Intracoronary Verapamil Research Articles

COMPARATIVE EFFICACY OF INTRACORONARY VERAPAMIL AND ADRENALINE IN MANAGING CORONARY NO-REFLOW DURING PRIMARY PCI IN STEMI PATIENTS AT A TERTIARY CARE HOSPITAL

Coronary No-Reflow (CNR) is a significant complication during Primary Percutaneous Coronary Intervention (PPCI) for ST-Elevation Myocardial Infarction (STEMI), often leading to poor clinical outcomes. Management strategies for CNR include various pharmacological agents, among which intracoronary verapamil and intracoronary adrenaline are commonly used alongside Glycoprotein IIb/IIIa inhibitors. Objective: This study aims to compare the effectiveness of intracoronary verapamil versus intracoronary adrenaline, alongside Glycoprotein IIb/IIIa inhibitors, in managing Coronary No-Reflow (CNR) during Primary Percutaneous Coronary Intervention (PPC1) for STEMI patients. Methodology: This randomized-control-trial was conducted at the Department of Cardiology, MTI Lady Reading Hospital Peshawar, Pakistan, from May 2023 to April 2024. Fifty patients diagnosed with CNR during PPC1 were randomised into two groups: adrenaline and verapamil. The primary outcome measures were TIMI Flow Grade (TFG) and Myocardial Blush Grade (MBG) immediately post-intervention. In contrast, secondary outcomes included Major Adverse Cardiovascular Events (MACE), myocardial infarction, stroke, target vessel revascularisation, mortality, and Left Ventricular Ejection Fraction (LVEF) assessed at baseline and one-month follow-up. Statistical analyses were performed using IBM SPSS version 20, with significance at P<0.05. Results: Baseline characteristics, procedural details, and initial TIMI flow grades were similar between groups. Adrenaline achieved universal TIMI 3 flow compared to 84% with verapamil (p=0.049), but no significant differences were noted in myocardial blush grades. Adrenaline led to significantly higher follow-up LVEF (45.0 ± 9.0 vs. 39.0 ± 9.0, p=0.027) and a more significant percentage change in LVEF (20.97% vs. 8.94%, p=0.042) than verapamil. Adverse event rates were comparable except for lower MACE incidence at 30 days with adrenaline (8.0% vs. 24.0%, p=0.039). Conclusion: Adrenaline notably enhanced TIMI 3 flow rates, improved left ventricular ejection fraction, and decreased significant adverse cardiovascular events at 30 days compared to verapamil. These findings suggest that adrenaline may be a superior option for improving coronary blood flow and early clinical outcomes in this patient population.

Intracoronary adenosine compared with adrenaline and verapamil in the treatment of no-reflow phenomenon following primary PCI in STEMI patients

Backgroundno-reflow can complicate up to 25% of pPCI and is associated with significant morbidity and mortality. We aimed to compare the outcomes of intracoronary epinephrine and verapamil with intracoronary adenosine in the treatment of no-reflow after primary percutaneous coronary intervention (pPCI). Methods108 STEMI patients had no-reflow during pPCI were assigned into four groups. Group 1, in which epinephrine and verapamil were injected through a well-cannulated guiding catheter. Group 2, in which same drugs were injected in the distal coronary bed through a microcatheter or perfusion catheter. Group 3, in which adenosine was injected through a guiding catheter. Group 4, in which adenosine was injected in distal coronary bed. Primary end point was the achievement of TIMI III flow and MBG II or III. Secondary end point was major adverse cardiovascular and cerebrovascular events (MACCEs) during hospital stay. ResultsThe study groups did not differ in their baseline characteristics. Primary end point was achieved in 15 (27.8%) patients in the guide-delivery arm compared with 34 (63%) patients in the local-delivery arm, p < 0.01. However, the primary end point did not differ between the epinephrine/verapamil group and the adenosine group (27 (50%) vs 22 (40.7%), p = 0.334). The secondary end points were similar between the study groups. ConclusionLocal delivery of epinephrine, verapamil and adenosine in the distal coronary bed is more effective in achieving TIMI III flow with MBG II or III compared with their guide-delivery in patients who suffered no-reflow during pPCI. There was no difference between epinephrine/verapamil Vs. adenosine.

