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[Minimum salvaged myocardium after rescue percutaneous coronary intervention: quantification by cardiac magnetic
Juan M Ruiz-Nodar1, Eloísa Feliu, Jessica Sánchez-Quiñones
1Departamento de Cardiología, Hospital General Universitario de Alicante, Alicante, España.
Insights
Rescue percutaneous coronary intervention (PCI) after failed fibrinolysis in ST elevation myocardial infarction offers minimal myocardial salvage. Long delays from pain onset to artery opening likely explain the limited benefit of rescue PCI.
Area of Science:
- Cardiology
- Interventional Cardiology
- Cardiovascular Imaging
Context:
- ST-elevation myocardial infarction (STEMI) management often involves fibrinolysis.
- Rescue percutaneous coronary intervention (PCI) is indicated when fibrinolysis fails.
- Limited data exists on the extent of myocardial salvage achievable with rescue PCI.
Purpose:
- To quantify myocardial salvage after rescue PCI in STEMI patients using cardiac magnetic resonance (CMR).
- To evaluate the relationship between timing of intervention and myocardial salvage.
- To assess the impact of initial coronary artery patency on salvage outcomes.
Summary:
- Fifty STEMI patients underwent CMR within 6 days of rescue PCI.
- Myocardial salvage was assessed by comparing edema (area at risk) and late gadolinium enhancement (infarct size).
- The mean salvaged myocardium was 3% ± 4%, with a myocardial salvage index (MSI) of 9% ± 8%, indicating minimal salvage.
Impact:
- Rescue PCI demonstrates very limited myocardial salvage, likely due to significant delays from symptom onset to reperfusion.
- Findings suggest that optimizing timely reperfusion strategies is crucial for improving outcomes in STEMI.
- Cardiac magnetic resonance is a valuable tool for quantifying myocardial salvage and infarct size post-intervention.
Introduction And Objectives:
When fibrinolysis fails in patients with ST elevation myocardial infarction, they are referred for a rescue percutaneous coronary intervention (PCI). However, there is still no evidence of how much myocardium potentially at risk we can actually salvage after rescue PCI.
Methods:
Fifty consecutive patients. Cardiac magnetic resonance was performed within 6 days. Myocardial necrosis was defined by the extent of abnormal late enhancement, myocardium at risk by extent of edema, and the amount of salvaged myocardium by the difference between myocardium at risk and myocardial necrosis. Finally, myocardial salvage index (MSI) resulted from the fraction (area-at-risk minus infarct-size)/area-at-risk.
Results:
The mean time elapsed between pain onset and fibrinolitic agent administration was 176 ± 113 min; time lysis-rescue=PCI 209 ± 122 min; time pain onset-PCI = 390 ± 152 min. The area at risk was 37% ± 13% and infarct size 34.5% ± 13%. Salvaged myocardium was 3% ± 4% and MSI 9 ± 8. Salvaged myocardium and MSI were similar between patients with the artery open on arrival at the catheterization lab (Thrombolysis in Myocardial Infarction [TIMI] 3) and those with TIMI flow ≤ 2 (3.3% ± 3.6% and 8.2 ± 6.9 in TIMI 0-2 vs 3.0% ± 3.7% and 10.8 ± 10.9 in TIMI 3; P=.80 and 0.31, respectively). No significant difference was observed between patients who went through rescue PCI within a shorter time and those with longer delay times.
Conclusions:
The myocardial salvage after rescue PCI quantified by cardiac magnetic resonance is very small. The long delay times between pain onset and the opening of the infarct-related artery with PCI are most probably the reason for such a minimal effect of rescue PCI.
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