No-reflow phenomenon medical therapy
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Jennifer Giuseffi, M.D.; David M. Leder, M.D.; Ayokunle Olubaniyi, M.B,B.S [2]
Overview
Treatment
When no-reflow phenomenon is diagnosed, the mainstay of treatment is pharmacologic. The optimal management of no-reflow after restoration of coronary blood flow is unknown. More emphases are laid on prevention rather than the treatment.
Supportive Care
Most patients experience chest pain, hypotension and cardiac arrhythmias, therefore, attention to supportive measures is highly recommended. This involves analgesia, intravenous fluids, intravenous inotropic agents, temporary cardiac pacing, and the use of intraaortic balloon pump support if necessary.
Exclude All Mechanical Causes
Restore normal blood flow through epicardial coronary arteries and microvasculature to prevent persistence of myocardial ischemia. No-reflow needs to be distinguished from slow-flow resulting from coronary artery dissection, thrombus, coronary vasospasm, or residual stenosis. These etiologies must be excluded as part of the treatment of no-reflow. Ultimately, the goals are to improve outcomes, relieve chest pain and alleviate myocardial ischemia.
Administration of Vasodilators
Medications such as verapamil,[1] adenosine and nitroprusside[2] through the intracoronary route have been used with results. There have been contrasting studies regarding the use of adenosine. In a study, administration of a high dose of intracoronary adenosine was proven to improve coronary flow, prevent no-reflow phenomenon, improve ventricular function, and is associated with a more favorable clinical course.[3] Conversely, a more recent study found no evidence that the administration of adenosine and verapamil can reduce all-cause mortality and improve outcomes, however, there was an increase incidence of adenosine-induced hypotension and bradycardia.[4] Intracoronary nitroprusside was shown to improve CTFCs among patients with no-reflow and also with a lower incidence of hypotension and bradycardia.[2]
References
- ↑ Werner, GS.; Lang, K.; Kuehnert, H.; Figulla, HR. (2002). "Intracoronary verapamil for reversal of no-reflow during coronary angioplasty for acute myocardial infarction". Catheter Cardiovasc Interv. 57 (4): 444–51. doi:10.1002/ccd.10375. PMID 12455077. Unknown parameter
|month=ignored (help) - ↑ 2.0 2.1 Hillegass, WB.; Dean, NA.; Liao, L.; Rhinehart, RG.; Myers, PR. (2001). "Treatment of no-reflow and impaired flow with the nitric oxide donor nitroprusside following percutaneous coronary interventions: initial human clinical experience". J Am Coll Cardiol. 37 (5): 1335–43. PMID 11300444. Unknown parameter
|month=ignored (help) - ↑ Marzilli, M.; Orsini, E.; Marraccini, P.; Testa, R. (2000). "Beneficial effects of intracoronary adenosine as an adjunct to primary angioplasty in acute myocardial infarction". Circulation. 101 (18): 2154–9. PMID 10801755. Unknown parameter
|month=ignored (help) - ↑ Aung Naing, K.; Li, L.; Su, Q.; Wu, T. (2013). "Adenosine and verapamil for no-reflow during primary percutaneous coronary intervention in people with acute myocardial infarction". Cochrane Database Syst Rev. 6: CD009503. doi:10.1002/14651858.CD009503.pub2. PMID 23736949.