Phenomenon of “de Winter” pattern, sign, or syndrome: A systematic scoping review and data analysis

Abstract

BACKGROUND

The de Winter (dW) pattern, sign, and syndrome is an ST-elevation myocardial infarction (STEMI) equivalent. The first two forms describe the electrocardiographic characteristics of this phenomenon, while dW syndrome additionally has symptoms indicative of acute coronary syndrome. Emerging evidence suggests that dW pattern precedes or alternates with STEMI patterns.

AIM

To improve the recognition of the dW pattern, dW sign, or dW syndrome, urge early aggressive treatment, and determine whether sex matters, by integrating contemporary knowledge through a systematic scoping review and data analysis.

METHODS

A comprehensive search was conducted across PubMed/MEDLINE and Google Scholar (November 2008 to June 2025), and literature data were analyzed. This scoping review adhered to the Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for scoping reviews checklist.

RESULTS

A total of 322 patients presenting with dW pattern were identified. Most patients were young males. Risk factors were primarily smoking, hypertension, and dyslipidemia. Sixteen cardiac arrest events occurred during hospitalization. The main culprit vessel was the left anterior descending artery (LAD) at 88.5%. Compared with the younger group, older patients had more LAD (84% vs 80%) and right coronary artery involvement (4% vs 1.0%). Left main coronary artery occlusion was more prevalent in the younger group (5.0% vs 2.4%). The frequency of total or near-occlusion of LAD and left main coronary artery was similar in the two age groups. Males showed a higher rate of severe LAD stenosis than females did (45.2% vs 17.7%). dW pattern followed by STEMI was noted in 40 cases, STEMI followed by dW pattern in 8 cases, and simultaneous STEMI and dW pattern in 10 cases. The overall mortality rate was 3%.

CONCLUSION

dW pattern, dW sign, and dW syndrome are commonly used interchangeably describing the dW phenomenon. Patients presenting with this phenomenon have unique demographics, risk factors, pathophysiology, and angiographic characteristics (i.e., distinct culprit lesions and coronary artery involvement). Early identification with a high index of suspicion is crucial and necessitates urgent intervention.

Key Words: Acute coronary syndrome; De Winter; Syndrome; Electrocardiographic pattern; ST-elevation myocardial infarction equivalent

Core Tip: The three forms of the de Winter (dW) phenomenon (dW pattern, dW sign, or syndrome) are used similarly in contemporary literature. This phenomenon has unique risk factors, pathophysiology, and angiographic characteristics. It should be managed as an indicator of ST-elevation myocardial infarction equivalent that requires urgent intervention. However, it is often underrecognized and therefore requires a high index of suspicion. Age and gender are associated with distinct culprit lesions and coronary artery involvement in this phenomenon. By integrating current evidence, prompt recognition and aggressive reperfusion strategies, such as those used in ST-elevation myocardial infarction protocols, are crucial for improving outcomes in this high-risk presentation.

INTRODUCTION

The de Winter (dW) pattern and “sign” indicate unique electrocardiographic (ECG) findings of the dW phenomenon, while dW syndrome additionally has symptoms indicative of acute coronary syndrome (ACS)[1]. Although dW pattern, dW sign, and dW syndrome are commonly used interchangeably in the literature, dW syndrome is preferable as it reflects the practical utility of this phenomenon and integrates ECG and clinical findings. In 1955, Pruitt described junctional ST-depression with tall symmetrical T waves in leads V3-V5 in a patient presenting with severe chest pain. In 2008, de Winter et al[1] revealed that an occlusion in the proximal left anterior descending (pLAD) coronary artery can occur in the absence of a clear ST-segment elevation myocardial infarction (STEMI) that was reported in 2% of anterior acute myocardial infarction (AMI)[2]. The ECG findings in dW pattern patients were obtained, on average, within 1.5 hours of symptom onset and were static[1]. In dW pattern, the ST segment displays a 1 mm to 3 mm upsloping depression at the J point in leads V1-V6, typically in V1-V4, which then progresses to tall, positive, symmetrical T waves[1].

When dW pattern is suspected, it should be considered a time-critical condition that requires treatment similar to that for STEMI, including coronary angiography (CAG) and percutaneous coronary intervention (PCI)[3]. If PCI is unavailable, then thrombolytic therapy can be administered if there are no contraindications[4]. Several reports have shown that dW pattern may be transient and subject to dynamic fluctuations, requiring serial ECG monitoring. The underlying risk factors of dW pattern are similar to those of ACS, and chest pain is the most common presenting symptom[5].

This review aims to integrate and evaluate the existing literature on the dW phenomenon, focusing on its up-to-date pathophysiology, diagnostic approaches, angiographic findings, treatment, and outcomes. By systematically reviewing and analyzing data from diverse studies, we will assess the clinical characteristics of dW pattern in males and females, define areas of uncertainty, and provide actionable recommendations for clinicians and researchers. Ultimately, this work would enhance understanding of the dW pattern and improve patient care through evidence-based recommendations.

MATERIALS AND METHODS

The primary objective of this review is to investigate the prevalence, pathophysiology, ECG, and angiographic findings of dW pattern in males and females. It also aims to evaluate the pharmacological and interventional treatment and assess the clinical outcomes. This review adhered to the Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for scoping reviews checklist.

