Aslanger pattern: A case report

Abstract

Patients with Aslanger pattern are characterized by a more conspicuous incidence of multivessel coronary artery disease, a more remarkable probability of chronic complete occlusion, and a more alarming rate of hospitalization. Owing to the insufficient understanding of electrocardiographic characteristics of Aslanger pattern by a multitude of clinicians, it is commonly undetected or misdiagnosed as reversible inferior myocardial ischemia, which gives rise to prolonged reperfusion time. The electrocardiographic characteristics of Aslanger pattern cannot be stereotyped. Aslanger pattern typically indicates a higher likelihood of multivessel disease and a prevalent occurrence of acute coronary occlusion, with electrocardiographic changes being complex in such cases of multivessel disease. Aslanger pattern must be managed in accordance with ST elevation myocardial infarction. Both emergency interventional therapy and coronary artery bypass grafting are appropriate.

Introduction

In 2020, Aslanger revolutionarily reported a specific type of electrocardiography (ECG) change in patients with acute myocardial infarction, with ST segment elevation in lead III, no ST segment elevation in lead II and aVF, and multiple lead ST segment depressions, which was termed as Aslanger pattern. Aslanger pattern describes a pathophysiologic process that is more compatible with ST elevation myocardial infarction (STEMI) rather than non-STEMI (NSTEMI). Patients with Aslanger pattern are characterized by a higher incidence of multivessel coronary artery disease, a higher probability of chronic total occlusion, and higher hospitalization and mortality rates. According to ST segment elevation of electrocardiographic characteristics, which is a crucial diagnostic indicator of acute myocardial infarction and one of the most valuable ECG findings, researchers have established a set of STEMI standards. However, it is crucial to acknowledge the limitations of these standards, as they overlook more than a quarter of acute coronary artery occlusions, leading to delayed revascularization.

Case report

A 59-year-old male patient was admitted to the hospital after experiencing “30 minutes of chest pain.” The patient developed chest pain without obvious cause. He arrived at the emergency department of The First People’s Hospital of Shaoguan City. An ECG suggested acute inferior wall myocardial infarction (Figure 1).

Figure 1.

ECG of the patient at the onset of chest pain. (Aslanger pattern ECG: sinus heart rate, III lead ST segment elevation, V2–V5 lead ST segment depression with T-wave terminal positive, aVR lead ST segment mild elevation). ECG: electrocardiography.

ECG interpretation: sinus heart rate, III lead ST segment elevation, V2–V5 lead ST segment depression with T-wave terminal positive, and aVR lead ST segment mild elevation. Acute troponin I level was 0.039 ng/mL (normal value: 0.0–0.05 ng/mL). A repeat high-sensitivity troponin I test 3 h later showed a level of 2990 ng/L (normal value: 0–500 ng/L). The patient experienced ventricular fibrillation in the emergency department. Electrical defibrillation was administered immediately. Subsequent to electrical defibrillation, it turned into sinus rhythm (based on ECG shown in Figure 2).

Figure 2.

ECG changes in sinus rhythm during and after the onset of ventricular fibrillation. ECG: electrocardiography.

The patient was sent to the intervention room for emergency interventional treatment. Previous history: He had a history of grade 2 hypertension. Personal history: Smoking history of more than 30 years, approximately 20 cigarettes/day. Preliminary diagnosis: Acute coronary syndrome and suspected acute inferior wall myocardial infarction. Emergency coronary angiography showed that the coronary artery was left dominant type. The left main coronary artery did not show significant stenosis. Opening stenosis of the left anterior descending coronary artery (LAD) was 50%–60%, and distal stenosis was 80%–90%. D2 proximal stenosis was 70%–80%, with thrombolysis in myocardial infarction (TIMI) grade 3. Proximal stenosis of the right carotid artery (RCA) was 30%–40%. Proximal stenosis of the posterior branch of the left ventricle was 60%–70%, with TIMI grade 3. The middle part of the left circumflex artery (LCX) was completely occluded, with TIMI grade 0. Considering LCX as the culprit blood vessel, interventional therapy was administered to LCX. Moreover, a 2.75 × 18-mm minimally invasive Firebird2 drug stent was implanted in the middle part of LCX. Then, a 3.0 × 9-mm Medtronic high-pressure balloon was used for dilation. No residual stenosis was found upon the re-examination of the angiography, as shown in Figure 3. Low density lipoprotein cholesterol level was 3.89 mmol/L (normal <3.36 mmol/L).

