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Patients presenting with acute coronary occlusion, manifested by ST segment elevation myocardial infarction (STEMI), benefit from prompt reperfusion therapy, including either fibrinolysis or primary percutaneous coronary intervention (PCI).1 When considering reperfusion therapy with either PCI or fibrinolysis, delays are associated with a markedly higher rate of short-term and long-term mortality2; furthermore, increased time to initiation of reperfusion therapy from symptom onset is associated with increased risk of poor cardiac function with heart failure and other cardiovascular comorbidities.3 In patients with left bundle branch block (LBBB), the diagnosis of acute myocardial infarction (AMI) resulting from acute coronary occlusion is much more difficult; in fact, the LBBB ECG pattern is considered a confounder to the diagnosis of AMI. This diagnostic difficulty results from the altered depolarisation pattern encountered in LBBB…of course, altered depolarisation results in altered repolarisation, producing ST segment/T wave configurations which obscure the ECG findings of myocardial ischaemia and infarction.
The diagnostic challenge does not infrequently result in delays in the initiation of both PCI and fibrinolysis with associated less optimal outcomes in terms of both mortality and subsequent development of heart failure.4 While the LBBB pattern frequently confounds the ECG diagnosis of AMI, these patients are usually very ill on presentation, experiencing cardiogenic shock, acute heart failure and malignant dysrhythmias; thus, the clinician must consider AMI as a potential explanation for the severity of presentation in these ill patients with LBBB. Improved early recognition of AMI in this challenging population may improve outcomes.
The analysis in this study by Nestelberger et al 5 is based on three large, prospective, multicentre studies with a central adjudication of AMI applying the universal definition of AMI. Nestelberger et al 5 prospectively evaluated the use of ECG criteria combined with high-sensitivity troponin determinations for the diagnosis of AMI in patients …
Contributors All authors contributed equally to this manuscript.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.
Patient consent for publication Not required.
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