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Published on: June 28, 2019
Treatment of Slow-Flow After Primary Percutaneous Coronary Intervention With Flow-Mediated Hyperemia: The Randomized
Josep Gomez-Lara1, Montserrat Gracida1, Fernando Rivero2
1Hospital Universitari de Bellvitge, Institut d' Investigació Biomèdica de Bellvitge (IDIBELL), Universitat de Barcelona, L' Hospitalet de Llobregat Barcelona Spain.
Insights
Neither pharmacologic nor flow-mediated hyperemia effectively restored coronary flow in ST-segment-elevation myocardial infarction patients experiencing no reflow. Both treatments demonstrated similar, limited efficacy, highlighting the need for improved strategies to manage no reflow complications.
Area of Science:
- Cardiology
- Interventional Cardiology
- Microcirculation Research
Background:
- No reflow phenomenon post-primary percutaneous coronary intervention in ST-elevation myocardial infarction is linked to adverse clinical outcomes.
- Current treatments for no reflow, despite improving Thrombolysis in Myocardial Infarction flow, remain suboptimal.
- Flow-mediated hyperemia induced by saline infusion presents a novel approach to managing no reflow.
Purpose of the Study:
- To compare the efficacy of pharmacologic hyperemia versus flow-mediated hyperemia in improving coronary flow in ST-elevation myocardial infarction patients with no reflow.
- To assess microcirculatory resistance and Thrombolysis in Myocardial Infarction frame count following interventions.
- To evaluate the diagnostic potential of thermodilution patterns during flow-mediated hyperemia.
Main Methods:
- The RAIN-FLOW study randomized 67 patients with ST-elevation myocardial infarction and no reflow.
- Intervention groups included pharmacologic hyperemia (adenosine or nitroprusside) and flow-mediated hyperemia (saline infusion).
- Outcomes measured included angiographic corrected Thrombolysis in Myocardial Infarction frame count and minimal microcirculatory resistance using thermodilution and pressure-thermistor wire.
Main Results:
- No significant difference was observed in Thrombolysis in Myocardial Infarction frame count (40.2±23.1 vs. 39.2±20.7, P=0.858) or minimal microcirculatory resistance (753.6±661.5 vs. 993.3±740.8 Wood units, P=0.174) between the groups.
- The rates of Thrombolysis in Myocardial Infarction 3 flow were similar (26.7% vs. 27.0%, P=0.899).
- Flow-mediated hyperemia revealed distinct thermodilution patterns indicating no reflow severity.
Conclusions:
- Both pharmacologic and flow-mediated hyperemia demonstrated limited and comparable efficacy in restoring coronary flow.
- Flow-mediated hyperemia, coupled with thermodilution, offers a method to characterize no reflow severity and treatment response.
- No reflow in ST-elevation myocardial infarction is associated with high rates of in-hospital adverse events, necessitating further research for prevention and treatment.
Abstract:
Background ST-segment-elevation myocardial infarction complicated with no reflow after primary percutaneous coronary intervention is associated with adverse outcomes. Although several hyperemic drugs have been shown to improve the Thrombolysis in Myocardial Infarction flow, optimal treatment of no reflow remains unsettled. Saline infusion at 20 mL/min via a dedicated microcatheter causes (flow-mediated) hyperemia. The objective is to compare the efficacy of pharmacologic versus flow-mediated hyperemia in patients with ST-segment-elevation myocardial infarction complicated with no reflow. Methods and Results In the RAIN-FLOW (Treatment of Slow-Flow After Primary Percutaneous Coronary Intervention With Flow-Mediated Hyperemia) study, 67 patients with ST-segment-elevation myocardial infarction and no reflow were randomized to receive either pharmacologic-mediated hyperemia with intracoronary adenosine or nitroprusside (n=30) versus flow-mediated hyperemia (n=37). The angiographic corrected Thrombolysis in Myocardial Infarction frame count and the minimal microcirculatory resistance, as assessed with intracoronary pressure-thermistor wire, dedicated microcatheter, and thermodilution techniques, were compared after study interventions. Both Thrombolysis in Myocardial Infarction frame count(40.2±23.1 versus 39.2±20.7; P=0.858) and minimal microcirculatory resistance (753.6±661.5 versus 993.3±740.8 Wood units; P=0.174) were similar between groups. Thrombolysis in Myocardial Infarction 3 flow was observed in 26.7% versus 27.0% (P=0.899). Flow-mediated hyperemia showed 2 different thermodilution patterns during saline infusion indicative of the severity of the no reflow phenomenon. In-hospital death and nonfatal heart failure were observed in 10.4% and 26.9%, respectively. Conclusions Both treatments showed similar (and limited) efficacy restoring coronary flow. Flow-mediated hyperemia with thermodilution pattern assessment allowed the simultaneous characterization of the no reflow degree and response to hyperemia. No reflow was associated with a high rate of adverse outcomes. Further research is warranted to prevent and to treat no reflow in patients with ST-segment-elevation myocardial infarction. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT04685941.
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