Figure 3.

(a) Distal LAD stenosis was 80%–90%. D2 proximal stenosis was 70%–80%; (b) Proximal stenosis of the RCA was 30%–40%. Proximal stenosis of the posterior branch of the left ventricle was 60%–70%, with TIMI grade 3; (c) the middle part of LCX was completely occluded, with TIMI grade 0; (d) a 2.75 × 18-mm minimally invasive Firebird2 drug stent was implanted in the middle part of LCX. Then, a 3.0 × 9-mm Medtronic high-pressure balloon was used for dilation. LAD: left anterior descending coronary artery; RCA: right carotid artery; TIMI: thrombolysis in myocardial infarction; LCX: left circumflex artery.

After LCX-percutaneous coronary intervention (PCI), the ECG changes of the patient were re-examined, as suggested in Figure 4 (in contrast to the first ECG analysis at admission to the hospital for chest pain: III leads fell back, the ST segment of V2–V4 leads returned to baseline, the ST segment of V5 and V6 leads was depressed with T-wave inversion, and the ST segment of aVR leads fell back). One month later, 80%–90% distal stenosis of the LAD was treated with 2.0 × 20-mm drug balloon dilatation.

Figure 4.

Compared with the first ECG analysis at admission to the hospital for chest pain: III leads fell back, the ST segment of V2–V4 leads returned to baseline, the ST segment of V5 and V6 leads was depressed with T-wave inversion, and the ST segment of aVR leads fell back. ECG: electrocardiography.

Discussion

Compared with patients with NSTEMI, patients with Aslanger pattern have a higher incidence of multivessel coronary artery disease, a higher probability of chronic complete occlusion, and a higher rate of hospitalization and mortality. ¹ The mechanism of Aslanger pattern may be the presence of transmural MI in the inferior wall on the basis of extensive subendocardial myocardial ischemia. In the case of extensive subendocardial ischemia, the comprehensive damage vector points were located at the upper right, which is similar to the direction of aVR leads, whereas the damage vector points were located at the bottom in the case of lower wall transmural MI. The resultant vector of the two vectors was directed to the right. Almost at a right angle to the aVF leads, it is projected to the negative of the II leads and the positive of the III leads, causing elevation of the III and/or aVR leads, and leftward of the I and V4–V6 leads, resulting in ST segment depression.^2,3

The V1 lead is the right thoracic lead, and the resultant vector may be slightly elevated to the right. In this case, coronary angiography showed complete occlusion in the middle part of LCX, combined with severe LAD stenosis and moderate stenosis in the distal left posterior ventricular branch of RCA. It is consistent with the coronary characteristics of multivessel disease in patients with Aslanger pattern. The culprit vessel is more common in the left circumflex branch than in the right coronary artery, which is consistent with thrombotic obstruction of LCX in this case. In the first ECG after LCX-PCI, the lower wall III leads fell back, the V2–V4 lead ST segment returned to baseline, the V5 and V6 lead ST segment was depressed with T-wave inversion, and the aVR lead ST segment fell back. Therefore, ST segment elevation in the III and aVR leads was analyzed as a result of LCX occlusion of the left dominant vessel, and ST segment depression in the V2–V4 leads was accompanied with positive T-wave endings.

However, ST segment depression was observed in the V5 and V6 leads after LCX-PCI, which was considered to be related to severe distal stenosis of the LAD. In this case, the elevation of V1 leads was not obvious. After 1 month, 80%–90% of the LAD stenosis was treated with medical balloon dilation. The ECG changes of the patient were re-examined after the second surgery and compared with the results of ECG analysis after the first LCX-PCI operation. The ST segment of the V5 and V6 leads returned to the baseline, and the T-wave was upright. This further confirmed that ST segment depression in V5 and V6 leads was caused by severe distal stenosis of the LAD, which was also in line with the coronary artery and electrocardiographic anatomical mechanism. Moreover, the corresponding coronary artery stenosis caused subendocardial myocardial ischemia, resulting in ST segment pressure and T-wave changes in the corresponding leads.

