Abstract
Background
The Aslanger pattern is a subtle electrocardiographic manifestation of inferior occlusion myocardial infarction that may not meet traditional ST-segment elevation criteria, particularly in the setting of multivessel coronary artery disease.
Case Summary
A 79-year-old man with known multivessel coronary artery disease presented with intermittent chest pain and was admitted for medical management of suspected unstable angina. Initial electrocardiogram (ECG) showed no acute ischemic changes. During hospitalization, he developed recurrent chest pain with subtle ECG findings consistent with the Aslanger pattern, which was not recognized at the time. Symptoms transiently resolved; however, on the following day, the ECG evolved to demonstrate overt inferior ST-segment elevation myocardial infarction. Emergent coronary angiography revealed left main and 3-vessel coronary artery disease with late stent thrombosis of the mid right coronary artery.
Discussion
This case illustrates how limited inferior wall injury combined with diffuse subendocardial ischemia in multivessel coronary artery disease can alter ST-segment vectors, masking an inferior occlusion myocardial infarction and delaying recognition.
Take-Home Message
Early recognition of the Aslanger pattern may facilitate timely diagnosis of inferior occlusion myocardial infarction and guide appropriate revascularization strategies in patients with multivessel coronary artery disease.
Key words: atherosclerosis, electrocardiogram, myocardial infarction
Visual Summary
Visual Summary.
Electrocardiographic Illustration of the Aslanger Pattern in Multivessel Coronary Artery Disease With Inferior Occlusion Myocardial Infarction
Competing inferior transmural and diffuse subendocardial ischemic vectors result in isolated ST-segment elevation in lead III with progression to overt inferior STEMI. CAD = coronary artery disease; OMI = occlusion myocardial infarction; STEMI = ST-segment elevation myocardial infarction.
History of Presentation
A 79-year-old man presented with intermittent chest pain. Serial cardiac biomarkers showed no significant dynamic change, and the presenting electrocardiogram (ECG) demonstrated no acute ischemic changes. He was admitted to the hospital for medical management of suspected unstable angina.
Take-Home Messages
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In the setting of multivessel coronary artery disease, limited inferior wall injury combined with diffuse subendocardial ischemia alters the resultant ST-segment vector, producing isolated ST-segment elevation in lead III (±aVR) without contiguous inferior lead involvement, characteristic of the Aslanger pattern.
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Failure to recognize this occlusion myocardial infarction pattern in the setting of multivessel coronary artery disease may delay emergent reperfusion, whereas early identification may guide revascularization by prioritizing lesions supplying the inferior wall for intervention.
Past Medical History
The patient had multivessel coronary artery disease with a history of multiple prior percutaneous coronary interventions and complex, high-risk multivessel coronary anatomy previously deemed not amenable to revascularization.
Investigations
The following day, the patient experienced a similar episode of transient chest pain accompanied by an ECG demonstrating subtle isolated ST-segment elevation confined to lead III without involvement of the other inferior leads, concomitant ST-segment depression in the lateral precordial leads (V4-V6) with terminally positive T waves, and a higher ST-segment in lead V1 compared with V2 (Figure 1).
Figure 1.
Electrocardiogram Demonstrating the Aslanger Pattern
Electrocardiogram showing isolated ST-segment elevation in lead III, ST-segment depression in the lateral precordial leads (V4-V6) with terminally positive T waves, and a higher ST-segment in lead V1 compared with V2.
Symptoms resolved after a single dose of sublingual nitroglycerin, and serial cardiac biomarkers remained without significant change. No further diagnostic escalation or cardiology involvement was pursued at that time. In the early hours of the following day, the patient developed recurrent chest pain of greater intensity. Repeat ECG demonstrated overt ST-segment elevation in the inferior leads, meeting criteria for an inferior ST-segment elevation myocardial infarction (STEMI) (Figure 2).
Figure 2.
Repeat Electrocardiogram Showing Overt ST-Segment Elevation in the Inferior Leads, Consistent With an Inferior STEMI
STEMI = ST-segment elevation myocardial infarction.
Management
After progression to overt STEMI, a STEMI protocol was activated, and the patient was taken emergently to the cardiac catheterization laboratory. Coronary angiography revealed known left main and 3-vessel coronary artery disease, with a late stent thrombosis of the mid right coronary artery identified as the culprit lesion causing a critical 90% stenosis, which was treated with plain old balloon angioplasty.
Outcome and Follow-Up
The patient underwent successful balloon angioplasty of the culprit right coronary artery lesion. Chest pain resolved after intervention, with improvement in ST-segment changes on subsequent ECG.
Discussion
The constellation of findings in the first ECG was consistent with the Aslanger pattern,1 a recognized manifestation of inferior occlusion myocardial infarction that may not meet traditional STEMI criteria, particularly in the setting of multivessel coronary artery disease.2 The subsequent ECG demonstrated progression to an overt inferior STEMI, reflecting an evolution in ECG expression. Failure to recognize the initial pattern resulted in delayed reperfusion.
The Aslanger pattern represents the vectorial result of competing injury currents. Inferior transmural ischemia generates an inferiorly directed injury vector, whereas diffuse subendocardial ischemia—commonly present in multivessel or left main coronary artery disease—produces opposing vectors that attenuate or cancel ST-segment elevation in contiguous inferior leads, particularly leads II and aVF. As a result, lead III, which is the most rightward and inferiorly oriented inferior lead, may remain the only lead demonstrating ST-segment elevation.
Importantly, manifestation of the Aslanger pattern requires a specific balance between inferior transmural ischemia and diffuse subendocardial ischemia. When these competing injury vectors are closely matched, ST-segment elevation in most inferior leads is neutralized. As inferior ischemia progresses or becomes more extensive—as occurred in this case—the inferior injury vector predominates, resulting in overt inferior STEMI. This ischemic transition may occur during early infarction, late infarction, or fluctuating ischemic states, explaining the dynamic ECG evolution observed.
An additional ECG observation was evolution of the QRS axis. The initial ECG showed a positive QRS complex in lead aVL with a slightly negative QRS in lead III, whereas the subsequent tracing demonstrated a negative QRS in lead aVL and a positive QRS in lead III, with terminal notching of the inferior QRS complexes. These findings suggest delayed conduction and loss of lateral wall electrical forces with mild rightward rotation of the mean QRS vector, consistent with evolving myocardial injury. Although not required for recognition of the Aslanger pattern, these changes further support dynamic ischemic involvement of the inferior and adjacent myocardial territories.
Conclusions
The Aslanger pattern represents an under-recognized ECG manifestation of inferior occlusion myocardial infarction in patients with multivessel coronary artery disease. Failure to identify this pattern may delay reperfusion and contribute to infarct progression.
Funding Support and Author Disclosures
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Disclaimer
The contents of this publication do not represent the views of the Veterans Affairs Caribbean Healthcare System, the U.S. Department of Veterans Affairs, or the United States Government.
Footnotes
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References
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