Data collection

A systematic scoping review of peer-reviewed articles published between November 2008 and June 2025 was carried out. Additionally, an analysis of the selected data was conducted. A thorough search was performed using medical terms and combinations such as the following: “de Winter sign” OR “de Winter pattern” OR “de Winter electrocardiographic pattern” OR “de Winter syndrome” OR “STEMI equivalent” across databases such as PubMed, Google Scholar, and Medical Subject Headings on the PubMed search engine. We also searched further among articles that fit the inclusion criteria, which were retrieved and included in the data.

Definition

dW pattern or dW sign: The ECG findings suggestive of dW pattern are: (1) A 1-3 mm upsloping ST-segment depression (STD) at the J point in the precordial leads V1-V6; (2) Tall, symmetric peaked T waves; (3) A normal or mildly prolonged QRS complex; (4) Poor R wave progression; and (5) Mild ST-segment elevation in lead augmented vector right (aVR) of > 0.5 mm (Figure 1)[1].

Figure 1 Electrocardiographic findings of de Winter pattern. ECG: Electrocardiographic; aVR: Augmented vector right electrocardiographic lead.

The dW syndrome: dW syndrome describes dW pattern or signs and symptoms suggestive of ACS, along with coronary angiographic findings. Most of the literature used the terms “dW pattern” and “dW syndrome” without a distinguishable definition.

Systematic selection of studies

Eligibility criteria: Eligible studies were identified by conducting a comprehensive search strategy using keywords and text words that highlighted diagnostics, interventions, and treatment options.

Inclusion criteria: Data included prospective, retrospective, case reports, and case series. Abstracts that include full pertinent details can be included. All age groups, genders, and different forms of presentation were included.

Exclusion criteria: Articles written in languages other than English were excluded, unless the abstract was written in English and contained all the required information, and cases of ACS without the characteristics of dW pattern. We also excluded systematic reviews and meta-analyses in which relevant individual cases were not identified or data were missing.

Data extraction and synthesis

Information sources and search methods: A comprehensive search was conducted across electronic databases, including PubMed/MEDLINE and Google Scholar, between November 2008 and June 2025.

Study selection: A systematic search was conducted using specific keywords.

Data collection process: A thorough manual search of eligible articles was conducted, and any duplicates were removed. Elmenyar E, Abbara MA, and Al-Ghoul Z independently searched, screened, and extracted the articles; all reached a consensus on eligibility, and the senior author reviewed the articles. The obtained information was categorized within tables that included the author(s), number of cases per article, gender, mean age, medical history, risk factors, presentation, medications used, laboratory findings as troponin, echocardiography findings, ejection fraction percentage, and ECG findings, including STEMI, non-STEMI, bundle branch block, atrial fibrillation, ventricular arrhythmias, and Wellens syndrome. Pharmacological treatment, CAG findings, PCI, extent of vessel stenosis, culprit lesion, and clinical outcome were analyzed.

Risk of bias assessment at the individual and across-studies levels: The risk of bias assessment was not applicable, as all cases were collected from case reports, case series, and retrospective studies. However, the risk could generally be low. No structured, large-scale, prospective studies, or randomized controlled trials addressed the subject of this review.

Statistical analysis

Data were presented as n (%), means ± SD, and medians (interquartile ranges) as applicable. Age (cut-off at 55 years) and sex (males vs females) were analyzed. Categorical variables were compared using the χ² test, while Student’s t-test was used for continuous variables. Statistical analysis was conducted using the Statistical Package for the Social Sciences version 21.0 (SPSS, Inc., Chicago, IL, United States).

RESULTS

A total of 322 patients presenting with dW pattern on ECG were retrieved from 159 papers (Figure 2). Three articles (n = 22) were case series[6-8], 149 articles (n = 165) were case reports, and seven articles were retrospective studies[1,2,9-13]. Table 1 shows case series and retrospective studies.

Figure 2  Study design (Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for scoping reviews).

Table 1 Case series and retrospective studies of de Winter pattern.

Ref.	Years	Study characteristics	Comments
de Winter et al[1]	2008	Retrospective; 30/1532 AMI (2%); mean age (52 years); male (94%)	(1) 76% isolated LAD disease; (2) Culprit pLAD, PCI done; (3) Wrap-around LAD (50%); and (4) Static status1: One died (3%)
Verouden et al[2]	2009	Retrospective; 35/1855 PCI of LAD	(1) Wrap-around LAD (57%); and (2) 67% had SVD
Xu et al[9]	2018	Retrospective; 15/449 AMI (3.4%); mean age (60 years); male (87%)	(1) 11/15 underwent PCI, 2 underwent successful thrombolysis, and 2 received conservative therapy; and (2) LAD was the culprit in 9
Shahri et al[6]	2022	Case series; 11 with dW pattern; mean age (56 years); male (54%)	(1) The culprit vessel is LAD; and (2) 5 MVD
de Winter et al[10]	2019	Retrospective; 11/701 AMI (1.6%); mean age (65 years); male 91%	(1) Culprit pLAD or mLAD; and (2) PCI not in a timely fashion; 3 died (27%)
Fuji and Ikari[12]	2024	Retrospective; 2/641 ACS; mean age (69 years); male (100%)	(1) Culprit LAD; and (2) 1 patient received PCI and 1 underwent CABG
Tang et al[13]	2024	Retrospective; 12/1865 AMI; mean age (49 years); male (100%)	(1) The culprit vessel was pLAD in 7 and mLAD in 3, LMCA in 1, and 1 in the ramus intermedius artery; (2) 53% had MVD; (3) 3 developed cardiogenic shock; and (4) The median door-to-balloon time was 94.5 minutes
Alireza et al[11]	2025	Retrospective; 30/967 AMI; mean age (61 years); male (67%)	(1) Culprit pLAD treated with PCI within 90 minutes of arrival (100%); (2) Wrap-around LAD (67%); (3) MVD (60%); and (4) Mortality 3%
Chyu et al[7]	2022	Case series; 4 had STEMI equivalent, 1/4 with dW pattern	Total occlusion of LAD after the first septal branch treated with PCI
Ni[8]	2022	Case series of 10 patients (9 males)	All showed dynamic evolution (the explanation was unclear, as no full text was available) 9 had PCI

¹First electrocardiographic > > pre-procedural electrocardiographic until angiographic findings.

