De Winter electrocardiographic pattern in a young patient with acute myocardial infarction

Abstract

A significant number of patients with acute coronary occlusion present with atypical electrocardiographic features in the emergency department. The de Winter pattern is suggestive of proximal left anterior descending coronary artery occlusion. Timely identification and immediate reperfusion is of utmost importance in these cases. The electrocardiographic pattern and its evolution in a young patient with acute myocardial infarction is described here.

Atypical patterns on the electrocardiogram (ECG) pose difficulty in diagnosing and treating acute coronary syndrome in the emergency department. Many ECG patterns indicating acute coronary occlusion other than ST elevation have been described, among which the de Winter pattern is a major one. In the original series by de Winter, this pattern occurred in 2% of patients with anterior myocardial infarction.¹ This ECG pattern had a high predictive value for acute occlusion of the proximal left anterior descending (LAD) coronary artery. Immediate reperfusion is lifesaving in most cases. This case report describes a young patient with the de Winter ECG pattern and temporal evolution of ECG changes following reperfusion.

CASE REPORT

A 33-year-old man with no comorbidities presented to the emergency department with a 4-hour history of chest pain. Pain was retrosternal with radiation to both arms, suggestive of typical angina. He was a nonsmoker, and there was no history of any substance abuse. His family history was negative. On examination his pulse rate was 86 beats/min and blood pressure was 110/76 mm Hg. Heart sounds were normal. His 12-lead ECG (Figure 1a) showed normal sinus rhythm with a rate of 86 beats/min. There was ST segment depression at the J point in leads V2 to V5. Upsloping ST depression of magnitude 1 to 4 mm was noted in the precordial leads with maximum ST depression in lead V4. The upsloping ST continued into tall symmetric positive T waves. Downsloping ST depression was noticed in leads III and aVF. There was 0.5 mm ST elevation in lead aVR. QRS duration was normal. PR and QT intervals were normal. The admission ECG thus showed a typical de Winter pattern. The admission troponin T level was 392 ng/L (normal, <40 ng/L). Transthoracic echocardiogram showed hypokinesia of apical and mid interventricular septum and apical anterior wall segments of the left ventricle. He had mild left ventricular systolic dysfunction with an ejection fraction of 48%.

Figure 1.

(a) 12-lead ECG in the emergency department showing de Winter pattern. (b) ECG 1 hour after angioplasty. (c) ECG 36 hours after angioplasty.

The patient was taken for immediate coronary angiogram through the right radial route. Loading doses of aspirin, ticagrelor, and atorvastatin were administered. Coronary angiogram (Figure 2a and b) showed 95% stenosis of the proximal LAD with thrombus. The left main, left circumflex, and right coronary arteries were normal. The proximal LAD lesion was dilated and stented using a 3.5 × 28 mm everolimus-eluting stent (Figure 2c). Percutaneous transluminal coronary angioplasty was done through the right femoral route, as he had a severe radial artery spasm following coronary angiogram. An ECG 1 hour after the procedure showed complete disappearance of the de Winter pattern (Figure 1b). After about 36 hours, the ECG showed T wave inversion in leads I, aVL, and V1–V6 (Figure 1c). An echocardiogram the next day showed mild hypokinesia and good left ventricular systolic function. The patient was discharged home after 3 days. Investigations for premature coronary artery disease, including serum homocysteine, lipid profile, and lipoprotein(a), were negative.

Figure 2.

Coronary angiogram showing a left anterior descending lesion in (a) an anterior-posterior cranial view and (b) a right anterior oblique caudal view. (c) Coronary angiogram after stenting of the proximal left anterior descending artery.

DISCUSSION

De Winter et al described a ST elevation myocardial infarction (STEMI)-equivalent ECG pattern in 2008.¹ It was characterized by 1- to 3-mm upsloping ST segment depression at the J point in leads V1 to V6 that continued into tall, positive symmetrical T waves. The QRS complexes were usually not widened or were only slightly widened, and in some there was a loss of precordial R wave progression. In most patients there was a 1- to 2-mm ST elevation in lead aVR. They identified this ECG pattern in 30 of 1532 patients with anterior myocardial infarction (2.0%). These ECG features were static, with persistence until the time of angiography which revealed LAD occlusion. The de Winter pattern was recorded on an average 1.5 hours after symptom onset. In our case, the ECG changes were typical of de Winter pattern except for a lower ST segment elevation in lead aVR. In our case, ECG changes normalized immediately after reperfusion but developed deep T wave inversions 36 hours later. Even though the de Winter sign was described in the proximal LAD lesion, similar patterns have been described in other coronaries as well.²

De Winter et al suggested different explanations for this ECG pattern. The presence of an anatomical variant of the Purkinje fibers, with endocardial conduction delay, could be a mechanism. Alternatively, ischemic ATP depletion may lead to lack of activation of sarcolemmal ATP-sensitive potassium channels, which can explain the lack of ST segment elevation, as has been shown in K_ATP knockout animal models of acute ischemia.³ Verouden et al suggested that the area of transmural ischemia might be so large that the injury current is directed toward lead aVR and away from the precordial leads.⁴ Some patients exhibiting the de Winter’s pattern who are not immediately reperfused may go on to develop overt ST elevation as well as Q waves.^5–7 Many patients show a static pattern until the time of reperfusion despite ongoing ischemia for prolonged periods of time. This suggests that this pattern may lie somewhere along the continuum of ischemic ECG changes between subendocardial ischemia and the transmural infarction associated with ST elevation.⁷

The prompt recognition of the ECG pattern by medical and paramedical staff is of utmost importance in the emergency department. The misdiagnosis rate is common because of the atypical ECG and the therapeutic window might be missed.⁸ Clinicians often categorize this pattern as non-STEMI and intervention may be delayed.^9,10 Moreover ECG software may not recognize this ECG pattern, and that can lead to misdiagnosis.

DISCLOSURE STATEMENT

The author reports no funding or conflicts of interest. Patient permission was obtained to publish the case.