DÄ internationalArchive20/2025Triage of Stable Patients With Suspected Acute Myocardial Infarction and Left Bundle Branch Block

Original article

Triage of Stable Patients With Suspected Acute Myocardial Infarction and Left Bundle Branch Block

A multicenter, propensity score–matched analysis

Dtsch Arztebl Int 2025; 122: 541-5. DOI: 10.3238/arztebl.m2025.0126

Macherey-Meyer, S; Heyne, S; Meertens, M M; Finke, K; Mauri, V; Terporten, J; Ahrens, I; Baer, F M; Eberhardt, F; Horlitz, M; Sinning, JM; Meissner, A; Rosswinkel, B; Baldus, S; Adler, C; Lee, S

Background: A pragmatic immediate invasive strategy is recommended in patients with ischemic symptoms and suspected left bundle branch block acute myocardial infarction (LBBB-AMI). It is important to identify patients with LBBB-AMI who do not need to be treated with the same strategy as those with ST-segment elevation myocardial infarction (STEMI). In this study, we aimed to compare the outcome of stable but symptomatic patients with suspected LBBB-AMI with that of matched STEMI patients.

Methods: All consecutive patients who were referred for percutaneous coronary intervention (PCI) in a metropolitan, multicenter STEMI network in Germany were analyzed and stratified according to their ECG findings (STEMI or LBBB). Propensity score matching (PSM) and adjusted analyses were performed.

Results: 4563 patients were included: 4219 (92.5%) with STEMI, and 344 (7.5%) with LBBB-AMI. After the identification of stable patients and PSM (n = 187 LBBB-AMI, n = 557 STEMI), the odds ratios for LBBB-AMI patients were 1.61 (95% confidence interval, [0.78; 3.32]) for in-hospital mortality, 0.56 [0.32; 0.91] for culprit lesion, and 2.18 [1.24; 3.84] for impaired patency of infarct-related artery after PCI. The median peak creatine kinase level was 1075 U/L in the STEMI patients and 478 U/L in the LBBB-AMI patients (estimated difference: –153 U/L [-504; 196]). Approximately, 70% of the LBBB-AMI patients had a culprit lesion in combination with myocardial necrosis implying acute stenosis.

Conclusion: Approximately, seven of ten symptomatic LBBB-AMI patients had acute culprit lesions requiring timely PCI. The findings support routine emergency coronary angiography in these patients. Future prospective trials should address more selective triage.

Cite this as:Macherey-Meyer S, Heyne S, Meertens MM, Finke K, Mauri V, Terporten J, Ahrens I, Baer FM, Eberhardt F, Horlitz M, Sinning JM, Meissner A, Rosswinkel B, Baldus S, Adler C, Lee S, on behalf of KIM e. V.: Triage of stable patients with suspected acute myocardial infarction and left bundle branch block: A multicenter, propensity score–matched analysis. Dtsch Arztebl Int 2025; 122: 541–5. DOI: 10.3238/arztebl.m2025.0126

LNSLNS

The electrocardiogram (ECG) is an important tool for timely triage of patients with persistent chest pain and suspected acute myocardial infarction (AMI) (1). In the event of typical ST-segment elevation in two contiguous ECG leads, patients are referred for immediate coronary angiography. The ECG criteria for conventional ST-segment elevation myocardial infarction (STEMI) are specific, but they have limitations: they cannot be used in patients with bundle branch block (1). Between 1% and 9% of patients with suspected AMI have a left bundle branch block (LBBB) (2, 3, 4, 5, 6, 7, 8, 9, 10, 11). Whether triage to immediate coronary angiography is beneficial in patients with LBBB-AMI remains controversial, as they have acute coronary occlusion less frequently than patients with STEMI (3, 6, 11, 12, 13, 14).

Several electrocardiographic criteria have been proposed—and subsequently refined—to predict AMI in the presence of LBBB (15, 16, 17, 18); however, their complexity limits applicability in daily routine. These ECG algorithms were not constructed or prospectively validated to predict culprit lesions or the need for emergency revascularization (6, 7, 19). ECG-based triage of LBBB-AMI is a frequent dilemma in modern emergency medicine.