AMI: Acute myocardial infarction; PCI: Percutaneous coronary intervention; LAD: Left anterior descending artery; dW: De Winter; ACS: Acute coronary syndrome; STEMI: ST-elevation myocardial infarction; pLAD: Proximal segment of the left anterior descending; SVD: Single vessel disease; MVD: Multi-vessel disease; mLAD: Mid segment of the left anterior descending; CABG: Coronary artery bypass grafting.

Demographics, clinical presentation, and comorbidities

The median age was 52 years, with an interquartile range of (42-62). Most patients presented with chest pain and tightness (82%) and shock or hemodynamic instability (5.2%). The main risk factors included smoking (50%), hypertension (32%), dyslipidemia (30%), diabetes mellitus (17.5%), and family history of ACS (16.8%). The median and interquartile range of the left ventricle ejection fraction were 45% (38-50). Positive troponin and creatine kinase myocardial band rates were 60% and 22%, respectively. Patients with dW pattern were divided into two age groups (< 55 yearsvs ≥ 55 years). The prevalence of culprit vessels, troponin levels, and severity of stenosis in the main vessels is shown in Table 2. Older patients had more LAD involvement (84% vs 80%) and right coronary artery (RCA) involvement (4% vs 1.0%) than the younger group did. Left main coronary artery (LMCA) occlusion was more prevalent in the younger group (5.0% vs 2.4%). With regard to severity, the frequency of total occlusion and near-occlusion in the LAD (42.7%) and LMCA (4.9%) was similar in both groups. The younger patients had higher serum troponin levels (55.3%).

Table 2 Characteristics of de Winter pattern by age.

Variables	< 55 years old (55%)	≥ 55 years old (45%)
Positive troponin	55.0%	44.0%
Mortality	1.9%	3.7%
Cardiac arrest	6.8%	4.9%
Severe LAD stenosis	42.7%	44.7%
Severe LCx	4.8%	7.3%
Severe RCA	2.9%	8.5%
Severe LMCA	4.9%	4.8%
Severe: ≥ 70% stenosis

LAD: Left anterior descending artery; LCx: Left circumflex; RCA: Right coronary artery; LMCA: Left main coronary artery.

The male sex predominated (89%). Females had no culprit lesions in the LMCA or RCA unlike males. The prevalence of LAD as the culprit vessel was similar in females and males (82%). However, females showed a higher rate of culprit left circumflex (LCx) artery than males did (6% vs 3%). Total occlusion and near-occlusion of LAD were higher in males than in females (45.2 vs 17.7%).

Dynamic ECG findings

The most common transformative ECG changes were STEMI[14-17], at 32.3%, of which 3.8% presented first with STEMI, then dW pattern[18-21], and 4.6% exhibited a precordial continuum of both patterns[22-25]. dW pattern followed by STEMI was noted in 40 cases, while STEMI followed by dW pattern was reported in 8 cases. STEMI following PCI for dW pattern was reported in 7 cases, STEMI following thrombolysis for dW pattern in 4 cases, and concomitant STEMI and dW pattern in 10 cases.

Associated ECG findings

Wellens’ ECG pattern was observed in 5.3%[26-35]. Two cases reported the coexistence of Wolff-Parkinson-White syndrome with dW pattern[36,37]. Five patients had bundle branch block, and six patients had atrial arrhythmia.

Angiographic findings and culprit lesion

In CAG, LAD was the culprit vessel in 277 patients (88%), with lesions located in the proximal region in 226 (72%), while 16 had no documentation beyond the ECG description. The other culprit vessels included LMCA (4.5%), diagonal branches (4.2%), LCx, and RCA (3.2% equally), and one case had an obtuse marginal (OM) artery and ramus intermedius stenosis[13]. The predominant site of occlusion within the LCx was the proximal region (10%). RCA stenosis was found in the proximal (5.3%) and middle segments (4.8%).

Medical, PCI, and surgical management

The medications used were dual antiplatelet therapy (38.8%), anticoagulant agents (19.6%), and nitroglycerin (15.3%). The overall use of thrombolytic treatment was 13%, Nineteen patients had efficient thrombolysis therapy, nine patients underwent PCI after stabilization, one underwent coronary artery bypass grafting, and the rest were safely discharged without further intervention. The following agents were used: Fibrin-specific tissue plasminogen activator (4.3%), streptokinase (4.7%), and prourokinase (1%). In four cases, the type of agent used was not specified. Three cases underwent coronary artery bypass grafting[12,38,39]. Around 120 patients underwent PCI, of whom 113 were primarily managed without prior thrombolysis.

