Efficacy of intracoronary nicardipine in the treatment of no-reflow during percutaneous coronary intervention
✍ Scribed by Raymond I. Huang; Parul Patel; Paul Walinsky; David L. Fischman; J. David Ogilby; Mark Awar; Craig Frankil; Michael P. Savage
- Publisher
- John Wiley and Sons
- Year
- 2006
- Tongue
- English
- Weight
- 105 KB
- Volume
- 68
- Category
- Article
- ISSN
- 1522-1946
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✦ Synopsis
Abstract
Objectives: The goal of this study was to evaluate the safety and efficacy of nicardipine in reversing no‐reflow during percutaneous coronary intervention (PCI). Background: No‐reflow is a common complication of PCI in patients with acute coronary syndromes or venous bypass graft disease. Although nicardipine has an attractive pharmacological profile and has been used clinically to treat no‐reflow, there is a paucity of published data regarding its effectiveness in this setting. Methods: We conducted a retrospective analysis of 72 consecutive patients who received intracoronary nicardipine to reverse no‐reflow during coronary intervention. Qualitative TIMI flow grade and quantitative TIMI frame count methods were used to assess the efficacy of nicardipine. Results: A mean of 460 ± 360 mcg of intracoronary nicardipine was used. No‐reflow was successfully reversed with complete restoration of TIMI 3 flow in 71 of 72 patients (98.6%). TIMI flow grade improved from 1.65 ± 0.53 prior to nicardipine to 2.97 ± 0.24 after treatment (P < 0.001). TIMI frame count decreased from 57 ± 40 at the time of no‐reflow to 15 ± 12 after nicardipine administration (P < 0.001). Nicardipine therapy was well tolerated without adverse hemodynamic or chronotropic effects.Conclusions: In this largest series to date, intracoronary nicardipine was demonstrated to be a safe and highly effective pharmacological agent to reverse no‐reflow during PCI. © 2006 Wiley‐Liss, Inc.
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Percutaneous intervention in acute myocardial infarction has been associated with a high incidence of "no reflow," ranging from 11% to 30%, with an increased risk of complications. The role of intracoronary adenosine for the prevention of this phenomenon has not been evaluated fully. We studied the
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