Uncommon culprit artery leading to atypical de winter electrocardiographic changes: a case report

Abstract

Background

A subset of patients with acute coronary artery occlusion requiring emergency revascularization, does not present with the typical ECG features of ST-segment elevation myocardial infarction (STEMI).Timely identification of these atypical presentations is crucial.

Case presentation

This report describes a 55-year-old male patient who was admitted to the emergency department with chest pain. The electrocardiogram (ECG) recorded atypical de Winter electrocardiographic changes and their evolution.

Results

Coronary angiography confirmed the occlusion of the second diagonal branch (D2). The patient’s condition improved after D2 balloon angioplasty.

Conclusion

De Winter electrocardiographic changes can also be observed in D2 occlusions and may present with milder manifestations. Timely recognition of these changes holds significant clinical value.

Background

A subset of patients with acute coronary artery occlusion requiring emergency revascularization, does not present with the typical ECG features of ST-segment elevation myocardial infarction (STEMI), despite having significant arterial stenosis or acute occlusion. Timely identification of these cases is crucial. De Winter electrocardiographic changes are one of the atypical ECG manifestations of acute myocardial ischemia, first described by de Winter et al. in 2008 [1]. This ECG feature is commonly seen in patients with proximal left anterior descending (LAD) artery occlusion. However, an increasing number of case reports in recent years suggest that de Winter ECG changes are also be associated with occlusion in other coronary arteries. This article reports a rare case of de Winter ECG changes caused by acute occlusion of the second diagonal branch (D2).

Case presentation

A 55-year-old male patient was admitted with 4 h of persistent, non-radiating precordial chest pain without other accompanying symptoms.Emergency routine electrocardiogram (ECG)(Fig. 1) showed sinus rhythm (75 bpm), QS pattern in lead aVL, preserved R wave amplitude in leads V1 to V3, upsloping ST-segment depression of 0.1 mv with upright T waves in leads V2 to V4, downsloping ST-segment depression of 0.05 mv with biphasic T waves in leads II, III and aVF, straightening of the ST-segment in leads aVL and I with loss of the ST-T wave angle in association with upright, symmetrically peaked T waves. ECG diagnosis: sinus rhythm, suspected de Winter ECG changes, in association with ischemia of the basal lateral wall. Elevated high-sensitivity troponin I on admission: 0.14 ng/ml (normal range < 0.11 ng/ml), normal levels of emergency myocardial enzymes, D-dimer, and electrolytes. History of diabetes mellitus. The attending physician suspected a de Winter ECG pattern, and administered enteric-coated aspirin 300 mg, clopidogrel 180 mg, and atorvastatin calcium 40 mg orally, and decided to repeat the ECG after anti-ischemic therapy had been administered. Subsequent repeated routine ECGs showed gradual “recovery” of ST-T changes to normal, with ECG at 4.5 h shown in Fig. 2: poor R wave progression in lead V2, no ST-T abnormalities, decreased T wave amplitudes in leads I, aVL, V2 to V4.The patient’s chest pain symptoms improved but did not completely resolve.Repeat high-sensitivity troponin I further increased to 0.65 ng/L. Coronary angiography at 5 h revealed: no stenosis in the left main (LM), 40% stenosis in the mid-segment of the left anterior descending (LAD) artery, 85% stenosis in the distal segment of LAD, occlusion of the second diagonal branch (D2), diffuse disease in the left circumflex (LCX) artery with approximately 50-60% stenosis, collateral supply of the right coronary artery (RCA) from the left coronary artery, 50% ostial RCA stenosis, and chronic occlusion in the proximal segment, as shown in Fig. 3. The patient underwent D2 drug-eluting balloon angioplasty, with post-procedural angiography showing TIMI III flow in the distal segment, as shown in Figure B. Postoperative repeat routine ECG (Fig. 4) showed abnormal Q waves in lead aVL, I and V2,horizontal ST-segment depression of 0.05 mv in leads II, III, and aVF, and inverted T waves in leads I and aVL. Echocardiography revealed a left ventricular ejection fraction of 68%. The patient improved and was discharged with a recommendation for scheduled treatment of the RCA occlusive lesion.

Fig. 1

The patient’s initial electrocardiogram in the emergency department

Fig. 2

The patient’s electrocardiogram re-examination at 4.5 h

Fig. 3

(a) Arrow indicates occlusion in D2. (b) Arrow indicates balloon angioplasty in D2 post-procedure. (c) Arrow indicates chronic occlusion in the proximal RCA

.