DISCUSSION

This work is an up-to-date, comprehensive review that includes 322 patients presenting with dW phenomenon in terms of dW pattern, dW sign, or dW syndrome. This review highlights the importance of the ECG recognition checklist, key differentials, management priorities, and pitfalls in diagnosing the dW phenomenon. A prior review on the same topic was published in 2024, including 66 patients with a limited analysis[40]. dW pattern was reported in 3.4% of patients with AMI, with a positive predictive value (PPV) of 95% to 100% for identifying an acute occlusion of the pLAD[9,41,42]. A subsequent study reported PPVs of 50% to 85.7% for dW pattern in predicting LAD occlusion[42]. However, the accuracy, sensitivity, and specificity of dW pattern for predicting the angiographic findings cannot be confidently obtained until well-designed large studies have been conducted. Early identification of STEMI-equivalent conditions, including dW pattern, is crucial for ensuring timely intervention, limiting infarct size and myocardial necrosis, reducing arrhythmias, and improving patient survival. Notably, dW pattern is easily misdiagnosed and needs a high index of suspicion.

Clinical significance of the dW phenomenon

The dW phenomenon is more prevalent in males, with a mean age of 52 and a mortality rate of 3% during the index admission[2,10,11,17,43,44]. However, this rate could be underestimated. Diabetes mellitus, unlike other STEMI, is not among the top three risk factors. Moreover, 7.8% sustained cardiac arrest during early hospitalization. Notably, among the 16 cardiac arrest cases, seven exhibited dynamic ECG changes (Table 3)[4,11,13,22,45-54]. Around 9% of dW syndrome patients had threatening ventricular arrhythmia. This prevalence of arrhythmia is similar to what has been reported in patients with STEMI[55].

Table 3 De Winter pattern and cardiac arrest (n = 16).

Ref.	Years	Comment	Outcome
Ghazali et al[4]	2020	Chest pain > > dW pattern followed by cardiac arrest > > STEMI	Survived
Tomcsányi et al[22]	2022	Chest pain > > simultaneous dW pattern and STE > cardiac arrest > > Stenting	Survived
Missaoui et al[45]	2020	Chest pain > > dW pattern with STE aVR > > thrombolytic agent > > > cardiac arrest > > stenting	Survived
John et al[46]	2020	Chest pain > > dW pattern > > STEMI > > cardiac arrest > > PCI	Survived
Fernandez-Vega et al[47]	2017	Cardiac arrest > > dW pattern > > PCI	Survived
Carr et al[48]	2016	Chest pain > > STD > > ECG normalization > > cardiac arrest > > dW pattern > > PCI	Survived
Alhatemi et al[49]	2024	Chest pain > > hyperacute T waves > > cardiac arrest > > dW pattern > > PCI	Survived
Wismiyarso et al[50]	2021	Chest pain > > dW pattern > > cardiac arrest > > ECG normalized after defibrillation > > PCI	Survived
Plane et al[51]	2019	Cardiac arrest > > dW pattern > > CAG and thrombus aspiration	Survived
Shepherd and Furiato[52]	2020	Chest pain > > dW pattern > > cardiac arrest > > PCI	Survived
Liu and Wang[53]	2020	Chest pain > > cardiac arrest > > STEMI > > dW pattern > > PCI	Survived
Rujuta et al[54]	2024	Chest pain > > dW pattern > > cardiac arrest > > Q waves and accelerated idioventricular rhythm > > Cardiogenic shock > > IABP > > PCI	Survived
Wang et al[56]	2022	Chest pain > > cardiac arrest > > dW pattern > > cardiac arrest > > STEMI > > PCI	Survived
Tang et al[13]	2024	2/12 dW pattern patients developed sudden cardiac arrest	Survived
Alireza et al[11]	2025	2/967 (7%) dW pattern > > VF	Not mentioned

dW: De Winter; STEMI: ST-elevation myocardial infarction; STE: ST-elevation; aVR: Augmented vector right; PCI: Percutaneous coronary intervention; STD: ST-segment depression; ECG: Electrocardiographic; CAG: Coronary angiography; IABP: Intra-aortic balloon pump; VF: Ventricular fibrillation.

The authors concluded that dW pattern is not an independent pattern but rather an early stage of STEMI that requires immediate intervention and reperfusion. However, timely thrombolysis can be successful when PCI is unavailable[9,17]. In dW pattern patients, the appearance of STD could be upsloping, horizontal, or down-sloping, and this is crucial in understanding the exact pathogenesis and prognosis[56]. Zhan et al[57] showed that a maximal STD pattern correlates with more critical ischemic changes within the subendocardial region in comparison to a non-upsloping STD. Maximal STD in dW pattern in lead V2 or V3 showed a PPV of 89% for all patients and 98% for those without an ST-segment elevation in V2 for identifying LAD as the culprit vessel[57]. Hence, upsloping STD > 1 mm at the J point with peaked T waves in the absence of ST-segment elevation in leads V2-V6 prompts urgent intervention in dW pattern patients[57,58]. This finding was supported by a retrospective study showing that STD upsloping is associated with higher rates of positive troponin levels, angiographic thrombus, in-hospital revascularization, overall mortality, and a lower ejection fraction compared with the non-upsloping STD group[59].

According to Zhan et al[57], pathological Q wave or poor R wave progression in leads V1-V4 was seen in 74% of dW pattern cases. Moreover, the reported rate of minimal ST-segment elevation in aVR was 100% in Verouden et al’s study[2], who proposed that widespread transmural ischemia results in ischemic current steering toward the aVR lead and away from the precordial leads. However, Wall et al[60] found that ST-segment elevation in aVR occurred in only 50% of patients with dW pattern. Notably, the more ST-segment elevation in the aVR lead, the more extensive myocardial ischemia and involvement of critical coronary arteries in dW pattern patients, such as LMCA[61].