Effect of post stenting Intracoronary Verapamil on Coronary Microcirculation in Primary PCI

Effect of post stenting Intracoronary Verapamil on Coronary Microcirculation in Primary PCI

The Immediate and Short-Term Outcomes of Patients with ST Elevation Myocardial Infarction with High Thrombus Burden Receiving Intracoronary Verapamil versus Epinephrine during Primary Percutaneous Coronary Intervention

Abstract Background When total coronary artery occlusion was found in the early hours of transmural myocardial infarction, most of our research interest and treatment strategies focused on epicardial coronary arteries. Little attention, however, is paid to the coronary microvasculature. When a coronary artery is occluded, detrimental changes occur in the cardiac capillaries and arterioles. After relief of the occlusion, blood flow to the ischemic tissue may still be impeded, a phenomenon known as no reflow. This abstract attempt to provide an in-depth understanding of this phenomenon and comparative review of two intracoronary agents used in no reflow settings. Aim of the Study This study is a comparative prospective study designed to compare between two agents‟ verapamil and adrenaline in treatment of no reflow in patients presenting with STEMI (ST elevation myocardial infarction) and a high thrombus burden developing no reflow during PPCI. Patients and Methods This study is a comparative prospective clinical trial designed to compare between two agents‟ verapamil and adrenaline in treatment of no reflow in patients presenting with STEMI and a high thrombus burden developing no reflow during PPCI. Results We have compared two of the proposed agents adrenaline and verapamil in the management of CNF and found out that verapamil is better in terms of improving LV functions but not the coronary flow. This further supported the consideration that MVO and CNF are two different entities and that we should be fully satisfied with restoration of coronary flow however all possible solutions should be spent to achieve adequate coronary perfusion so as not to give any change to MVO and microvascular dysfunction. We need a better understanding of the pathology of CNF and MVO for better solutions. It is time that we include agents more concerned with the ischemic reperfusion injury, looking at it not solely as a mechanical issue but also as an inflammatory and cellular pathology. Fighting the No reflow should be broad spectrum until such time we have a deep insight to the main pathology behind it. Conclusion The study concluded that the verapamil and adrenaline were not superior the standard treatment in term of TFG, but the verapamil was superior to both groups in improving the MBG while the adrenaline was not superior to the control group. The short-term outcomes were better in verapamil group than the adrenaline and control group who were equivocal.

Treatment of Refractory No-Reflow in Cardiac Catheterization Laboratory; Role of Intracoronary Verapamil (A Case Report)

The no reflow phenomenon is a feared complication in Percutaneous Coronary Intervention (PCI) procedures including elective as well as primary PCI (Percutaneous Coronary Intervention), and results in worse prognosis. A number of etiological factors are involved in pathogenesis of no reflow phenomenon. These include distal athero embolization, ischemic and reperfusion injury, microvascular spasm and endothelial dysfunction. The treatment of no reflow depends on underlying mechanism and includes pharmacological as well as non-pharmacological interventions. Pharmacological agents include vasodilators like adenosine, sodium nitroprusside, verapamil, in addition to adrenaline (intracoronary) and, GpIIa/IIIb inhibitors. Non pharmacological measures include mechanical thrombus aspiration. Among pharmacological agents, Verapamil is usually the least preferred agent because of its negative ionotropic effect. Here, we describe a case of refractory no reflow in a patient undergoing primary PCI to right coronary artery (RCA), which was treated with a no. of pharmacological agents as well as aspiration thrombectomy but without much success and finally responded to intracoronary verapamil.

