Features and outcome of no-reflow after percutaneous coronary intervention

Abbo, Katherine M.; Dooris, Mark; Glazier, Sue; O’Neill, William W.; Byrd, David R.; Grines, Cindy L.; Safian, Robert D.

doi:10.1016/s0002-9149(99)80410-x

Cited by 261 publications

(144 citation statements)

References 15 publications

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“…Because tirofiban blocks the final common pathway of platelet aggregation and administration of tirofiban quickly resolved the no-reflow phenomenon, our experience is consistent with previous studies suggesting that platelets play a major role in noreflow phenomenon. 5) Why did tirofiban restore the flow in our patient but not in previous studies? [15][16][17] The most striking difference is our route of intracoronary administration rather than the intravenous adminstration used in previous studies.…”

Section: Discussioncontrasting

confidence: 57%

“…3) No-reflow phenomenon may lead to acute myocardial infarction and result in inhospital mortality. 4) Intracoronary administration of verapamil, 1) adenosine, 5) nicorandil, 6) papaverine, 7) urokinase, 8) or tissue-type plasminogen activator through the intravenous route 9) has been attempted to treat no-reflow phenomenon. However, none was found to promptly and effectively restore the coronary flow.…”

Section: Discussionmentioning

confidence: 99%

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Restoration of Normal Coronary Flow With Tirofiban by Intracoronary Administration for No-reflow Phenomenon After Stent Deployment

et al. 2005

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SUMMARYNo-reflow phenomenon is frequently observed during percutaneous coronary intervention in patients with acute coronary syndrome. It may jeopardize hemodynamic status or result in ischemic chest pain in these patients. Currently, there is no adequate solution for this problem. We report our experience with an acute coronary syndrome patient who developed no-reflow phenomenon associated with ST segment elevation and shock after percuteneous coronary balloon dilatation and stent deployment. Intracoronary administration of tirofiban immediately restored the coronary flow of the target vessel, and the disastrous condition reversed. Our experience suggests that intracoronary administration of tirofiban can be considered as an option in case of no-reflow phenomenon during percutaneous coronary intervention. (Int Heart J 2005; 46: 139-145)

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Section: Discussioncontrasting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Restoration of Normal Coronary Flow With Tirofiban by Intracoronary Administration for No-reflow Phenomenon After Stent Deployment

et al. 2005

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“…In these cases, distal embolization of plaque or thrombus from the lesion site is the likely mechanism. 11,12 Webb et al 13 reported the presence of particulate material in 21 of 23 distal protection device procedures, in which pathological examination revealed the presence of particles with a necrotic core of cholesterol clefts, lipid-rich macrophages, and fibrins.…”

Section: Discussionmentioning

confidence: 99%

No-Reflow Phenomenon and Lesion Morphology in Patients With Acute Myocardial Infarction

et al. 2002

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Background-The no-reflow phenomenon is associated with poor functional and clinical outcomes for patients with acute myocardial infarction (AMI). In the era of primary intervention, accurately identifying lesions at high risk of no reflow is of crucial importance. At present, no study into the relationship between lesion morphology and no reflow has been performed. The aim of this study was to investigate the relationship between preintervention intravascular ultrasound (IVUS) lesion morphology and the no-reflow phenomenon. Methods and Results-This study comprised 100 consecutive patients with AMI who underwent preintervention IVUS and were successfully recanalized with primary balloon angioplasty or stenting. IVUS was again performed to identify and exclude any mechanical vessel obstruction in cases of thrombolysis in myocardial infarction flow grade 0, 1, or 2 after intervention in the absence of angiographic stenosis. Angiographic no reflow was seen in 13 patients (13%). Univariate analysis indicated that hypercholesterolemia, fissure and dissection, lipid pool-like image, lesion, and reference external elastic membrane cross-sectional area correlate with the no-reflow phenomenon. Multivariate logistic regression analysis showed that lipid pool-like image (PϽ0.05; odds ratio 118; 95% CI, 1.28 to 11 008) and lesion elastic membrane cross-sectional area (PϽ0.05; odds ratio 1.55; 95% CI 1.01 to 2.38) are independent predictive factors of no-reflow phenomenon after reperfusion for AMI. Conclusions-Large vessels with lipid pool-like image are at high risk for no reflow after primary intervention for AMI.Also, plaque content may play a role in damage to the microcirculation after primary intervention for AMI.

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“…[1][2][3] The most common intracoronary agents used to induce hyperemia include adenosine, diltiazem, verapamil, papaverine, nitroglycerin, epinephrine, nicardipine, and sodium nitroprusside. 4 -10 The coronary hyperemic and systemic hemodynamic effects vary among and between these pharmacological agents.…”

mentioning

confidence: 99%

Coronary Hyperemic Dose Responses of Intracoronary Sodium Nitroprusside

Parham¹,

Bouhasin²,

Ciaramita³

et al. 2004

Circulation

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Background-Sodium nitroprusside is one of several agents considered effective for treating the no-reflow phenomenon during acute coronary interventions. However, the coronary hyperemic dose responses and systemic hemodynamic effects of intracoronary nitroprusside have yet to be determined in humans. The purpose of this study was to compare the hyperemic and hemodynamic responses of intracoronary nitroprusside to intracoronary adenosine in patients during cardiac catheterization with angiographically normal anterior descending arteries. Methods and Results-In 21 patients, coronary blood flow velocity (0.014-inch Doppler flow wire), heart rate, and blood pressure were measured in unobstructed left anterior descending coronary arteries at rest, after intracoronary adenosine (30-to 50-g boluses), and after 3 serial doses (0.3-, 0.6-, and 0.9-g/kg boluses) of intracoronary nitroprusside. Coronary reserve was calculated as hyperemia/basal coronary flow velocity. In an additional 9 patients with intermediate stenoses (53Ϯ7%), 14 fractional flow reserve (FFR) measurements (using 0.014-inch pressure wire) were performed with both intracoronary adenosine and nitroprusside (0.6 g/kg). Intracoronary nitroprusside produced equivalent coronary hyperemia with a longer duration (Ϸ25%) compared with intracoronary adenosine. Intracoronary nitroprusside (0.9 g/kg) decreased systolic blood pressure by Ͻ20%, with minimal change in heart rate, whereas intracoronary adenosine had no effect on these parameters. FFR measurements with intracoronary nitroprusside were identical to those obtained with intracoronary adenosine (rϭ0.97). Conclusions-Compared with adenosine, intracoronary nitroprusside produces an equivalent but more prolonged coronary hyperemic response in normal coronary arteries. Intracoronary nitroprusside, in doses commonly used for the treatment of the no-reflow phenomenon, can produce sustained coronary hyperemia without detrimental systemic hemodynamics. On the basis of FFR measurements compared with adenosine, sodium nitroprusside also appears to be a suitable hyperemic stimulus for coronary physiological measurements.

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Features and outcome of no-reflow after percutaneous coronary intervention

Cited by 261 publications

References 15 publications

Restoration of Normal Coronary Flow With Tirofiban by Intracoronary Administration for No-reflow Phenomenon After Stent Deployment

Restoration of Normal Coronary Flow With Tirofiban by Intracoronary Administration for No-reflow Phenomenon After Stent Deployment

No-Reflow Phenomenon and Lesion Morphology in Patients With Acute Myocardial Infarction

Coronary Hyperemic Dose Responses of Intracoronary Sodium Nitroprusside

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