Fig. 4

Post-balloon angioplasty re-examination electrocardiogram of the patient’s D2

Discussion

In 2008, de Winter et al. reviewed the electrocardiograms (ECGs) of 1,532 cases of acute coronary syndrome (ACS) with proximal left anterior descending (LAD) artery occlusion and found that 30 of these cases did not present the typical hyperacute ECG pattern of ST-elevation myocardial infarction (STEMI) [1]. The characteristic ECG features of the de Winter pattern include: (1) depression of the J point by 1–3 mm in precordial leads V1-V6, with upsloping ST-segment depression followed by tall, symmetric T waves; (2) a normal or slightly widened QRS complex; (3) poor R wave progression in some patients; and (4) mild ST-segment elevation in lead aVR. The 2018 Fourth Universal Definition of Myocardial Infarction guidelines by the European Society of Cardiology [2] first mentioned the de Winter ECG pattern, recognizing it as an atypical manifestation of acute myocardial ischemia due to LAD occlusion. The most logical explanation for the tall, peaked T wave and moderate ST-segment depression is the occurrence of a delay in repolarization in the subendocardial region, with a change in the transmembrane action potential shape (slow rise time and long duration).However, an increasing number of case reports have indicated that this ECG pattern is not exclusive to LAD proximal-mid occlusion, and it has been associated with occlusions of the left main (LM), left circumflex (LCX), right coronary artery (RCA), multiple-vessel disease, the first diagonal branch (D1), and the intermediate branch [3,4,5,6,7,8].

In this case, the ECG on admission showed upsloping ST-segment depression and upright T waves in leads V2-V4, without ST-segment elevation. Combined with the patient’s persistent chest pain and elevated troponin I levels, this suggested a diagnosis of a case of ACS manifesting the de Winter ECG changes and taller than normal T waves in leads aVL and I, indicating that the likely culprit vessel was the proximal LAD.Careful observation (show in Fig. 1) revealed a QS pattern in lead aVL and a low-amplitude r wave in lead V2,suggesting that the ischemic area also involved the aVL and V2 lead regions.Potential culprit vessel differential diagnosis: (1) Considering the Littmann’s concept of dual plane representation of leads V1-V3, aVL and V2 can be viewed as being “siblings.”In high lateral STEMI, the ST segments are usually elevated in leads I and aVL which is frequently accompanied by ST elevation in V2, but not in V1 or V3 (“South African Flag Sign”). This pattern is usually due to thrombotic occlusion of the first diagonal branch of the left anterior descending coronary artery [9].Yet, the evolution of ECG changes favored mid-anterior MI(ST-T changes in leads V2-V4).(2)In the hyperacute phase of ischemia caused by LCX occlusion, typically there is ST depression in V1,and the T waves in V1 to V2 are mostly negative.In the course of evolving myocardial infarction (MI) caused by LCX occlusion, after a number of hours, the amplitude of the R wave increases, the magnitude of the ST depression decreases, and the terminal component of the T wave becomes positive, corresponding to a mirror pattern of evolved lateral MI (Q waves, ST elevation with terminal T wave inversion).LCX occlusion can be ruled out.On the other hand, in LAD subocclusion (or occlusion with collaterals), ST depression in lead V1 is less prominent, and typically, the terminal portion of the T waves is positive, especially in V2 to V4.The amplitude of the positive T-wave component is often greater than the amplitude of the ST depression [10].Coronary angiography in this patient revealed D2 occlusion. According to the research by Tomcsányi J et al.,in the corresponding electrocardiographic leads, transmural ischemia is represented by ST-segment elevation, near-transmural by hyperacute T wave, and severe but subendocardial ischemia by de Winter sign [11].Thus, in the present case, leads aVL, I and V2 very likely manifest changes of ischemia having different severity (more severe sub-endocardial ischemia captured by leads aVL and I than in V2,the changes in leads aVL and I was compatible with the hyperacute phase of acute coronary artery occlusion).Regarding the evolution of the de Winter electrocardiogram, it was initially believed that from persistent ST-segment depression all the way to LAD reperfusion therapy, this characteristic electrocardiogram did not evolve [2].However, subsequent research suggested that these ECG changes could be transient or persistent, with de Winter and STEMI/Wellens ECG patterns potentially interchanging [10,11,12,13].In this patient, coronary angiography confirmed acute D2 occlusion, with mild de Winter ECG changes (compared to typical de Winter changes [1, 3,4,5,6,7,8, 11,12,13], this patient had a smaller range of precordial leads involved, limited to V2-V4,with mild ST-segment depression and less pronounced T waves).Subsequently, it presented a rare evolution gradually transforming to “normal ST-T”.After reperfusion, abnormal Q waves appeared in lead V2, and inverted T waves changed in leads I and aVL. This case has important clinical value, but similar cases are rarely reported.Based on our patient’s ECG manifestations, the D2 supplied the mid-anterior LV wall and such an ECG presentation of a D2 occlusion may be due to collateral circulation not visible by invasive angiography precluding the subepicardium from becoming ischemic, hence manifesting as ST-segment elevation.The ischemic process that occurred in the patient left a series of manifestations on the electrocardiogram.Understanding the diversity of de Winter electrocardiographic changes better can aid in early and effective diagnosis.

Conclusion

In the context of the patient’s multi-vessel coronary artery disease, the acute occlusion of D2 caused atypical de Winter ECG changes, which can serve as a reference for future clinical practice.