Intracoronary epinephrine and verapamil in the refractory no-reflow phenomenon in patients with acute myocardial infarction

Despite modern advances in performing percutaneous coronary interventions, refractory no-reflow remains a serious problem that worsens in-hospital and long-term prognosis. Low-dose adrenaline may exhibit potent beta-receptor agonist properties that mediate coronary vasodilation.Aim. To evaluate the efficacy and safety of intracoronary administration of epinephrine and verapamil, as well as their combination, compared with standard treatment in patients with ST-segment elevation myocardial infarction (STEMI) and refractory no-reflow during percutaneous coronary interventions.Material and methods. Patients with STEMI and refractory no-reflow will be randomized into 4 groups: standard therapy, intracoronary adrenaline, intracoronary verapamil, intracoronary epinephrine + verapamil. All patients will be assessed for epicardial blood flow using the Thrombolysis in Myocardial Infarction (TIMI) and Myocardial Blush Grade (MBG) scales, peak troponin levels, ST segment changes, echocardiography, magnetic roesnance imaging, and dynamic single photon emission computed tomography.Results. Based on the pharmacodynamic effects of epinephrine and verapamil, their combination is expected to have a more potent vasodilating effect.Conclusion. If the Intracoronary administration of EPInephrine and VERapamil in the refractory no-reflow phenomenon (EPIVER) study will be successful, a novel, more effective method for managing refractory no-reflow phenomenon will appear. This will ensure better preservation of left ventricular systolic function, as well as improve the prognosis and clinical course of the disease.

Association of High Density Cholesterol With Hyperemic Epicardial Flow and Frame Count Reserve in Patients With Moderate Coronary Lesions and Slow Coronary Flow.

BackgroundPatients with microvascular angina and non-obstructive coronary atherosclerotic disease have an elevated risk of adverse events and all-cause mortality compared with individuals without ischaemic heart disease. The diagnosis coronary microvascular dysfunction in this setting relies on the detection of impaired coronary flow at rest or on calculation of coronary flow reserve. Previous studies demonstrate that the coronary flow reserve assessed by the corrected thrombolysis in myocardial infarction method - the frame count reserve is an objective quantitative alternative to other widely used invasive methods for microvascular status evaluation.PurposeWe assessed the significance of clinical, hemodynamic, angiographic variables and therapy with reference to FCR in a small group of patients with up to moderate atherosclerotic coronary lesions and slow coronary flow. Materials and methods: Frame count reserve was evaluated in 15 patients without flow-limiting (>50%) coronary stenoses admitted with unstable angina. Frame count reserve was calculated by dividing the baseline corrected thrombolysis in myocardial infarction frame count (cTFC) by the cTFC assessed after intracoronary infusion of 100 µg of the calcium channel blocker - verapamil.ResultsThe values of frame count reserve correlate positively with the levels of high density cholesterol (r= 0.900, p=0.001), inversely coronary flow after the application of verapamil - cTFCv (r= - 0.534, p=0.049). cTFCv was positively related with the levels of high density lipoproteins (r = - 0.645; p= 0.044) and was negatively influenced by the presence of atherosclerotic lesions at quantitative angiography (42.8±19.1 (n=8) vs 23±5.4 (n=7), p=0.029).The therapy with β-blocker and long-acting nitrate was associated with insignificantly higher frame count reserves after intracoronary verapamil compared to the continuous intake only of β-blocker or β-blocker and verapamil (2.1±0.78 vs 1.34±0.14 vs 1.70±0.70, p=NS).ConclusionsHigher high-density lipoproteins relate to higher frame count reserves evaluated using verapamil. The improved blood flow after this microvascular vasodilator is consistently positively related to high-density cholesterol and the lack of atherosclerosis at conventional coronary angiography. The combined intake of micro- and macrovascular vasodilator could be associated with higher frame count reserves compared to therapy with β-blocker and one vasodilating drug.

COMPARISON OF INTRACORONARY VERAPAMIL VS ADENOSINE FOR RESTORATION OF CORONARY BLOOD FLOW POST PERCUTANEOUS CORONARY INTERVENTION (PCI) IN PATIENTS WITH NO-REFLOW