Pathophysiology of dW pattern

It is theorized that dW pattern is likely caused by regional subendocardial ischemia, with myocardial protection occurring through various mechanisms, such as collateral blood flow, ischemic preconditioning, or maintained forward blood flow (Figure 2)[11,62,63]. Importantly, assessment of the ischemia vector direction helps identify the site of greater ischemia, and the amount of ST-segment elevation indicates its severity[64]. The proposed mechanism underlying the lack of ST-segment elevation in an LAD occlusion involves an anatomical deviation within the Purkinje fibers, resulting in delayed endocardial conduction[2]. Furthermore, ischemic adenosine triphosphate (ATP) depletion results in the inactivation of sarcolemmal ATP-sensitive potassium channels, precluding ST-segment elevation[2]. In support of this theory, Li et al[65] reported an animal study showing that mice deficient in ATP-sensitive potassium channels (K_ATP knockout) lacked ST elevation following LAD ligation.

As for the STD in dW pattern, it is due to the negative voltage difference between ischemic subendocardial and normal subepicardial action potentials during the plateau phase[62]. This difference, caused by subendocardial ischemia, aligns with the transmembrane action potential summation theory, which leads to STD on the surface ECG[62]. Potentially, the upsloping STD and tall, peaked T waves occur due to hypoxia-induced changes in ATP-sensitive potassium channels, which delay repolarization in the subendocardial region and alter the shape of the transmembrane action potential[66]. Cardiac magnetic resonance imaging proposed an interplay of differential action potential expression and collateral circulation as a possible explanation of dW pattern[67].

Is dW pattern a static or dynamic phenomenon?

The dW pattern has been regarded as a transient phenomenon rather than a static one, as it may progress to STEMI or start as STEMI and then progress to dW pattern[16]. This implies the importance of continuous ECG monitoring in patients with dW pattern. Such a dynamic ECG change is due to dW pattern reflecting subendocardial ischemia, but as it advances to transmural ischemia, the pattern evolves into a STEMI appearance[68]. Xu et al[9] reported an average time to ECG evolution from dW pattern to STEMI of approximately 114 minutes in 13 patients.

Our review revealed that 69 patients exhibited ECG transformation: 51 developed a STEMI following the initial ECG of dW pattern, 8 presented with a STEMI that later transformed into dW pattern, and 10 patients presented with concomitant ECG findings[11,22-25,69]. One case report, including a 31-year-old male, showed dW pattern as a transient event after LAD stenting (at the time of reperfusion)[70]. In this patient, the classic ST-segment elevation was observed in the initial ECG (as a total LAD occlusion) before and after reperfusion. At the same time, dW pattern appeared between (reflecting subtotal occlusion with spontaneous recanalization). Theoretically, Zhao et al[70] categorized dW pattern into two phenomena. The first category is static, in which the J-point depression remains until LAD patency is achieved; this category does not progress to STEMI. The second category is dynamic, in which STEMI pattern transformed into dW pattern, and vice versa, depending on the total LAD occlusion and spontaneous recanalization state transitions. Furthermore, Pica et al[71] reported a case of STEMI due to acute stent thrombosis following PCI therapy for dW pattern in the LAD. This patient was in a hyperglycemic state, which could lead to the non-opening of ATP-sensitive potassium channels, resulting in differences in ischemic ECG changes[71].

Simultaneous dW pattern and STEMI

To further elaborate on cases showing ECGs with concomitant STEMI and dW pattern, Tomcsányi et al[22] reported two cases with an ECG showing ST-segment elevation in V1-V3, a transient isoelectric ST segment with a subsequent tall T wave in lead V4, and upsloping ST depression in leads V5-V6, followed by tall T waves. These patients were found to have type III LAD (a large wrap-around vessel). The coexistence of both patterns is not relevant to the inactivation of sarcolemmal ATP-sensitive potassium channels or anatomical atypia in the Purkinje fibers[22]. Instead, the different ischemic changes and their extent across the myocardial layers led to this ST segment continuum such that transmural ischemia occurs in the proximal anterior wall, which exhibits near-transmural ischemia as it extends distally. By contrast, in the most distal region, ischemia intensifies but remains limited to the subendocardium[22].

Simultaneous occlusion of two major vessels is a rare event that requires careful ECG interpretation, especially in hemodynamically unstable patients, as described by Tsuchida et al[25]. Their case report raised the following question: Is dW pattern an STD or merely a reciprocal change? ST-T deviation patterns can vary with the temporal sequence and anatomical dominance of the two infarct-related arteries (LAD and RCA) in a patient presenting with bradycardia, ST elevation in the inferior leads, and dW pattern.

dW pattern and Wellens syndrome

Notably, 10 cases reported ECG evolution from dW pattern to Wellens syndrome. The ECG pattern in Wellens is mainly marked by deep inverted T waves in leads V1-V4, persisting for weeks after the resolution of chest pain, and is also considered a STEMI equivalent[29]. dW pattern patients exhibiting the Wellens pattern were found to have non-complete occlusion in the pLAD[30]. Wang et al[30] concluded that the sequential appearance of both patterns (dW pattern > > > Wellens) within a short time contributes to a higher diagnostic accuracy of non-complete or near-complete LAD occlusion. Ratzenböck et al[33] concluded that Wellens ECG could indicate myocardial reperfusion after successful stenting of LAD in a patient presenting with dW pattern. Moreover, the Wellens pattern may be related to vasospasm or the dissolution of a possible thrombus following medical therapy[33].