Meanwhile, the European Society of Cardiology (ESC) recommends a pragmatic approach to patient triage: LBBB patients with signs and symptoms highly suspicious for ongoing myocardial ischemia should be managed in the same way as STEMI patients (1). This approach might give rise to frequent false-positive emergency activation of catheterization laboratories (13). Consequently, these patients are less often referred for an immediate invasive STEMI-equivalent strategy and experience delayed treatment in daily routine (2, 3, 4, 11, 20). The rate of emergency coronary angiography in suspected LBBB-AMI varies between 12% and 83% in the published literature, depending on the cohort, with higher rates reported in dedicated STEMI networks and lower rates in unselected chest pain cohorts (3, 11, 14). Hence, patient selection requires refinement. Derived from the non-ST-segment elevation acute coronary syndrome (NSTE-ACS) population (1), we hypothesized that symptomatic patients with suspected LBBB-AMI without clinical criteria for emergency coronary angiography are potential candidates for a delayed invasive strategy. The aim of the present study was therefore to characterize stable LBBB-AMI patients and to analyze outcomes in comparison to matched STEMI patients.

Material and methods

This retrospective, observational, multicenter cohort study included all consecutive patients diagnosed and treated in a local metropolitan infarction network (Cologne Infarct Model [Kölner Infarkt Modell, KIM]) within the period 1 January 2005 to 30 December 2020 in Cologne, Germany. The concept of KIM was described previously (21, 22, 23).

Patients without evidence of hemodynamic instability, acute heart failure, mechanical complications, life-threatening arrhythmia, or cardiac arrest were identified (Table 1). Then, propensity score matching (PSM) was used to control for potential confounding with regard to the outcome of treatment. Odds ratios (OR) and 95% confidence intervals (CI) were determined. The outcomes measured were:

  • In-hospital mortality
  • Cardiogenic shock
  • Culprit lesions
  • Stent implantation rate
  • Patency of the infarct-related artery (IRA) following percutaneous coronary intervention (PCI) (impairment defined by thrombolysis in myocardial infarction [TIMI] flow 0–2 = slow flow or no reflow)
  • Enzymatic infarct size (assessed using peak creatine kinase [CK] which has been described as a well correlating surrogate [24]).
Patient and procedural characteristics of the PSM cohort
Table 1
Patient and procedural characteristics of the PSM cohort

Further details are listed in the eMethods.

Results

Unadjusted analysis

A total of 4768 patients were registered in the infarction network. Of these, 4563 were eligible for analysis: 4219 (92.5%) with STEMI and 344 (7.5%) with LBBB-AMI (eFigure 1). The remaining 205 patients were excluded due to incomplete data on infarction type. The patient characteristics are summarized in eTable 1. The immediate invasive strategy was the predominant approach in both groups (99.0% and 98.2%).

Flow chart
eFigure 1
Flow chart
Patient and procedural characteristics
eTable 1
Patient and procedural characteristics

The unadjusted groups were imbalanced, with LBBB-AMI patients being the more morbid subgroup. LBBB-AMI patients were older, were more often transferred by the emergency medical services, and more often presented with pulmonary edema or ventricular fibrillation. They also more frequently required resuscitation, intubation, or administration of vasopressors. LBBB-AMI patients had a shorter symptom-to-contact time, and they were more likely to have oral anticoagulants or acetylsalicylic acid in their long-term medication.

The quantitative outcome analysis is presented in eTable 2. In-hospital mortality was 22.6% in the LBBB-AMI and 8.2% in the STEMI group (OR 3.26; 95% confidence interval [2.47; 4.30]). Cardiogenic shock was diagnosed in 33.9% of LBBB-AMI and 12.7% of STEMI patients (OR 3.54 [2.64; 4.76]). A culprit lesion was identified in 77.9% of LBBB-AMI and 89.8% of STEMI patients (OR 0.40 [0.30; 0.53]), and the corresponding stent implantation rates were 69.3% and 83.3%, respectively (OR 0.45 [0.35; 0.58]). Impaired flow in the IRA after PCI was found in 24.6% of LBBB-AMI and 12.6% of STEMI patients (OR 2.26 [1.70; 3.00]). The median peak CK level was 1141 U/L in STEMI and 800 U/L in LBBB-AMI patients. At discharge, LBBB-AMI patients were more often diagnosed with impaired systolic left ventricular function (eTable 2).

