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Incidence and treatment of 'no-reflow' after percutaneous coronary intervention
R N Piana1, G Y Paik, M Moscucci
1Charles A. Dana Research Institute, Boston, MA.
Insights
The no-reflow phenomenon, a reduction in coronary blood flow during interventions, affects 2% of patients. Intracoronary verapamil effectively restores flow, suggesting microvascular spasm as the cause.
Area of Science:
- Cardiology
- Interventional Cardiology
Background:
- The no-reflow phenomenon is a rare complication during percutaneous coronary intervention (PCI).
- It presents as reduced antegrade epicardial coronary flow with ischemia, despite no apparent dissection or obstruction.
- Previous studies suggested intracoronary verapamil may reverse this condition.
Purpose of the Study:
- To determine the prevalence of the no-reflow phenomenon during PCI.
- To evaluate the effectiveness of intracoronary verapamil in treating no-reflow.
- To explore the potential etiology of the no-reflow phenomenon.
Main Methods:
- A retrospective review of 1919 PCI procedures performed between January 1991 and April 1993.
- Identification of patients meeting criteria for the no-reflow phenomenon.
- Treatment analysis of patients receiving intracoronary verapamil for no-reflow versus mechanical obstruction.
Main Results:
- The no-reflow phenomenon occurred in 2.0% of PCI procedures (39 patients).
- Intracoronary verapamil improved TIMI flow grade in 89% of no-reflow patients.
- Verapamil showed minimal benefit in patients with mechanical obstruction (19% improvement).
Conclusions:
- The no-reflow phenomenon is observed in 2% of coronary interventions.
- Intracoronary verapamil administration is an effective treatment for no-reflow.
- The prompt response to verapamil suggests distal microvascular spasm as the likely cause.
Background:
Profound reduction in antegrade epicardial coronary flow with concomitant ischemia is seen occasionally during percutaneous coronary intervention despite the absence of evident vessel dissection, obstruction, or distal vessel embolic cutoff. In a prior small series of cases, this "no-reflow" phenomenon appeared to be promptly reversed by the intra-coronary administration of verapamil.
Methods And Results:
To further understand the prevalence of this syndrome and its responsiveness to the proposed therapy, we reviewed 1919 percutaneous interventions performed between January 1991 and April 1993. During the study period, 39 patients (2.0%) met our criteria for no reflow, 37 of whom were treated with intracoronary nitroglycerin followed by intracoronary verapamil and 2 of whom received intracoronary nitroglycerin alone. An additional 16 patients (0.8%) were given verapamil as part of the management of a flow-limiting dissection or distal embolus (mechanical obstruction). Intracoronary verapamil (50 to 900 micrograms, total dose) improved TIMI flow grade in 89% of no-reflow patients and markedly reduced the number of cineframes between contrast injection and opacification of a selected distal landmark (from 91 +/- 56 to 38 +/- 21 frames, P < .001). By contrast, only 19% of patients with epicardial mechanical obstruction showed improvement in TIMI flow grade after verapamil, with minimal reduction in frames to opacification (from 107 +/- 42 to 101 +/- 69, P = .73).
Conclusions:
The no-reflow phenomenon--reduction in distal flow without apparent dissection or distal embolization--occurs in 2% of coronary interventions. It generally responds promptly to intracoronary verapamil administration, suggesting that distal microvascular spasm may be its etiology.