Atypical angiographic presentation of dW pattern

dW pattern on the ECG would be present in any ECG lead and would be associated with acute occlusion of any coronary artery. The precordial lead with upsloping STD holds significance in identifying LAD as the culprit artery in dW pattern patients. However, as more cases emerge in the literature, it has become apparent that dW pattern can occur when vessels other than the LAD are occluded. Hence, Rachmi et al[72] highlighted the importance of additional findings alongside the classic STD appearance, such as non-upsloping STD, STE, Q waves, and R/S ratio, in identifying the culprit vessel in dW pattern patients. According to our review, the LCx, RCA, LMCA, diagonal branches (D1 and D2), or OM occlusion can be the affected vessel in dW pattern patients.

LMCA and dW pattern

Nine cases in the literature attribute dW pattern to LMCA stenosis[13,38,39,43,73-76]. Numerous studies have established the link between aVR ST-segment elevation and diffuse STD in patients with significant LMCA disease or extensive CAD[77-79].

Zhan et al[74] described an LMCA occlusion in a patient presenting with a dW pattern that resembled an LAD occlusion. However, the ECG illustrated global subendocardial ischemia, as leads V4-V5 showed maximal STD with T wave inversion in V5-V6, which warranted the possibility of an occlusion in the LMCA rather than LAD. Furthermore, they proposed that collateral circulation from the LAD and ischemic preconditioning prevented deterioration in the patients. Moreover, Sunbul et al[38] reported a dW pattern with LMCA occlusion, which was prominently visible in leads V3-V6. Kashou et al[75] reported severe LMCA stenosis followed by a complete LAD occlusion, which demonstrated dW pattern with maximal STD in lead V5. The proposed explanation for the involvement of the anterolateral leads is diffuse subendocardial ischemia within the corresponding ventricular walls and transmural ischemia in the basal interventricular septum due to the lack of collateral circulation from the LAD[75].

RCA, LCx, and dW pattern

Six cases reported RCA to be the isolated-injury artery in dW pattern patients[25,80-84]. Typically, ST-segment changes within leads II, III, augmented voltage foot, and V4-V6 correlate with RCA occlusion[56]. Tsutsumi and Tsukahara[81] presented similar ECG findings in the inferolateral leads in dW pattern, which were also confirmed by an echocardiogram. Chen et al[80] described the presence of junctional rhythm resulting from absent blood flow to the sinoatrial and atrioventricular nodes due to RCA occlusion in dW pattern.

LCx is involved almost concomitantly with LAD in most cases; however, six cases reported LCx as the culprit lesion[6,85-89]. STD at the J point with upsloping ST-segments and hyperacute T wave in the inferior and lateral wall leads is associated with acute LCX occlusion[85]. Manno et al[86] showed that an upright T wave in lead V1 is more common in patients with isolated LCx artery disease. An acute occlusion of the LCx artery causes a lack of blood supply to the inferobasal and lateral areas within the left ventricle, hence resulting in a posterolateral myocardial infarction[89]. Additionally, a peaked R wave, unlike S waves, in leads V1-V2 indicates the presence of a posterior infarct, as it is reflective of Q waves in posterior leads[72]. Rachmi et al[72] reported a case of a posterolateral myocardial infarction, characterized by prominent R waves in leads V1-V2 and ST-segment elevation in leads I and augmented voltage left arm, alongside the classic dW pattern. The post-procedural ECG further confirmed the LCx occlusion, as it revealed prominent ST-segment elevation in leads V5-V6. Additionally, echocardiography findings revealed hypokinesis in the basal-mid-apical anterolateral and inferolateral segments[72].

OM, diagonal, and dW pattern

Xu et al[24] presented a rare dW pattern with an occluded OM artery; the ECG showed dW pattern and a STEMI in the posterior leads. Moreover, there are eight cases with the diagonal branch reported as the culprit vessel in dW pattern[9,32,90-95]. Montero Cabezas et al[92] reported the incidence of dW pattern due to a lesion in the D1 branch with a seemingly patent LAD. However, following reperfusion, the ECG illustrated a typical D1 infarct with a persistent ST-segment elevation in the anterolateral leads from V2-V6 with negative T waves and Q waves in lead I and augmented voltage left arm[92].

PCI vs thrombolysis in dW pattern/dW syndrome

The ideal management of dW pattern/dW syndrome requires early revascularization with PCI, as it is a STEMI equivalent[96]. International guidelines do not yet recommend the use of thrombolytic agents for dW pattern[97,98]. However, thrombolytic agents have been reported to be effective, particularly in resource-limited settings. Six cases reported failed thrombolysis, necessitating the transfer of the patients to centers equipped with catheterization laboratories[9,45,55,99]. Among 11% of patients who were prescribed thrombolytic therapy in non-PCI centers, 82% had successful reperfusion[55]. This reperfusion rate in dW pattern patients was similar to that reported in STEMI patients[55]. Xu et al[9] reported successful resolution of a STEMI that developed after dW pattern in one patient after thrombolytic therapy without further revascularization. At the same time, two cases failed, and one patient experienced vessel blockage again[9]. Xiao et al[99] reported inefficient use of reteplase, leading to anterior STEMI that resolved only after PCI. In 2019, the Chinese Guidelines for the Diagnosis and Treatment of Acute STEMI recommended that patients with dW syndrome need to be managed as a distinct STEMI subtype; however, in non-PCI centers, no clear guidance is available on whether intravenous thrombolytic therapy should be preferred for dW syndrome patients[99]. Large-scale studies are needed to evaluate the use of thrombolytic agents in dW pattern when PCI is unavailable or in cases of patient refusal, as their safe use remains controversial.