Objective: To determine the efficacy of intracoronary verapamil vs adenosine in restoration of coronary blood flow, post PCI in patients with No-Reflow.&#x0D; Study Design: Double blind (patient/operator blind) randomized control trial.&#x0D; Place and Duration of Study: Cath lab of AFIC &amp; NIHD Rawalpindi, from Feb 2019 to Aug 2019.&#x0D; Methodology: A total of ninety (n=90) patients of either gender between age 25-80 years of age who underwent angioplasty for STEMI/NSTEMI demonstrating No-Reflow (thrombolysis in myocardial infarction 0,1,2) post PCI were enrolled and were randomized into two groups. Group A received verapamil 500 µg in 10 ml heparinized saline, given slowly over 1 minute and group B received adenosine 60 µg in 10 ml of heparinized saline, given quickly. After the administration of both drugs repeat angiogram was carried out and thrombolysis in Myocardial Infarction flow was assessed. Restoration of blood flow was defined as achievement of thrombolysis in myocardial infarction 3 grade.&#x0D; Results: Efficacy (restoration of thrombolysis in Myocardial Infarction grade 3) was better with intracoronary administration of verapamil when compared with intracoronary administration 2 of adenosine (84.4% vs 80%). The difference was, however, not statistically significant (p=0.581).&#x0D; Conclusion: Efficacy (restoration of thrombolysis in myocardial infarction grade 3) was not statistically significant between intracoronary administration of verapamil and adenosine in no-reflow cases after PCI in patients with STEMI/NSTEMI.

Post-dilatation improves stent apposition in patients with ST-segment elevation myocardial infarction receiving primary percutaneous intervention: A multicenter, randomized controlled trial using optical coherence tomography.

Stent failure is more likely in the lipid rich and thrombus laden culprit lesions underlying ST-segment elevation myocardial infarction (STEMI). This study assessed the effectiveness of post-dilatation in primary percutaneous coronary intervention (pPCI) for acute STEMI. The multi-center POST-STEMI trial enrolled 41 consecutive STEMI patients with symptom onset <12 hours undergoing manual thrombus aspiration and Promus Element stent implantation. Patients were randomly assigned to control group (n=20) or post-dilatation group (n=21) in which a non-compliant balloon was inflated to >16 atm pressure. Strut apposition and coverage were evaluated by optical coherence tomography (OCT) after intracoronary verapamil administration via thrombus aspiration catheter, post pPCI and at 7-month follow-up. The primary endpoint was rate of incomplete strut apposition (ISA) at 7 months after pPCI. There were similar baseline characteristics except for stent length (21.9 [SD 6.5] mm vs. 26.0 [SD 5.8] mm, respectively, P=0.03). In post-dilatation vs. control group, ISA rate was lower (2.5% vs. 4.5%, P=0.04) immediately after pPCI without affecting final TIMI flow 3 rate (95.2% vs. 95.0%, P>0.05) or corrected TIMI frame counts (22.6±9.4 vs. 22.0±9.7, P>0.05); and at 7-month follow-up (0.7% vs. 1.8%, P<0.0001), the primary study endpoint, with similar strut coverage (98.5% vs. 98.4%, P=0.63) and 1-year rate of major adverse cardiovascular events (MACE). In STEMI patients, post-dilatation after stent implantation and thrombus aspiration improved strut apposition up to 7 months without affecting coronary blood flow or 1-year MACE rate. Larger and longer term studies are warranted to further assess safety (ClinicalTrials.gov identifier: NCT02121223).

Coronary artery vasospasm and cardiogenic shock as the initial presentation for eosinophilic granulomatosis with polyangiitis

A 68-year-old woman presented to our hospital with unstable angina and was admitted for further evaluation. While hospitalized, she developed persistent angina with hypotension along with ST-segment elevation in leads V1–V2 along with lead aVR elevation on 12-lead electrocardiogram. Coronary angiography revealed diffuse multi-vessel coronary vasospasm most notably in the left anterior descending artery (LAD). Due to incomplete resolution of vasospasm with intracoronary verapamil and nitroglycerin, along with hemodynamic compromise requiring an intra-aortic balloon pump, percutaneous coronary intervention (PCI) of the LAD was performed. Clinical workup revealed hypereosinophlia and elevated IgE; diagnosis of eosinophilic granulomatosis with polyangiitis was confirmed with evidence of radiographic migratory pulmonary infiltrates and airway obstruction on spirometry. The patient had recurrent angina after PCI but her symptoms resolved fully after a course of corticosteroids. We attribute her refractory vasospastic angina to previously undiagnosed small/medium-vessel vasculitis.<Learning objective: We present a case of refractory coronary artery vasospasm in the setting of eosinophilic granulomatosis with polyangiitis (EGPA). Typically, calcium channel blockers and nitrates are used to treat hyperreactive narrowing of the coronary vasculature but we propose this case was refractory to standard treatment due to the underlying pathology of EGPA. Alternative causes of coronary vasospasm when standard therapies fail should be considered.>

