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*Corresponding Author: Hüsnü Değirmenci, Faculty of Medicine, Department of Cardiology, Erzincan Binali Yıldırım University, Erzincan/Turkey.
Citation: Hüsnü Değirmenci (2021) Current Approach to the No Reflow Phenomenon J, Heart and Vasculature 1(1); DOI: 10.31579/JHV-2021/002
Copyright: © Değirmenci, This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received: 08 February 2021 | Accepted: 19 February 2021 | Published: 27 February 2021
Keywords: no reflow, microvascular obstruction, timi 1-2 flow, timi frame count, myocardial blush grade, treatment
Coronary no reflow phenomenon is a decrease in myocardial tissue perfusion despite the patency of the epicardial coronary arteries. Microvascular obstruction due to various reasons is the main pathological mechanism. In coronary no reflow phenomenon, TIMI 1-2 flow and high TIMI frame count are observed. Since microvascular obstruction continues intermittently despite TIMI 3 flow, myocardial blush grade provides a better evaluation in the evaluation of no reflow phenomenon. In patients with TIMI 3 flow, myocardial blush being below grade 2 is considered as a no reflow phenomenon. Thrombus aspiration, antiplatelet agents, adenosine, sodium nitroprusside, epinephrine constitute the main treatment.
Coronary no reflow phenomenon is defined as myocardial tissue hypoperfusion that develops despite the patency of epicardial coronary arteries [1]. While no reflow phenomenon is observed in 0.6-5% of cases with elective percutaneous coronary intervention, it is seen in 60% of cases with primary percutaneous coronary intervention [1, 2]. Especially in patients diagnosed with ST segment elevation myocardial infarction, no reflow phenomenon is common in percutaneous coronary interventions, saphenous vein graft attempts and atheroctomy [2]. This phenomenon especially causes complications of early post myocardial infarction, left ventricular remodeling, recurrent hospitalizations and mortality [2]. Therefore, we presented the current approach to the coronary no reflow phenomenon.
Epicardial stenosis, epicardial spasm, local thrombus, and dissection should be ruled out for diagnosis [3]. No reflow phenomenon is defined as the decrease in myocardial flow and myocardial perfusion despite reperfusion with percutaneous coronary intervention during acute myocardial infarction. TIMI flow grade system, TIMI frame count and myocardial blush grade are used to evaluate coronary blood flow. In coronary no reflow phenomenon, TIMI 1-2 flow and high TIMI frame count are observed. Since microvascular obstruction continues intermittently despite TIMI 3 flow, myocardial blush grade provides a better evaluation in the evaluation of no reflow phenomenon [4]. In patients with TIMI 3 flow, myocardial blush being below grade 2 is considered as a no reflow phenomenon [4-6]. No reflow phenomenon is often caused by microvascular obstruction due to various reasons. This phenomenon is evaluated in two classes: intervention-related or reperfusion [7]. Echocardiography, coronary angiography, magnetic resonance imaging, computed tomography and biomarkers can be used for diagnosis. Noninvasive echocardiographic evaluation of myocardial perfusion by myocardial contrast echocardiography plays an important role in determining microvascular no reflow phenomenon. Reduced tissue contrast enhancement on MRI with contrast enhancement suggests no reflow phenomenon. Multidetector computed tomography suggests noreflow phenomenon with decreased myocardial perfusion. Even after successful percutaneous coronary intervention, an increase in troponin levels can be seen in 70% of patients. This rise is suggestive of a no reflow phenomenon [7].
Over 65, smoking, previous myocardial infarction, high killip class, high serum creatine levels, high C reactive protein level, low vitamin D level, prolonged intervention time, low ejection fraction, low TIMI flow grade, initial major perfusion defect, acute Hyperglycemia, hyperlipidemia, hypertension, and low echoic content of the lesion are risk factors for the no reflow phenomenon [7,8]. The No-reflow phenomenon and comparison to the normal-flow population postprimary percutaneous coronary intervention for ST elevation myocardial infarction: case – control (NORM PPCI) study evaluated predictors and incidence of the no-reflow phenomenon. In this study, no reflow phenomenon was observed in 24 (13.9%) of 173 patients with ST segment elevation myocardial infarction. No reflow phenomenon has been found to be associated with complex lesion, systolic hypertension and low weight [9].
Endothelial dysfunction, reperfusion injury, ischemia-related injury, distal thromboembolism due to percutaneous coronary intervention, individual sensitivity, myocardial cell swelling and microvascular arterial spasm play an important role in etiopathogenesis. Increase in neutrophil platelet aggregates, increase in free oxygen radicals, increase in endothelin 1 level and thromboxan A 1 level, increase in mean platelet volume and reactivity in patients with risk factors play an important role in the pathogenesis of no reflow phenomenon [7].
