Key result
Occluded culprit vessel yields no difference in 5-year mortality vs patent vessel in NSTEMI.
Why the study?
Patients with NSTEMI and an occluded culprit vessel represent a unique subset, but their long-term outcomes remain unclear.
Does pre-procedural TIMI 0-1 flow (occluded culprit vessel) increase long-term mortality compared to TIMI 2-3 flow in NSTEMI patients undergoing PCI?
Cohort (n=1,525)
No
Does pre-procedural TIMI 0-1 flow (occluded culprit vessel) increase long-term mortality compared to TIMI 2-3 flow in NSTEMI patients undergoing PCI?
Hazard Ratio: 1.08 (95% CI 0.49–2.32)
Absolute Event Rate: 16% vs 18%
p-value: p=0.34
NSTEMI patients presenting with occluded culprit vessels have similar long-term mortality following PCI compared to those with patent vessels, suggesting equivalent benefit from revascularization.
Similar long-term mortality after PCI in NSTEMI regardless of culprit patency; leaves open whether pre-procedural TIMI flow should guide decisions.
Background/Objectives: People with non-ST-segment elevation myocardial infarction (NSTEMI) with an occluded culprit vessel represent a unique subset of patients; however, their long-term outcomes remain unclear. This study aimed to compare 5-year mortality between NSTEMI patients treated with percutaneous coronary intervention (PCI) based on TIMI flow states in the culprit vessel on presentation (TIMI 0-1 compared to TIMI 2-3). Methods: A retrospective analysis of prospectively collected data of all NSTEMI patients who underwent PCI from 2012 to 2019 at a tertiary cardiac center (The Freeman Hospital, Newcastle-Upon-Tyne, UK) with follow up for 5 years until January 2024. Patients were identified from the database and categorized based on pre-procedural TIMI flow in the culprit vessel. A propensity score was used to pair TIMI 0-1 patients with a matched cohort of TIMI 2-3 patients. The primary outcome was 5-year all-cause mortality. Results: A total of 775 patients with TIMI 0-1 flow were matched with 750 patients who had TIMI 2-3 flow. Patients with TIMI 0-1 flow were more likely to have transient ST elevation (24% vs. 18%, p < 0.001) or Q waves (4% vs. 1%, p < 0.001) compared with patients who had TIMI 2-3 flow. They were also more likely to have moderately to severely impaired left ventricular systolic function compared with patients with TIMI 2-3 flow (21% vs. 16%, p = 0.01). In-hospital mortality (1.2% vs. 1.2%, p = NS), 1-year mortality (5% vs. 6.9%, p = NS), and 5-year mortality (16% vs. 18%, p = 0.34) were not significantly different between the two groups. The use of glycoprotein IIb/IIIa antagonists was associated with lower mortality, HR 0.64 (0.46 to 0.87). Conclusions: NSTEMI patients with occluded culprit vessels who underwent PCI had similar in-hospital and long-term outcomes to patients with patent culprit vessels. The use of glycoprotein IIb/IIIa inhibitors appears to be associated with lower mortality.
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Abdeldayem et al. (2026) conducted a cohort in NSTEMI with percutaneous coronary intervention (n=1,525). Pre-procedural TIMI 0-1 flow (occluded culprit vessel) vs. Pre-procedural TIMI 2-3 flow (patent culprit vessel) was evaluated on 5-year all-cause mortality (HR 1.08, 95% CI 0.49-2.32, p=0.34). NSTEMI patients with an occluded culprit vessel (TIMI 0-1) undergoing PCI had similar 5-year all-cause mortality compared to those with a patent vessel (16% vs 18%, p=0.34).
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