GW26-e4476 Administration of intracoronary verapamil via self-made perfusion balloon to Treat No-Reflow Phenomenon following PCI in patients with Acute Coronary Syndromes

To evaluate the efficacy and safety of intracoronary administration of verapamil through self-made perfusion balloon, with 2∼4 holes punctured by needle at the end of a rapid exchange balloon, to treat impaired blood flow (no/slow reflow phenomenon, NSF) in patients with acute coronary syndrome (

«No-reflow» phenomenon: clinical aspects of reperfusion failure

«No-reflow» phenomenon is the most striking example of myocardial reperfusion clinical failure. It is caused by a lack of adequate blood flow in tissues after successful recanalization of infarct-related artery and is of multifactorial nature. The main reason for «no-reflow» is microvascular damage, of both structural and functional nature. Microvascular microemboli formation is also of particular importance in developing this phenomenon. In patients with acute coronary syndrome undergoing thrombolysis, percutaneous coronary intervention or coronary artery bypass surgery, the risk for «no-reflow» is about 30% or more. In case of planned endovascular interventions, «no-reflow» prevalence ranges from 0.3 to 2%. Patients with «no-reflow» have highly increased risk of complications such as reduced systolic function, heart muscle remodeling, dilatation, cardiac chambers hypertrophy/hyperplasia, left ventricular aneurysm etc. In addition, «no-reflow» increases the risk of death. Predisposition for «no-reflow» might be associated with a number of local and systemic factors. For diagnosing this phenomenon, angiographic grading of coronary blood flow restoration (Thrombolysis in Myocardial Infarction - TIMI) and myocardial perfusion (Myocardial Blush Grade - MBG) is recommended. For the most accurate «no-reflow» diagnosis, different methods for myocardium visualization might be used. The most studied treatments of ongoing «no-reflow» are: vasodilators administered intracoronary (verapamil, adenosine, sodium nitroprusside) at percutaneous coronary intervention or coronary artery bypass surgery; systemic antiplatelet agents; mechanical protection from distal embolization. Given the multifactorial nature of the «no-reflow», further search for the novel methods for prevention and treatment of this phenomenon is needed.

No-reflow phenomenon during PCI in acute myocardial infarction

No-reflow phenomenon complicates percutaneous coronary intervention in acute myocardial infarction. It significantly affects cardiac prognosis and clinical outcome. The underlying causes of no-reflow are ischaemia/reperfusion-related injury, coronary microcirculation injury and distal embolisation. Thrombolysis in myocardial infarction, myocardial blush grade and myocardial contrast echocardiography are commonly used to diagnose no-reflow phenomenon. Several pharmacological agents and mechanical devices effectively prevent and treat no-reflow. This article presents a patient with acute myocardial infarction who experienced no-reflow phenomenon during percutaneous coronary intervention. He is successfully treated with intracoronary nitroprusside, nitroglycerin (TNG), intra-arterial verapamil and intravenous abciximab.

Local Intracoronary Eptifibatide versus Mechanical Aspiration in Patients with Acute ST-Elevation Myocardial Infarction.

