MUNICH — Switching from a 3-hour to a 1-hour high-sensitivity cardiac troponin pathway for patients with suspected myocardial infarction (MI) was safe, but unexpectedly, did not shorten emergency department (ED) stays in a large, pragmatic, real-world trial.

Despite delivering the second troponin result about 2 hours earlier, the accelerated pathway left median ED length of stay unchanged at 309 minutes, suggesting that simply making diagnostic information available sooner may not be enough to improve patient flow.

“The time point of diagnosis seems to be a different time point from the time point of ED discharge,” said principal investigator Christian Mueller, MD, of University Hospital Basel in Switzerland, presenting the findings here at the European Society of Cardiology (ESC) Congress 2026. “The availability of nurses and physicians rather than the availability of the information was the rate-limiting step,” he said.

The findings suggest hospitals hoping to improve ED throughput will need to address the broader workflow surrounding diagnosis and discharge, rather than simply accelerating biomarker testing. “We need to get the information in a smart way to the brain of the physician, and also we need to facilitate all the workflow after the diagnosis is made,” Mueller said during a press briefing prior to the session.

PRESC1SE-MI was simultaneously published in The Lancet.

Real-World Testing

Acute chest pain is one of the most common reasons for presentation to the ED, but only about 10% of these patients are ultimately found to have acute MI, said Mueller, adding that rapid identification of those who can safely be ruled out was important both clinically and for overcrowded EDs.

High-sensitivity cardiac troponin (hs-cTn) assays have progressively shortened assessment of suspected MI from repeat testing at around 6 hours to 3 hours, and subsequently, the ESC 0/1-hour pathway. 

The 0/1-hour approach has had a class I ESC recommendation since 2015, but uptake has been slow. Most evidence for its use has come from diagnostic studies and early-adopting hospitals, but questions remain about safe and effective implementation in hospitals that still use the older 0/3-hour pathway. 

PRESC1SE-MI used a pragmatic, stepped-wedge, cluster-randomized design involving 19 hospitals in 10 countries across four continents. Hospitals initially used their existing 0/3-hour pathway and were then randomized to earlier or later implementation of the 0/1-hour approach. 

Overall, the primary analysis included 67,624 patient presentations comprising 36,464 managed using the 0/3-hour pathway and 31,160 using the 0/1-hour pathway. The study was designed to test the 0/1-hour pathway for noninferiority on safety and superiority on efficacy. 

The primary safety endpoint was the composite of death from any cause or a new type 1 MI within 30 days. The primary efficacy endpoint was ED length of stay. The median age of patients was 59 years, approximately 45% were women, and 22% had known coronary artery disease. Eligible patients presented to the ED with acute nontraumatic chest pain and suspected MI.

ED Throughput

The 0/1-hour strategy met the prespecified criterion for noninferiority for the primary safety outcome. The composite outcome (all-cause death or new type 1 MI) occurred in 1.1% of presentations using the 0/1-hour pathway and 1.2% using the 0/3-hour pathway (adjusted odds ratio [OR], 0.93; 95% CI, 0.77-1.13; P for noninferiority = .0004).

The components of the composite, however, moved in different directions. All-cause death occurred in 0.8% with the 0/1-hour pathway vs 1.1% with the 0/3-hour pathway (adjusted OR, 0.84; 95% CI, 0.67-1.06), whereas new type 1 MI occurred in 0.3% vs 0.2%, respectively (adjusted OR, 1.55; 95% CI, 1.07-2.24). 

Mueller said the divergence requires further investigation. Exploratory subgroup analyses also suggested possible differences according to sex and the presence of known coronary artery disease, although these findings were hypothesis-generating and require confirmation. 

“We observed heterogeneity regarding sex and known coronary artery disease, with an apparent reduction in the primary safety outcome in women and in patients without known coronary artery disease,” he said.

The bigger surprise came with the efficacy endpoint. Implementation clearly accelerated testing. The median time to the second hs-cTn measurement fell from 190 minutes with the 0/3-hour pathway to 86 minutes with the 0/1-hour strategy. Yet median ED length of stay was 309 minutes for both strategies (ratio of adjusted median times, 1.00; 95% CI, 0.97-1.02; P = .65). Direct discharge from the ED increased only modestly from 71% to 74%. 

