Beyond Standalone Diagnostic Accuracy: Contextual and Methodological Considerations in ECG Interpretation for Suspected Pulmonary Embolism

To the Editor,We read with great interest the article by Smaniotto et al, entitled "Classical ECG findings in pulmonary embolism have minimal diagnostic accuracy: A cross-sectional study". 1 The authors should be congratulated for addressing a clinically relevant and frequently misunderstood issue: the limited diagnostic value of classical electrocardiographic (ECG) signs in suspected pulmonary embolism (PE).Their findings provide an important corrective to the persistent overemphasis on "classic" ECG patterns, particularly S1Q3T3, right bundle branch block, right ventricular (RV) strain, and sinus tachycardia.In their cohort of patients undergoing computed tomography pulmonary angiography for suspected PE, classical ECG abnormalities modestly increased post-test probability but were insufficient to rule in or rule out PE when used in isolation.This message is highly relevant for emergency, respiratory, and cardiovascular practice.However, we believe that the broader interpretation should not be that the ECG is clinically unhelpful in suspected PE.Rather, the study reinforces a more precise conclusion: the ECG is a poor standalone diagnostic test for PE, but it remains valuable as a contextual bedside tool.Its role is not to confirm or exclude PE independently, but to support differential diagnosis, identify alternative causes of acute chest pain or dyspnea, recognize rhythm disturbances, and provide indirect information about RV pressure overload or hemodynamic stress.This distinction between diagnostic accuracy and physiological interpretation is important.ECG abnormalities such as anterior and inferior T-wave inversion, right bundle branch block, right-axis deviation, S1Q3T3, and sinus tachycardia are neither specific nor sufficiently sensitive for PE.Nevertheless, when present in the appropriate clinical context, they may reflect acute RV strain, increased pulmonary vascular resistance, or evolving cardiopulmonary compromise.Conversely, their absence should not reassure clinicians when clinical probability, hypoxemia, syncope, D-dimer, imaging, or biomarkers suggest PE. 2 The study also highlights the need to move beyond binary interpretation of ECG findings.Traditional teaching often frames the ECG in PE as a search for named patterns, particularly S1Q3T3.This approach may be misleading because PErelated ECG changes represent a spectrum of cardiopulmonary stress rather than pathognomonic diagnostic signatures.In clinical practice, the ECG should be interpreted together with pre-test probability, oxygenation, hemodynamic status, cardiac biomarkers, computed tomography evidence of RV enlargement, and echocardiographic findings when available.A further point concerns heart rate interpretation.Smaniotto et al found sinus tachycardia to be independently associated with PE, but tachycardia is not universal in acute PE.Patients may present with normocardia or even unexpectedly low heart rates, particularly in the presence of beta-blockers, calcium-channel blockers, anti-arrhythmic drugs, pacemakers, conduction disease, advanced age, autonomic dysfunction, syncope, or severe hypoxemic deterioration.Thus, absence of tachycardia should not be interpreted as evidence against PE.A normal or slow pulse may be falsely reassuring when discordant with dyspnea, hypoxemia, syncope, RV strain, or poor perfusion.This is especially relevant because many clinical tools and bedside heuristics treat heart rate asymmetrically: tachycardia increases suspicion or risk classification, whereas absence of tachycardia may implicitly lower concern.The study by Smaniotto et al indirectly supports the need for more nuanced heart-rate interpretation in PE.Future studies should examine