Objectives. We compared local delivery of intracoronary eptifibatide via perfusion catheter to thrombus aspiration in primary PCI. Background. Perfusion catheter increases local concentration of the drugs at the culprit site and prolongs their residency time. Methods. 75 patients with acute STEMI were randomized to three groups: 25 received local intracoronary eptifibatide and verapamil via perfusion catheter; 25 patients were managed by Diver CE thrombectomy device and 25 patients by primary PCI without thrombus aspiration. Primary end point was assessment of postprocedural TIMI flow, MPG, and corrected TIMI frame count (cTFC) in the culprit vessel. Results. Perfusion catheter was superior to thrombus aspiration and conventional PCI as regards MBG (68% versus 36% in Diver CE and 20% in the control arm; P value = 0.002), with shorter cTFC rates than thrombectomy and control groups (20.76 ± 4.44 versus 26.68 ± 8.40 and 28.16 ± 5.96, resp.; P = 0.001). TIMI flow was not different between the 3 groups. Eptifibatide led to less time to peak CK (13.12 hours versus 16.5 and 19.5 hours, respectively, P value = 0.001). Conclusion. Local intracoronary eptifibatide by perfusion catheter reduces thrombus burden with better results in microvascular perfusion assessed by cTFC and MBG compared to aspiration device or conventional PCI.

GW24-e0004 Safety and effectiveness of verapamil preventing no-reflow: A systematic review

ObjectivesTo evaluate the clinical efficacy and safety of verapamil injection for preventing slow-flow/no-reflow phenomenon after percutaneous coronary intervention.MethodsWe searched the Cochrane Central Register of Controlled Trials (CENTRAL) (Issue 2, 2012),...

Short‐term Effect of Verapamil on Coronary No‐Reflow Associated With Percutaneous Coronary Intervention in Patients With Acute Coronary Syndrome: A Systematic Review and Meta‐analysis of Randomized Controlled Trials

To evaluate the clinical efficacy and safety of intracoronary verapamil injection in the prevention and treatment of coronary no-reflow after percutaneous coronary intervention (PCI). Intracoronary verapamil injection may be beneficial in preventing no-reflow/slow-flow after PCI. We searched PubMed, Embase, and the Cochrane Central Register of Controlled Trials database. Randomized trials comparing the efficacy and safety of intracoronary verapamil infusion vs control in patients with acute coronary syndrome (ACS) were included. Meta-analysis was performed by RevMan 5.0 software (Cochrane Collaboration, Copenhagen, Denmark) . Seven trials involving 539 patients were included in the analysis. Verapamil treatment was significantly more effective in decreasing the incidence of no-reflow (risk ratio [RR]: 0.33; 95% confidence interval [CI]: 0.23 to 0.50) as well as reducing the corrected thrombolysis in myocardial infarction (TIMI) frame count (CTFC) (weighted mean difference: -11.62; 95% CI: -16.04 to -7.21) and improving the TIMI myocardial perfusion grade (TMPG) (RR: 0.43; 95% CI: 0.29 to 0.64). Verapamil also reduced the 30-day wall motion index (WMI) compared to the control. Moreover, the procedure reduced the incidence of major adverse cardiac events (MACEs) in ACS patients during hospitalization (RR: 0.37; 95% CI: 0.17 to 0.80) and 2 months after PCI (RR: 0.56; 95% CI: 0.33 to 0.95). However, administration of verapamil did not provide an additional improvement of left ventricular ejection fraction regardless of the time that had passed post-PCI. Intracoronary verapamil injection is beneficial in preventing no-reflow/slow-flow, reducing CTFC, improving TMPG, and lowering WMI. It is also likely to reduce the 2-month MACEs in ACS patients post-PCI.

Severe coronary vasospasm

A 50-year-old man, with chronic kidney disease and on dialysis, underwent coronary angiography in the context of acute coronary syndrome, which revealed focal lesions (type A) in the proximal left anterior descending and mid circumflex arteries. Ad-hoc angioplasty was performed on both lesions with direct stenting. An immediate drop in arterial blood pressure was observed and the angiogram showed new lesions with reduced flow throughout the coronary tree, progressing to cardiogenic shock and electromechanical dissociation. During cardiopulmonary resuscitation maneuvers, intracoronary verapamil was administered and TIMI 3 flow, sinus rhythm and a rise in blood pressure were obtained. Clinical stability was progressively restored. The patient was discharged medicated with calcium channel blockers and nitrates. During follow-up, he was twice readmitted for unstable angina. Coronary angiography revealed findings that could easily have been interpreted as new obstructive lesions, but these resolved after administration of intracoronary nitrates.