Clinical outcome analysis in stable patients following propensity score matching
Table 2
Clinical outcome analysis in stable patients following propensity score matching
Clinical outcome analysis in the unadjusted cohort
eTable 2
Clinical outcome analysis in the unadjusted cohort

Propensity score-matched analysis

Overall, 744 stable patients were eligible after PSM: 557 (75%) with STEMI and 187 (25%) with LBBB-AMI. The groups were well balanced within the adjusted covariates for logit propensity score calculation, and logit propensity score distribution was also similar between the groups (eFigure 2).

Group balance before and after propensity score matching
eFigure 2
Group balance before and after propensity score matching

The quantitative outcome analysis within the matched cohort is presented in Table 2. In-hospital mortality was 6.5% in the LBBB-AMI and 5.4% in the STEMI group (OR 1.21 [0.61; 2.42]). Cardiogenic shock was diagnosed in 6.9% of LBBB-AMI and 4.1% of STEMI patients (OR 1.75 [0.76; 4.07]). A culprit lesion was identified in 78.4% of LBBB-AMI and 86.7% of STEMI patients (OR 0.56 [0.36; 0.86]), and the corresponding stent implantation rates were 71.3% and 79.8%, respectively (OR 0.63 [0.42; 0.93]). Impaired flow in the IRA after PCI was found in 21.8% of LBBB-AMI and 14.3% of STEMI patients (OR 1.67 [1.05; 2.63]). The median peak CK level was 1075 U/L in STEMI and 478 U/L in LBBB-AMI (calculated difference: –153 U/L [−504; 196]).

Notably, LBBB-AMI patients with an identified culprit lesion had a median peak CK of 881 U/L (interquartile range [IQR] 2283), indicating acute lesions defined by the combination of flow-limiting stenosis and myocardial necrosis. The corresponding value was 1249.5 U/L (IQR 2394) in STEMI patients. Approximately 70% of LBBB-AMI patients presented with the combination of culprit lesion and myocardial necrosis indicating the need for the immediate invasive strategy.

At discharge, it was still the case that a higher proportion of LBBB-AMI patients than of STEMI patients had impaired systolic left ventricular function (Table 2).

Discussion

The present study is the first to focus on STEMI-equivalent treatment of stable patients with LBBB in combination with chest pain or an angina equivalent. The major findings in a well-matched cohort were as follows:

  • Seven out of ten symptomatic patients suspected to have LBBB-AMI had a culprit lesion in combination with myocardial necrosis, indicating acute stenosis.
  • LBBB-AMI patients more often had impaired IRA flow following PCI.
  • Lower peak CK levels, indicating a lower enzymatic infarct size, were detected in suspected LBBB-AMI patients, irrespective of whether or not a culprit lesion was identified.

