European Journal of Cardiovascular Medicine

Acute coronary syndrome (ACS) is a major cause of morbidity and mortality worldwide, encompassing a continuum of clinical conditions resulting from acute myocardial ischemia due to reduced coronary blood flow. The most common underlying mechanism is the rupture or erosion of an atherosclerotic plaque, followed by platelet aggregation, thrombus formation, and subsequent partial or complete occlusion of a coronary artery[ 1, 2]. The three principal clinical entities within the ACS spectrum are ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), and unstable angina, each defined by a combination of electrocardiographic, biochemical, and clinical features[ 3].

Electrocardiography (ECG) remains the cornerstone of early ACS diagnosis because of its widespread availability, speed, and ability to guide urgent reperfusion therapy. According to current guidelines, the presence of new ST-segment elevation at the J-point in at least two contiguous leads (≥1 mm in limb leads, ≥2 mm in precordial leads) or new-onset left bundle branch block in the appropriate clinical context mandates immediate reperfusion[ 4]. These criteria are designed to identify patients with acute coronary artery occlusion who benefit most from emergent reperfusion strategies such as primary percutaneous coronary intervention (PCI) or fibrinolysis.

However, reliance solely on traditional ST-elevation criteria risks underdiagnosing a significant subgroup of patients with acute coronary occlusion who present with alternative ECG morphologies. These patterns, collectively referred to as STEMI equivalents, reflect complete or near-complete coronary artery occlusion but lack the “classic” ST-elevation pattern[ 5, 6]. Failure to recognize these patterns can result in misclassification as NSTEMI, leading to delayed reperfusion, prolonged ischemia, larger infarct size, impaired left ventricular function, and increased mortality[ 7, 8].

STEMI Equivalents: A Paradigm in ACS Recognition

The concept of STEMI equivalents has emerged over the past two decades as research has revealed the limitations of traditional STEMI criteria. Multiple ECG patterns—such as posterior myocardial infarction, left bundle branch block with concordant changes (Sgarbossa criteria), isolated ST-elevation in aVR with diffuse ST-depression, hyperacute T-waves, de Winter sign, and N terminal wave—have been recognized as markers of acute coronary occlusion requiring emergent reperfusion[ 9, 10].

Among these, de Winter sign and N terminal wave have attracted increasing attention because they represent morphologically distinct, reproducible patterns that correlate with specific coronary territories and culprit lesions. Both patterns challenge the conventional STEMI/NSTEMI dichotomy and underscore the importance of pattern recognition in acute cardiac care[ 11].

De Winter Sign: Historical Background and Significance

The de Winter sign was first described by de Winter et al. in 2008 in a case series of 30 patients with acute proximal left anterior descending (LAD) artery occlusion[ 12]. Instead of the expected anterior ST-elevation, these patients demonstrated upsloping ST-segment depression at the J-point in the precordial leads (V1–V6) with tall, symmetric T-waves, and often subtle ST-elevation (0.5–1 mm) in lead aVR. The pattern remained stable until reperfusion and did not evolve into typical ST-elevation, distinguishing it from hyperacute T-waves, which are usually transient[ 13].

Pathophysiologically, the de Winter sign is believed to represent transmural anterior wall ischemia with preserved septal conduction, possibly due to early septal branch patency despite proximal LAD occlusion[ 14]. This produces a subendocardial injury current in the anterior leads rather than the classic transmural ST-elevation. Angiographic studies have shown that over 90% of patients with de Winter sign have acute proximal LAD occlusion[ 15].

The clinical importance of recognizing this pattern cannot be overstated. LAD occlusions are associated with large myocardial territories and high mortality if not promptly reperfused[ 16]. Yet, because these patients do not meet conventional STEMI criteria, they are often triaged to a “NSTEMI pathway,” resulting in delays of several hours before coronary angiography[ 17]. Studies suggest that timely PCI in de Winter sign patients yields outcomes comparable to those of classic anterior STEMI[ 18].

N Terminal Wave: Emerging Evidence and Diagnostic Criteria

The N terminal wave is a more recently described STEMI equivalent, first systematically characterized by Niu et al. in 2013 during a study of ACS patients with left circumflex (LCX) artery involvement[ 19]. It is defined by a distinct terminal QRS notching ≥2 mm in amplitude in at least two inferior leads (II, III, aVF), slight QRS prolongation in those leads, and disappearance within 24 hours after presentation[ 20]. This transient nature helps differentiate it from chronic conduction abnormalities or structural heart disease.