Grave vasoespasmo coronário

A 50-year-old man, with chronic kidney disease and on dialysis, underwent coronary angiography in the context of acute coronary syndrome, which revealed focal lesions (type A) in the proximal left anterior descending and mid circumflex arteries. Ad-hoc angioplasty was performed on both lesions with direct stenting. An immediate drop in arterial blood pressure was observed and the angiogram showed new lesions with reduced flow throughout the coronary tree, progressing to cardiogenic shock and electromechanical dissociation. During cardiopulmonary resuscitation maneuvers, intracoronary verapamil was administered and TIMI 3 flow, sinus rhythm and a rise in blood pressure were obtained. Clinical stability was progressively restored. The patient was discharged medicated with calcium channel blockers and nitrates. During follow-up, he was twice readmitted for unstable angina. Coronary angiography revealed findings that could easily have been interpreted as new obstructive lesions, but these resolved after administration of intracoronary nitrates.

Intracoronary Vasodilators for the No-Reflow Phenomenon

Objective: To review the literature relating to the use of intracoronary vasodilators to prevent and/or treat the no-reflow phenomenon in patients undergoing percutaneous coronary intervention (PCI). Data Sources: A literature search was conducted using MEDLINE (1966–March 2008) and Science Citation Index (1945–March 2008) using the search terms vasodilators, no-reflow, and intracoronary. Study Selection and Data Extraction: English-language clinical trials and case series were selected from articles retrieved. References of reviewed articles were examined for additional sources. Studies relating to the use of intracoronary vasodilators in the prevention and/or treatment of no-reflow in PCI were evaluated for safety and efficacy data. Articles relating to agents not available in the US were excluded. Data Synthesis: Evidence of intracoronary adenosine's utility in no-reflow treatment is limited. Its use in no-reflow prevention was associated with outcomes ranging from no difference to nearly an 88% reduction in no-reflow development; the drug was generally well tolerated. No-reflow treatment with intracoronary verapamil improved flow in 87–100% of cases. Preventive trials with verapamil failed to demonstrate efficacy. Atrioventricular block requiring treatment was the most commonly reported adverse event with intracoronary verapamil. Literature on intracoronary diltiazem and intracoronary nicardipine is limited. Both agents produced greater than 95% efficacy in no-reflow treatment, while prevention studies found no-reflow developing in less than 4% of patients. Although adverse event reporting was limited, hemodynamic instability was noted in patients receiving diltiazem. Response rates ranged from 73% to 100% when intracoronary nitroprusside was studied as treatment for no-reflow associated with acute myocardial infarction (AMI). Systemic hypotension was noted with nitroprusside administration. Conclusions: The available data are predominately from case series and retrospective reviews. Prevention of no-reflow with intracoronary vasodilators in elective PCI is not warranted. Nitroprusside should be considered first-line treatment in no-reflow associated with AMI.

Management of ‘no‐reflow’ complicating reperfusion therapy

No-reflow phenomenon, defined as inadequate myocardial perfusion of the adequately dilated target vessel without evidence of angiographic mechanical obstruction. It is a multifactorial, well-recognised, secondary phenomenon following reperfusion therapy such as thrombolysis or percutaneous coronary interventions (PCI). The pathophysiological mechanisms leading to the no-reflow state are incompletely understood. Embolization of the atheromatous material to the distal vasculature and intense arteriole vasospasm caused by microembolization of platelet-rich thrombi that release vasoactive agents resulting in microvascular obstructions are likely mechanisms. Current prophylaxis and management strategies are derived from limited clinical data. Intracoronary verapamil, adenosine and nitroprusside have been most frequently studied and administered for angiographic no-reflow during PCI for acute myocardial infarction or saphenous vein graft (SVG) lesions and have been shown to improve epicardial flow and microvascular perfusion. The use of distal embolic protection devices in SVG interventions also provide microvascular protection and improve clinical outcomes. However, by far the most important measures are prevention and anticipation during PCI as once no-reflow established, complete reversal of the situation may not be possible.