table 2]


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