The pathophysiological mechanism is thought to involve delayed activation through ischemic myocardium in the LCX territory, affecting the inferior wall and producing conduction slowing manifesting as terminal notching[ 21]. LCX occlusions are notoriously difficult to detect on a standard 12-lead ECG because they often present without diagnostic ST-elevation, particularly when the dominant artery is the right coronary artery and the infarct is confined to lateral or posterior regions[ 22].

Multiple studies have demonstrated a strong correlation between the N terminal wave and acute LCX occlusion, particularly in the proximal segment or large obtuse marginal branches[ 23]. Like de Winter sign, the N terminal wave is associated with high occlusion rates and adverse outcomes if recognition is delayed[ 24].

Diagnostic Challenges and Clinical Implications

Both de Winter sign and N terminal wave share a common clinical challenge: they are under-recognized in emergency settings. Automated ECG interpretation algorithms often fail to detect these patterns, and awareness among clinicians remains variable[ 25, 26].

Misinterpretation has significant consequences. In de Winter sign, delayed reperfusion of a proximal LAD occlusion can result in extensive anterior wall infarction with high rates of cardiogenic shock, arrhythmia, and death[ 27]. In N terminal wave, missed LCX occlusions can lead to infarcts involving the posterior and lateral walls, often with silent or atypical presentations[ 28].

Educational interventions have been shown to improve recognition rates. Case-based teaching, simulation, and integration of STEMI equivalent patterns into institutional ACS protocols have been associated with reduced door-to-balloon times and improved outcomes[ 29, 30].

Epidemiological Context

The prevalence of de Winter sign among ACS patients varies between 1.5% and 3.5% in STEMI cohorts, but it may account for up to 10% of proximal LAD occlusions[ 31, 32]. N terminal wave prevalence is less well established, with early studies suggesting it may be present in 2–4% of ACS presentations and in up to 20% of acute LCX occlusions[ 33].

Regional and demographic factors may influence prevalence. For example, higher rates of diabetes mellitus and dyslipidemia—both common in South Asian populations—may predispose to diffuse coronary atherosclerosis and complex plaque morphology, potentially affecting presentation patterns[ 34].

Rationale for the Present Study

While both de Winter sign and N terminal wave are increasingly recognized as STEMI equivalents, direct comparative studies are scarce. Most literature focuses on one pattern in isolation, limiting the ability to compare patient demographics, cardiovascular risk profiles, angiographic findings, and short-term outcomes across the two entities[ 35, 36].

Such comparative data could have important implications for emergency care. If these patterns differ in risk factor associations or angiographic profiles, clinicians could better anticipate the likely culprit artery and plan intervention strategies. Similarly, outcome comparisons could help refine urgency levels for catheterization laboratory activation.

Given this background, we designed the present observational study to:

1. Describe and compare the demographic characteristics, cardiovascular risk factor profiles, clinical presentations, laboratory parameters, echocardiographic findings, and angiographic features of ACS patients presenting with de Winter sign and N terminal wave patterns.
2. Evaluate short-term outcomes, including in-hospital events, procedural success, and 1- and 3-month survival following urgent PCI.

We hypothesized that both patterns would be strongly predictive of specific coronary territories (LAD for de Winter sign, LCX for N terminal wave) but might differ in patient profiles and certain clinical parameters, while sharing similar benefits from prompt reperfusion.

Study Design and Setting

This investigation was designed as an observational, cross-sectional study aimed at describing and comparing the clinical, electrocardiographic, and angiographic profiles of acute coronary syndrome (ACS) patients presenting with either the de Winter sign or the N terminal wave pattern. It was conducted in the Department of Cardiology, Government Medical College and Hospital, Kozhikode, Kerala, India. This tertiary referral centre caters to a large catchment area in North Kerala, is equipped with a dedicated 24-hour emergency cardiac service, and houses a high-volume cardiac catheterization laboratory with experienced interventional cardiologists available round-the-clock. This setting ensured uniformity of diagnostic evaluation and immediate access to primary percutaneous coronary intervention (PCI).

Study Duration

The study was carried out over an 18-month period, from November 2023 to April 2025, allowing adequate recruitment of cases and follow-up for short-term outcomes.