“Despite having the troponin result available including the second troponin result about 2 hours earlier, it did not result in shorter ED lengths of stay,” Mueller reported.

One explanation may be how the pathway was integrated into clinical workflow, Mueller suggested. Results became available in the electronic health record, but there was no automatic alert or integration into a clinical decision-support tool. Subsequent processes including physician review, further investigations, consultations, bed availability, and discharge arrangements could therefore remain bottlenecks. 

Safety Findings of Meta-Analysis

A second presentation provided a broader assessment of the randomized evidence. Jasper Boeddinghaus, MD, of University Hospital Bonn in Germany, presented an individual-participant-data meta-analysis of five randomized trials involving 110,933 patient presentations from 46 sites in 14 countries.

There was no clear difference in the composite safety endpoint of all-cause death or new type 1 MI within 30 days (pooled OR, 0.83; 95% CI, 0.45-1.53).

There was also no overall reduction in ED length of stay (pooled ratio, 1.03; 95% CI, 0.85-1.25), although there was substantial heterogeneity between trials. The pooled estimate for direct ED discharge was also inconclusive (OR, 1.31; 95% CI, 0.79-2.16). PRESC1SE-MI was by far the largest study and accounted for around 61% of patients in the meta-analysis. 

Boeddinghaus cautioned that the meta-analysis should be regarded as complementary to, rather than superseding, the individual trials.

Downstream Workflow 

Discussing both studies, Lori B. Daniels, MD, MAS, professor of cardiovascular medicine at the University of California San Diego, praised the real-world design of PRESC1SE-MI as a “massively ambitious logistical achievement” to pull off an “implementation trial like this, coordinating a protocol switch across 19 hospitals, 10 countries, and four continents.” She added that “a large implementation trial plus an updated meta-analysis is exactly the evidence that we’ve been missing.”

“Taken together, the studies provided a reassuring message on safety, with the composite finding showing noninferiority of a 0/1-hour versus a 0/3-hour pathway, but a more nuanced one regarding efficiency,” Daniels said. 

“We need to manage expectations. Faster serial biomarker testing alone won’t fix ED overcrowding. There are factors downstream, maybe in bed flow, imaging, and disposition decisions,” she said, pointing out that “studying other ED time points that ‘total length of stay’ can’t see [identify] might help.”

Daniels nevertheless highlighted the divergence within the PRESC1SE-MI safety endpoint, particularly the numerically higher incidence of new type 1 MI with the accelerated pathway, as something warranting additional scrutiny. “The new MI safety signal also deserves vigilance, not necessarily alarm, and deserves further study.” She also noted that the observed rate of the primary safety outcome of around 1.2% was considerably lower than anticipated compared with the 3% assumed in the trial’s sample-size calculation.

Overall, however, she said the findings should reassure clinicians already using accelerated troponin testing. “The 0/1-hour pathway is safe enough to keep using for fast rule-out,” Daniels concluded, “but don’t expect it alone to fix ED overcrowding.”

PRESC1SE-MI was funded by the Swiss National Science Foundation, Swiss Heart Foundation, University Hospital Basel, University of Basel, Foundation for Cardiovascular Research Basel, Fondazione Ricerca Molinette, Idorsia, and Roche. Mueller has reported institutional research grants from Innosuisse, Abbott, AstraZeneca, Beckman Coulter, bioMérieux, Boehringer Ingelheim, Mindray, MSD, Novartis, Novo Nordisk, Ortho Clinical Diagnostics, Quidel, SpinChip, Upstream, and SphingoTec; and institutional speaker or consulting honoraria from Abbott, AstraZeneca, Bayer, Boehringer Ingelheim, BMS, Daiichi Sankyo, Eli Lilly, Idorsia, MSD, Novartis, Novo Nordisk, Roche, Sanofi, Siemens, and SpinChip. Boeddinghaus has reported research grants from the University of Basel, University Hospital Basel, Division of Internal Medicine, Swiss Academy of Medical Sciences, Gottfried and Julia Bangerter-Rhyner Foundation, Freie Akademische Gesellschaft Basel, Swiss National Science Foundation, and Swiss Heart Foundation. He has also reported research support from Teleflex; honoraria from Siemens, Roche Diagnostics, QuidelOrtho, and Beckman Coulter; and travel support from Medtronic and Vascular Medical, all outside the submitted work.