In the present registry, patients with LBBB in combination with ischemic symptoms were urgently referred for immediate coronary angiography—the local triage is closely oriented on the pragmatic ESC guidelines. The ECG was interpreted by experienced and trained emergency physicians: this constitutes an important patient selection step. Overall, emergency coronary angiography was performed in 98.2% of suspected LBBB-AMI patients. Conversely, the management of these patients differed substantially from that described in the published literature. In other designated infarction networks, only 43.6% to 83% of suspected LBBB-AMI patients were referred for emergency coronary angiography (3, 11, 14). In emergency departments with less homogeneous chest pain cohorts, up to 10% of LBBB patients were triaged to emergency catheter examination (2, 25). Even delayed invasive coronary angiography was performed in only a minority of these suspected LBBB-AMI patients (2, 6, 25). Invasive treatment strategies are inconsistently applied. Their indication and timing define the dilemma of LBBB-AMI triage: On the one hand, identification of patients with acute coronary occlusion requiring emergency catheterization is of utmost interest, but on the other hand, discrimination of those LBBB patients with non-occlusive AMI is necessary to reduce unnecessary use of catheterization laboratory resources. While unadjusted analyses have indicated increased in-hospital and 1-year mortality rates and a higher prevalence of cardiogenic shock in LBBB-AMI than in STEMI (2, 3, 14, 20, 26), this has not been the case in adjusted comparison studies or in the present study considering clinical status and comorbidities (2, 3, 20). Unadjusted analysis of these outcomes is misleading, as suspected LBBB-AMI patients are per se a more morbid cohort. It is underlying chronic diseases rather than the suspected AMI event that tend to determine LBBB patients’ poorer prognosis (2, 3, 14, 20).

The present adjusted analysis leant on the assumption that suspected LBBB-AMI patients with chest pain or an equivalent without concurrent hemodynamic, respiratory, or electric instability criteria might be candidates for a delayed catheterization strategy. This hypothesis was adopted from patients with NSTE-ACS, in whom early or delayed invasive coronary angiography is recommended in the absence of the above-mentioned criteria (1, 27, 28). Following this practice, a culprit lesion was identified and treated in almost 80% of stable LBBB-AMI patients. The culprit lesion and coronary artery flow were assessed by the treating cardiologists, all of them experienced in interventional techniques. Around 22% of stable LBBB-AMI patients had TIMI 0–2 flow rate following PCI, compared with 14.3% of stable STEMI patients. As these patients were classified as “stable”, hemodynamic constraints such as shock do not explicitly explain this observation. Instead, stenosis characteristics or treatment strategies remain as potential confounders. Further explanation is required, and false-positive assessment of culprit lesions seems to be the most imputable factor considering the biomarker findings: In the suspected LBBB-AMI group, some patients had peak CK levels below the upper limit of normal. This is in line with prior reports (7). It seems plausible that in these patients chronic or subacute flow-limiting stenosis was present, rather than acute occlusion, and was misclassified as a culprit lesion. Nonetheless, in the remaining subgroup still seven out of ten stable LBBB-AMI patients had an acute stenosis. In these patients, the median peak CK was elevated more than five times the upper limit of normal, and this strengthens the validity of acute lesions. The high prevalence of true culprit lesions supports routine emergency coronary angiography in patients with suspected LBBB-AMI.

Even though pragmatic triage in a selected LBBB-AMI group is supported by our data, more targeted patient selection would be desirable. A few attempts at optimizing LBBB-AMI triage have been reported. Established ECG algorithms as stand-alone tool have limited accuracy in predicting acute coronary occlusion or the need for emergency coronary angiogram in LBBB-AMI (29) or STEMI (30). As another option, the utility of bedside echocardiography for better prediction of AMI in LBBB patients by evaluation of regional wall motion abnormalities has been tested in the emergency room setting. To date, however, the results have not been reliable (31).

Instead, a broader approach taking the whole clinical context into consideration might add value. An integrated concept combining ECG criteria with highly sensitive cardiac troponin T measurement has been proposed to predict AMI in chest pain patients with LBBB (6). However, this approach depends on the turnover time of biomarkers, delays coronary angiography, and does not discriminate sufficiently clearly between AMI and occlusive myocardial infarction (6). Especially those LBBB-AMI patients with type 2 myocardial infarction (32) should not, in theory, require an immediate reperfusion strategy.

While an optimized triage strategy has yet to be defined, the following open research questions can be derived from the present analysis and the pre-existing literature:

  • What is the optimal timing of coronary angiography in LBBB-AMI and in the subgroup of stable patients?
  • Should the pragmatic “one size fits all” approach of the ESC be routinely applied in all LBBB patients with ischemic signs and symptoms?
  • Should the presence of a culprit lesion or an acute coronary occlusion be preferred outcomes to (re)validate treatment algorithms (ECG +/- biomarkers), and define the optimal time to coronary angiography?