Resolution of dW sign or dW pattern

With regard to ECG evolution following reperfusion therapy, STEMI was observed in seven patients who underwent PCI for dW pattern, including five with LAD, one with LCx, and one with diagonal branch occlusions. The postprocedural ECG evolution from dW pattern to a STEMI, commonly in the anterior wall, can be attributed to microcirculatory impairment and progressive myocardial necrosis[100]. Another probable explanation is the rupture of plaque remnants, which embolize distally, or the akinesis of wall motion following intervention[101]. However, the evolution to STEMI with Q waves in leads I and aVR following reperfusion is a standard finding in a diagonal branch occlusion[98,102]. Furthermore, four of the patients who received primary thrombolytic therapy showed an evolving STEMI after reperfusion therapy, which necessitated PCI[9,99,103].

Atypical presentations of dW pattern/dW syndrome

Several case reports in the literature described conditions associated with dW pattern, thereby expanding the range of presentations of this phenomenon (Table 4). For instance, acute stent thrombosis and myocarditis have been noted to present with dW pattern likely due to overlapping pathophysiological mechanisms, including the inactivation of sarcolemmal ATP-sensitive potassium channels or anatomical variants in the Purkinje fibers[104,105]. Molina-Lopez et al[106] described a patient who developed a dW pattern following aortic valve repair, which was attributed to severe aortic stenosis that resulted in elevated left ventricular pressure and ischemia, and was associated with the Bezold-Jarisch reflex. Chen et al[107] reported a dW pattern following chest pain in a patient at the end of an elective PCI procedure. The troponin level became positive, and no stenosis was detected on the CAG. The patient’s symptoms were alleviated, and dW pattern disappeared after treatment with diltiazem.

Table 4 Unique conditions presenting with de Winter pattern.

Ref.	Years	Medical condition
García-Izquierdo et al[104]	2018	Myocarditis
Porciuncula et al[105]	2019	Acute stent thrombosis
Chen et al[107]	2020	After elective PCI (asymptomatic and no STEMI-equivalent on arrival)
Molina-Lopez et al[106]	2024	Post aortic stenosis repair
Ando et al[108]	2020	Vasospastic angina
Azdaki et al[44]; Hirase et al[91]	2021; 2020	Spontaneous coronary artery dissection
Dai et al[110]	2021	Kounis syndrome
Al-Assaf et al[5]	2024	Blunt chest trauma
Zhang et al[109]	2022	Type A aortic dissection
Daas et al[111]	2025	Coronary artery ectasia
Li et al[112]	2025	Pheochromocytoma
Wei et al[113]	2022	Stroke-heart syndrome

PCI: Percutaneous coronary intervention; STEMI: ST-elevation myocardial infarction.

Furthermore, Ando et al[108] reported a case of vasospastic angina with transient ischemic changes that possibly mimicked the dW pattern. A separate report by Zhang et al[109] described a dW pattern in a patient with type A aortic dissection, likely resulting from compression of the LMCA, LAD, and LCx. Al-Assaf et al[5] documented another interesting case with blunt chest trauma, in which they suggested that dW pattern was due to AMI caused by rupture of a pre-existing atherosclerotic plaque. Additionally, Dai et al[110] proposed that the ECG manifestations in Kounis syndrome may resemble those of the dW pattern, although this relationship requires further clarification.

Spontaneous coronary artery dissection, ectasia, and dW pattern

Other reports have demonstrated that dW pattern can be caused by spontaneous coronary artery dissection in the diagonal branch in instances where a large diagonal branch occlusion is distributed parallel to the LAD[91]. This patient received no specific therapy and had an uneventful recovery. Another patient with extensive myocardial infarction due to spontaneous coronary artery dissection of the LAD was treated initially with a thrombolytic agent. The patient’s condition deteriorated; subsequently, the patient expired. Post-mortem examination confirmed the diagnosis, as CAG was not feasible[44].

dW pattern has also been seen in a patient who had congenital coronary artery ectasia in addition to a plaque rupture within the coronary artery. The mechanism that led to dW pattern is thought to be triggered by a plaque rupturing within the dilated coronary artery, causing a spontaneous dissection, which then results in a series of ischemic changes[111].

Pheochromocytoma and dW pattern

A patient with pheochromocytoma presented with ECG findings of dW pattern, attributed to coronary vasospasm due to increased catecholamine secretion from the tumor instead of it being a typical myocardial infarction[112].

Stroke-heart syndrome and dW pattern

Wei et al[113] described a patient who suffered from a cerebellar and pontine stroke, which induced a myocardial infarction manifesting as dW pattern on ECG. This collection of findings was classified as stroke-heart syndrome. It was hypothesized that autonomic dysregulation was caused by a stroke resulting in an uncontrolled catecholamine surge, which augments inflammation and leads to myocardial ischemia, causing the findings of dW pattern on the ECG[113].

STEMI-equivalent differential diagnosis

In addition to the dW pattern/dW syndrome, STEMI-equivalent conditions include Wellens syndrome, posterior myocardial infarction, T wave precordial instability, and delayed activation wave[113]. Posterior MI is seen with STD in leads V1-V3, unlike dW pattern, where STD typically involves V1-V4 and with dominant R waves[114]. STD must measure more than 0.5 mm and may sometimes progress into leads V5-V6[59]. Also, posterior MIs are linked with an acute inferior or lateral myocardial infarction[114].

