Treatment of no-reflow in degenerated saphenous vein graft interventions: Comparison of intracoronary verapamil and nitroglycerin

Kaplan, Barry M.; Benzuly, Keith H.; Kinn, James W.; Bowers, Thomas A.; Tilli, Frank V.; Grines, Cindy L.; O’Neill, William W.; Safian, Robert D.

doi:10.1002/(sici)1097-0304(199610)39:2<113::aid-ccd1>3.0.co;2-i

Cited by 130 publications

(59 citation statements)

References 15 publications

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“…2 If vasoconstriction is one of the mechanisms, this would explain the favorable response seen with administration of a calcium antagonist. 12,16,17 Recent studies have demonstrated that TIMI 2 grade flow after PCI, which we defined as angiographic no reflow, may be caused by microvascular dysfunction sustained in the ischemic region. 12,18 Many mechanisms have been postulated for this microvascular dysfunction, including free radicals, 19 -21 cardiac sympathetic reflexes with resulting ␣-adrenergic macrovascular and microvascular constriction, 16 regional changes in angiotensin II receptor density, 22 and selectin-regulated interactions between activated polymorphonuclear leukocytes and the endothelium.…”

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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Section: Discussionmentioning

confidence: 99%

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

et al. 2002

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“…In cases of impaired flow during PCI, combination therapy of adenosine and nitroprusside has been shown to be safe and provides better improvement in coronary flow and MACE, as compared with adenosine alone [68] . Small trials suggest that there may be a role for prophylactic use of intracoronary calcium channel blockers, especially verapamil, because they seem to prevent no-reflow in some patients by reversing the calcium-mediated distal microvascular spasm [71,72] . Although the benefit of intracoronary delivery of adjunctive pharmacologic agents such as calcium channel blockers, adenosine and nitroprusside is limited to small studies showing reduction of embolization rates and not clinical outcomes, they are still useful in the catheterization laboratory.…”

Section: Vasodilatorsmentioning

confidence: 99%

Coronary thrombus in patients undergoing primary PCI for STEMI: Prognostic significance and management

Vecchio¹

2014

WJC

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Acute ST-elevation myocardial infarction (STEMI) usually results from coronary atherosclerotic plaque disruption with superimposed thrombus formation. Detection of coronary thrombi is a poor prognostic indicator, which is mostly proportional to their size and composition. Particularly, intracoronary thrombi impair both epicardial blood flow and myocardial perfusion, by occluding major coronary arteries and causing distal embolization, respectively. Thus, although primary percutaneous coronary intervention is the preferred treatement strategy in STEMI setting, the associated use of adjunctive antithrombotic drugs and/or percutaneous thrombectomy is crucial to optimize therapy of STEMI patients, by improving either angiographical and clinical outcomes. This review article will focus on the prognostic significance of intracoronary thrombi and on current antithrombotic pharmacological and interventional strategies used in the setting of STEMI to manage thrombotic lesions.© 2014 Baishideng Publishing Group Inc. All rights reserved. Key words: ST-elevation myocardial infarction; Intracoronary thrombosis; Primary percutaneous coronary intervention; Antithrombotic therapies; Coronary thrombectomyCore tip: Intracoronary thrombosis, is the basic pathophysiologic event in acute ST-elevation myocardial infarction (STEMI), and thrombi are very frequently detected in STEMI patients undergoing primary percutaneous coronary intervention (PPCI). Thrombus burden and components are important determinants of prognosis in STEMI, being well-known risk factors for longterm adverse cardiovascular events, distal embolization and stent thrombosis. As a result, percutaneous management of lesions with a consistent thrombotic burden is still challenging in the setting of PPCI for STEMI. Therefore, several pharmacological and interventional strategies, such as thrombectomy have been developed in order to improve PPCI's safety and efficacy, by reducing thrombus burden.

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“…Despite the limited effects on coronary blood flow, the ability to produce epicardial vasodilation and blunt coronary vasospasm without adversely altering coronary flow reserve made IC calcium channel blockers the favored agents for the treatment of the no-reflow phenomenon. [15][16][17][18][19][20][21] Fugit et al 15 examined IC nicardipine, diltiazem, and verapamil to define their effects on coronary blood flow velocity in humans. IC nicardipine (200 g), diltiazem (1 mg), and verapamil (200 g) were serially administered in a randomized, double-blinded fashion in minimally diseased LAD and circumflex arteries in 9 patients.…”

Section: Comparison With Other Pharmacological Hyperemic Stimulimentioning

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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Treatment of no-reflow in degenerated saphenous vein graft interventions: Comparison of intracoronary verapamil and nitroglycerin

Cited by 130 publications

References 15 publications

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

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

Coronary thrombus in patients undergoing primary PCI for STEMI: Prognostic significance and management

Coronary Hyperemic Dose Responses of Intracoronary Sodium Nitroprusside

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