Summarizing and analyzing ECG changes of patients before and after two operations, ECG characteristics of Aslanger pattern are unlikely to be uniform. Aslanger pattern is more suggestive of multivessel lesions, and the ECG changes reflected by multivessel lesions are very complex. In cases of multivessel disease, ST segment elevation caused by occlusive vessels may be difficult to identify due to ST segment downshift caused by other ischemic stenosis vessels, and the elevation and downshift of ST segment may cancel each other out. The degree of multivessel stenosis and the location of the stenosis may affect the ECG characteristics of Aslanger pattern. The main ECG changes of Aslanger pattern are ST segment elevation in lead III, no ST segment elevation in lead II and aVF, which may be accompanied with ST segment elevation in lead AVR, ST segment depression in lead chest, and positive terminal T wave. The ECG changes of the thoracic leads are not specific and depend on the location and severity of LAD stenosis as well as the vascular diameters of RCA, LAD, and LCX.

Conclusion

Determining the presence of acute coronary occlusion (ACO) by ECG is a complex process. STEMI criteria were derived in the 1980s using only a set of myocardial enzyme data from patients with AMI, without the use of angiographic data. In recent decades, advances in coronary angiography, coronary CTA, and ECG interpretation have demonstrated that the STEMI pattern is flawed for identification (ACO). In 25% of patients diagnosed with NSTEMI, complete occlusion of the culprit vessel was found on delayed angiography. ⁴

We need to recognize the limitations of the current criteria, and new ECG findings are needed to compensate for the limitations^5,6 of this diagnostic criterion. In summary, it is extremely important to improve the understanding of ECG characteristics of Aslanger pattern. Moreover, for patients with Aslanger pattern, emergency coronary interventional therapy, antiplatelet aggregation therapy, and targeted treatment such as stabilizing plate should be administered. The occurrence of Aslanger pattern suggests that the culprit vessel is more common in the left circumflex branch than in the RCA. In addition, Aslanger pattern belongs to the high-risk group ACS, which further belongs to acute coronary artery occlusion myocardial infarction and is recommended to be treated as acute inferior STEMI. Timely coronary interventional therapy or coronary artery bypass grafting may save patients’ lives and reduce the mortality rate of AMI.^7,8 Currently, ECG with Aslanger pattern is often undetected or misdiagnosed as reversible inferior wall myocardial ischemia due to the lack of understanding of ECG characteristics by many clinicians, resulting in prolonged reperfusion time. Aslanger pattern must be managed according to STEMI; both emergency interventional therapy and coronary artery bypass grafting are appropriate. Thrombolytic therapy can be considered in the absence of interventional conditions, warranting further confirmation in future studies. ⁹

STEMI criteria are not the most accurate markers of ACO. The STEMI/NSTEMI model is highly flawed and hinders our progress in the diagnosis of ACO. We not only need to use STEMI patterns to identify ACO but should also actively look for new ECG patterns to indicate ACO. ¹⁰ New patterns should include the diagnosis of Wellens syndrome, De-Winter syndrome, and Aslanger syndrome. In the NSTEMI model, some studies have suggested that the maximum ST segment depression in leads V1–V4 (STDmaxV1–4) should be used as an index of posterior obstructive myocardial infarction(OMI) because a study demonstrated a specificity of 97% for the diagnosis of OMI, which is suggestive of ischemic STDmaxV1-4, and a specificity of 96% for OMI requiring PCI. ¹¹ The new OMI/NOMI paradigm is not limited to ECG; ultrasound, biomarkers, computed tomography, and conventional angiography are also requested if ECG results are inconclusive. It is expected that with the development of science, relevant computer models will help assist in the judgment of ACO.