Wellens syndrome, which may signify an impending myocardial infarction, can appear on the ECG as two distinctive T wave changes. The first type is characterized by deeply inverted T waves in leads V2 and V3, while the second type presents with biphasic T waves in leads V2 and V3 after angina relief[30,115,116]. It is also worth mentioning that no Q waves can be seen in Wellens and that precordial R wave progression is absent[115], indicating that reperfusion is the underlying mechanism in a non-complete occluded vessel. Furthermore, acute occlusion of the LCx may sometimes develop a rare ECG pattern, known as the delayed activation wave[117]. This pattern is characterized by a notch-like appearance in the terminal QRS complex, known as the N wave, with a height of at least 2 mm relative to the PR segment[59]. These notches can appear on different leads, with reports stating that they appear on leads I, II, III, augmented voltage foot, and augmented voltage left arm[117].

Another STEMI equivalent is T wave precordial instability, also known as loss of precordial T wave balance. The key factor in this pattern is the T wave amplitude, which is greater in V1 than in V6, and an upright T wave is present in V1[59]. This pattern is critical to know, as not all patients’ ECGs presenting with it are suffering from coronary artery occlusion; it may be explained as ventricular early repolarization[118,119]. Figure 3 shows the typical and atypical ECG presentations of LAD stenosis, in addition to the types of STEMI equivalent.

Figure 3 ST-elevation myocardial infarction-equivalent and de Winter pattern. STEMI: ST-elevation myocardial infarction; dWP: De Winter pattern; pLAD: Proximal segment of the left anterior descending; mLAD: Mid segment of the left anterior descending; dLAD: Distal segment of the left anterior descending; ATP: Adenosine triphosphate; LAD: Left anterior descending; NSTEMI: Non-ST-elevation myocardial infarction; RV: Right ventricle; RCA: Right coronary artery; LCx: Left circumflex; MI: Myocardial infarction; STE: ST-segment elevation; aVR: Augmented vector right ECG lead; STD: ST-segment depression; aVL: Augmented vector left ECG lead.

Pitfalls of dW syndrome/dW pattern

The major pitfalls in managing dW syndrome/pattern include its frequent misdiagnosis as non-STEMI, leading to inappropriate patient triage, and the failure to recognize its dynamic ECG evolution, which results in critical delays in urgent revascularization.

Management of dW syndrome/dW pattern

Currently, the clinical management of dW syndrome/dW pattern primarily requires attention to: (1) Guidelines and consensus on the management of the dW phenomenon are needed; (2) ECG alone may fail to predict the angiographic finding in 30% of ACS cases; therefore, a differential diagnosis list and a high index of suspicion should be maintained to reduce time-to-treat and mortality; (3) Collaboration is necessary between primary care, the emergency department team, and cardiologists (interprofessional team); (4) A serial ECG is recommended whenever dW pattern is suspected; (5) dW pattern or dW syndrome should be considered a STEMI equivalent, although it is not explicitly detailed in the American Heart Association/American College of Cardiology guidelines; (6) Continuous monitoring is needed as dW pattern can evolve into classic STEMI; (7) Early cardiologist consultation, optimized medications, and admission to a monitored intensive care unit are recommended; (8) CAG, timely revascularization using PCI, or, otherwise, thrombolytic therapy can be administered if there is no contraindication; and (9) The impact of dW pattern on the left ventricle function requires assessment.

Limitations

The prevalence of dW pattern is low or underestimated, requiring a review of ECG databases in Department of Emergency and Cardiac Catheterization Units. Risk of bias assessment and study quality were not performed in this work, as we identified only a few retrospective studies with dW pattern subgroups, along with a few case series (159 papers yielded 322 cases). Follow-up of post-charge dW pattern patients was not documented. The individual culprit vessel was not specified for each patient’s age and gender in some retrospective studies. Comparisons by sex and age should be interpreted cautiously, as they are mainly based on scattered cases or case series. Given the small and uneven subgroups, statistical testing may yield misleading results and lead to overinterpretation. However, systematic reviews of case reports have shown considerable impact in reducing unfavorable outcomes for documenting clinical patterns and therapy outcomes in uncommon disorders[55]. The time to diagnose and intervene was not captured, as it was not specified in most cases. However, door-to-balloon was reported in three studies[10,11,13]. The time to evolution was rarely reported. The question now is, which of these three forms - dW pattern, dW sign, or dW syndrome - should be treated promptly? The literature did not differentiate among these three terms, which were often used interchangeably, and did not describe their silent form (silent pattern or sign). Therefore, this issue needs further elaboration and guidelines.

CONCLUSION

The three forms of the dW phenomenon (dW pattern, dW sign, and dW syndrome) are commonly used in most of the literature, with no consensus on the criteria for the chosen therapy. dW syndrome is preferable whenever associated clinical manifestations are present. This phenomenon has unique risk factors, pathophysiology, and angiographic characteristics. It should be managed as an indicator of a STEMI equivalent requiring urgent intervention. However, it is often underrecognized and therefore requires a high index of suspicion. Age and gender have distinct culprit lesions and coronary artery involvement in patients with dW pattern. Despite advances in understanding its dynamic nature and the clinical significance of STEMI equivalents, challenges persist in timely diagnosis and management. This review emphasizes the importance of enhancing clinician awareness, establishing standardized diagnostic protocols, and conducting further research into the pathophysiological mechanisms of this condition. By integrating current evidence, we emphasize that prompt recognition and aggressive reperfusion strategies, such as those used in STEMI protocols, are crucial for improving outcomes in this high-risk presentation.