Limitations

This retrospective study needs to be interpreted in the context of the preselected patient cohort from a STEMI network: These patients had acute chest pain or an angina equivalent combined with LBBB at first medical contact (FMC), and they were intentionally referred for immediate coronary angiography. This preselection explains the high rate of coronary angiography in the investigated cohort. Moreover, this strategy increased the prevalence of culprit lesions, and the findings laid out above cannot be directly generalized to a broader LBBB cohort of patients with lower AMI prevalence. It remains uncertain how treating physicians assessed the ECG at FMC and the explicit clinical status. The registry does not file ECG recordings or ECG interpretations. Hence, retrospective assessment and adjudication is not possible.

A further limitation is that the time of onset of LBBB in the LBBB-AMI group was unknown—the registry structure does not permit differentiation between “pre-existing,” “new,” and “presumably new” conduction disturbance. However, this approach, irrespective of LBBB onset, reflects the pragmatic ESC guideline perspective and mirrors the challenge in everyday clinical practice. Moreover, pre-existing chronic diseases not documented in the registry may have contributed to decision making and the relationship between treatment and outcome. Missing data may also have had an impact on the observed effects and the treatment outcome relationship.

Notably, adjustment of the documented covariates dramatically reduced mortality rates in LBBB-AMI patients. This indicates unmeasured bias and a relevant impact of age on the treatment result, as LBBB-AMI patients are typically older than those with STEMI (2, 3). Propensity score matching was used to perform an adjusted analysis but is restricted to available or documented parameters. As the registry only included prespecified variables, bias arising from unmeasured variables was present.

Coronary angiograms are not archived in the registry. Consequently, we could not double-check the judgement of the experienced interventional cardiologists who performed the treatment. Finally, the 15-year treatment period implies performance bias. Guideline recommendations on the triage strategy remained constant, but revascularization techniques have evolved and this may have influenced the outcome of treatment.

Conclusion

Approximately seven out of ten symptomatic LBBB-AMI patients triaged within a STEMI network had acute lesions with myocardial necrosis requiring timely revascularization. This supports routine emergency coronary angiography in these symptomatic patients. Future prospective studies should aim to establish if even more selective triage is feasible and to clarify the role of clinical phenotypes.

Ethics statement

The study complies with the Declaration of Helsinki. The local ethical review board approved the registry study (No. 06–064), and written informed consent was obtained from all patients.

Acknowledgments

We thank all patients and physicians who participated in KIM. We further thank Tim Becker, Khalid Salem, and Greta Sommer for data extraction, and Petra Daniels and Jasmin Behler for their valuable support in the administration of KIM.

Funding

The KIM registry was funded in part by the Elisabeth and Rudolf Hirsch foundation.

Data sharing statement

The original data are available upon reasonable request from the authors.

Conflict of interest statement

SMM has received travel expenses from Bayer Vital AG and research grants from the Elisabeth and Rudolf Hirsch Foundation.

SH has received travel expenses from Eli Lilly and research grants from the German Heart Foundation.

JMS has received research grants from Boston Scientific, Edwards Lifesciences, and Medtronic, and was proctor for Medtronic and Boston Scientific. He is a scientific advisory board member for Abbott, Abiomed, Boston Scientific, Boehringer Ingelheim, and Medtronic, and has received speaker honoraria and travel expenses from Abbott, Abiomed, Astra Zeneca, Bayer, Boehringer Ingelheim, Boston Scientific, Bristol Myers Squibb, Edwards Lifesciences, Medtronic, Novartis, Novo Nordisk, Pfizer, Shockwave Medical, and Zoll,

SB has received lecture fees and travel expenses from Abbott, Edwards, AstraZeneca and JenaValve, and research grants from Abbott and AstraZeneca.

The remaining authors declare that no conflict of interest exists.