No reflow development risk score is determined according to age, thrombus burden and microcirculatory resistance index level (ATI Score). According to these parameters, age 50 and over is 1 point. If thrombus load is 4, 1 point; If 5, 3 points are given. If the microcirculatory resistance index is between 40-100, 1 point; If 100 and above, 2 points are awarded. According to this evaluation, the maximum score is 6. If the ATI score is 4 and above, 95.1% microcirculatory resistance index is 40U and above. Microvascular resistance index is a parameter that has been used for a long time, showing coronary microvascular functions. Its normal value is 25 and below. Generally, this index is not affected by epicardial vascular stenosis. As a standardized coronary pressure wire is used, it is possible to measure fractional flow reserve simultaneously. Therefore, macrovascular and microvascular dysfunction can be distinguished. Microvascular resistance can simply be formulated as distal microvascular pressure x transit time of blood (10-13). ATI score over 4 was found to be associated with large infarct volume and left ventricular remodeling [14, 15].
The most important invasive intervention that reduces the no reflow phenomenon is thrombus aspiration. The REMEDIA study is the first study showing that manual thrombectomy reduces the no reflow phenomenon, especially in patients with high thrombus burden [16]. In addition, in the TAPAS study, it was shown that improvement in myocardial perfusion was achieved with manual thrombus aspiration. In this study, it was shown that mortality decreased in 1-year follow-up [17].
Clopidogrel reduces the no reflow phenomenon by inhibiting platelet aggregation by P2Y12 inhibition. Ticagrelor reduces the uptake of adenosine into the cell by inhibition of adenosine transporter ENT-1. Thus, extracellular adenosine increases. The increase in adenosine causes coronary vasodilation. Ticagrelor also inhibits platelet aggregation. Kangrelor provides reversible P2Y12 inhibition. Thus, it inhibits platelet aggregation [18-22].
Glycoprotein 2b / 3a inhibitors such as abciximab and tirofiban reduce the no reflow phenomenon by reducing distal embolization and thrombus burden. Abciximab can be administered as a 12-hour infusion followed by a 0.25 mg / kg IV bolus [23, 24].
In the Randomized Evaluation Of Intracoronary Nitroprusside vs Adenosine After Thrombus-aspiration During Primary Percutaneous Coronary Intervention for the Prevention of No Reflow in Acute Myocardial Infarction (THE REOPEN-AMI STUDY) study (25) adenosine (80 microgram bolus followed by 2 mg; 33 cc saline followed by slow bolus in 2 minutes) and nitroprusside (60 microgram fast bolus followed by 100 microgram; 33 cc 5% dextrose 2 min slow bolus) was compared. All of these patients were given abciximab before the procedure and thrombus aspiration was performed during the procedure. In this study, a significant improvement in ST segment resolution was observed with the addition of adenosine to thrombus aspiration. Improvement in ST segment resolution is an indication that microvascular obstruction has improved. In the adenosine no reflow phenomenon, intravenous or intracoronary can be applied. Adenosine can be administered at a bolus dose of 100-200 micrograms (intracoronary) or as an intravenous infusion of 50-70 micrograms / kg / min for 3 hours. Or, a 120 microgram bolus followed by a slow infusion with 2 mg over 2 minutes [4].
In the AMISTAD and AMISTAD 2 studies, adenosine has been shown to reduce infarct volume. However, it did not improve clinical outcomes in patients with delayed reperfusion [26-28].
In some studies, it has been shown that sodium nitroprusside provides a significant hyperemic effect with its vasodilator effect and reduces the no reflow phenomenon [4]. Nitroprusside 60-100 micrograms intracoronary bolus is administered.
Calcium channel blockers of nondihydropride have also been shown to reduce the no-reflow phenomenon and reduce 6-month adverse cardiovascular events. Verapamil can be administered as 0.1-0.5 mg intracoronary followed by oral tablets [4]. Diltiazem can be administered as 0.4 mg intracoronary.
Nicorandil provides coronary vasodilation by increasing nicotinamide nitrate levels and opening mitochondrial potassium channels. Nicorandil can be administered as an intravenous 4mg bolus and 6mg / hour infusion following 0.5 mg intracoronary administration. It is followed by an oral tablet [29, 30].
In a small retrospective study of the refractory no reflow phenomenon, at least 100 micrograms of epinephrine (in the range of 100-400 micrograms) has been shown to be beneficial. Adenosine or nitroprusside can also be used in the resistant no reflow phenomenon [31].
In the no reflow phenomenon, intravenous atrial natriuretic peptide, intravenous cyclosporine or intracoronary dipyridamole may also be used [4].
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