Manuscript received on 21 January 2025, revised version accepted on 7 July 2025

Corresponding author
Dr. med. Sascha Macherey-Meyer

sascha.macherey-meyer@uk-koeln.de

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University of Cologne, Faculty of Medicine and University Hospital Cologne, Clinic III for Internal Medicine, Cologne, Germany: Dr. med. Sascha Macherey-Meyer, Dr. med. Sebastian Heyne, Dr. med. Max Maria Meertens, Dr. med. Karl Finke, Dr. med. Victor Mauri, Dr. med. Johannes Terporten, Prof. Dr. med. Stephan Baldus, Dr. med. Christoph Adler, Dr. med. Samuel Lee
Cardiology III Angiology, Department of Cardiology, University Hospital, University of Mainz, Mainz, Germany: Dr. med. Max Maria Meertens
Department of Cardiology and Internal Intensive Care Medicine, Augustinerinnen Teaching Hospital, Cologne, Germany: Prof. Dr. med. Ingo Ahrens
Department of Medicine and Cardio-Diabetes Center Cologne, St. Antonius Hospital, Cologne, Germany: Prof. Dr. med. Frank Michael Baer
Cardiology and Internal Intensive Care Medicine, Protestant Hospital Köln-Kalk, Cologne, Germany: Dr. med. Frank Eberhardt
Department of Cardiology, Electrophysiology, and Rhythmology, Porz am Rhein Hospital gGmbH, Cologne, Germany: Prof. Dr. med. Marc Horlitz
Internal Medicine III – Cardiology, St. Vinzenz Hospital, Cologne, Germany: Prof. Dr. med. Jan-Malte Sinning
Department of Medicine II, Cologne Municipal Hospitals gGmbH, Merheim Hospital, Cologne, Germany: Prof. Dr. med. Axel Meissner
Institute for Medical Statistics and Bioinformatics, Medical Faculty and University Hospital, University of Cologne, Germany: Benjamin Rosswinkel
Patient and procedural characteristics of the PSM cohort
Table 1
Patient and procedural characteristics of the PSM cohort
Clinical outcome analysis in stable patients following propensity score matching
Table 2
Clinical outcome analysis in stable patients following propensity score matching
Flow chart
eFigure 1
Flow chart
Group balance before and after propensity score matching
eFigure 2
Group balance before and after propensity score matching
Patient and procedural characteristics
eTable 1
Patient and procedural characteristics
Clinical outcome analysis in the unadjusted cohort
eTable 2
Clinical outcome analysis in the unadjusted cohort
1.Byrne RA, Rossello X, Coughlan JJ, et al.: 2023 ESC Guidelines for the management of acute coronary syndromes. Eur Heart J 2023; 44: 3720–6 CrossRef MEDLINE
2.Stenestrand U, Tabrizi F, Lindback J, Englund A, Rosenqvist M, Wallentin L: Comorbidity and myocardial dysfunction are the main explanations for the higher 1-year mortality in acute myocardial infarction with left bundle-branch block. Circulation 2004; 110: 1896–902 CrossRef MEDLINE
3.Yeo KK, Li S, Amsterdam EA, et al.: Comparison of clinical characteristics, treatments and outcomes of patients with ST-elevation acute myocardial infarction with versus without new or presumed new left bundle branch block (from NCDR(R)). Am J Cardiol 2012; 109: 497–501 CrossRef MEDLINE
4. Sgarbossa EB, Pinski SL, Topol EJ, et al.: Acute myocardial infarction and complete bundle branch block at hospital admission: Clinical characteristics and outcome in the thrombolytic era. GUSTO-I Investigators. Global utilization of streptokinase and t-PA [tissue-type plasminogen activator] for occluded coronary arteries. J Am Coll Cardiol 1998; 31: 105–10 CrossRef MEDLINE
5.Neeland IJ, Kontos MC, de Lemos JA: Evolving considerations in the management of patients with left bundle branch block and suspected myocardial infarction. J Am Coll Cardiol 2012; 60: 96–105 CrossRef MEDLINE PubMed Central
6.Nestelberger T, Cullen L, Lindahl B, et al.: Diagnosis of acute myocardial infarction in the presence of left bundle branch block. Heart 2019; 105: 1559–67 CrossRef MEDLINE
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