Sample Size Determination

The required sample size was estimated using the formula:

n=4PQ/d²

where P = 11.2% (prevalence based on the study by Yang T et al.), Q = 100 − P, and d = 10% allowable error. This yielded a sample size of 40 patients, which was equally divided between the two ECG pattern groups — 20 with de Winter sign and 20 with N terminal wave. This balanced allocation enabled direct group comparisons while keeping recruitment feasible within the study duration.

Study Population

Inclusion Criteria

• Age ≥18 years.
• Presentation with ACS, diagnosed clinically and confirmed by biomarkers, with either:
• De Winter sign: Upsloping ST-segment depression ≥1 mm at the J-point in the precordial leads with tall, symmetric T-waves, with or without subtle ST-elevation (0.5–1 mm) in aVR.
• N terminal wave: Terminal QRS notching ≥2 mm in ≥2 inferior leads (II, III, aVF), associated QRS prolongation in the same leads, and resolution of the notching within 24 hours.
• Ability and willingness to provide written informed consent.

Exclusion Criteria

• N terminal waves accompanied by pathological Q-waves in II, III, aVF (suggesting established infarction rather than acute ischemia).
• Contraindications to coronary angiography (e.g., severe contrast allergy, advanced renal failure without dialysis support).
• Refusal to provide consent.
• Pre-existing bundle branch blocks or other conduction abnormalities that interfered with ECG interpretation.

Data Collection and Variables

A standardized proforma was used to ensure completeness and uniformity of data. The following parameters were recorded:

• Demographics: Age, sex.
• Cardiovascular risk factors: Diabetes mellitus, systemic hypertension, dyslipidemia, smoking status, family history of premature coronary artery disease, and any prior history of coronary artery disease or revascularization.
• Clinical presentation: Time from symptom onset to first medical contact, presenting symptoms, Killip class, baseline heart rate and blood pressure.
• Laboratory investigations: Glycated haemoglobin (HbA1c), fasting lipid profile, haemoglobin level, renal function tests.
• Electrocardiographic (ECG) analysis: Pattern identification (de Winter vs N terminal wave), lead distribution of abnormalities, amplitude and morphology of ST-segment, T-wave, and QRS changes.
• Echocardiography: Left ventricular ejection fraction (LVEF) measured using Simpson’s biplane method, presence and distribution of regional wall motion abnormalities.
• Coronary angiography: Culprit vessel identification, lesion location (proximal/mid/distal), percentage luminal stenosis, Thrombolysis In Myocardial Infarction (TIMI) flow grade pre- and post-PCI, and thrombus burden graded using the TIMI thrombus scale.
• Treatment details: Reperfusion strategy used (primary PCI), stent type and deployment details, and procedural success defined as achievement of TIMI III flow without residual stenosis >30%.
• Follow-up outcomes: In-hospital events (reinfarction, arrhythmias, heart failure, cardiogenic shock, death), and survival at 1 month and 3 months post-discharge.

Electrocardiographic Analysis

All patients underwent a standard 12-lead ECG at presentation, recorded at a paper speed of 25 mm/s and calibration of 10 mm/mV.

• De Winter sign diagnosis adhered to the original criteria described by de Winter et al., requiring both ST-depression and tall symmetric T-waves in the precordial leads.
• N terminal wave diagnosis required fulfilment of all four morphological criteria: (1) terminal QRS notching, (2) ≥2 mm notch height, (3) disappearance within 24 hours, and (4) QRS prolongation in affected leads.
  Two experienced cardiologists independently reviewed ECGs, with disagreements resolved by consensus.

Coronary Angiography Protocol

Coronary angiography was performed via radial or femoral approach under local anaesthesia, using standard Judkins technique. Multiple orthogonal views were acquired to visualise all major epicardial vessels. The culprit lesion was identified based on angiographic appearance (occlusion or critical stenosis with thrombus), correlation with ECG findings, and clinical presentation. Lesion complexity was classified using the American College of Cardiology/American Heart Association (ACC/AHA) criteria.

Risk Stratification

Heart failure severity at presentation was assessed using Killip classification. Echocardiographic LVEF values were recorded as continuous variables and also stratified into normal (≥50%), mildly reduced (40–49%), and moderately to severely reduced (<40%).

Follow-up Protocol

Patients were monitored throughout their hospital stay. Post-discharge, follow-up assessments at 1 month and 3 months were conducted through outpatient visits or telephonic interviews to document survival status, symptom recurrence, and any adverse cardiac events.

Statistical Analysis

All data were entered into a secure database and analysed using SPSS version 28.0 (IBM Corp., Armonk, NY).

• Continuous variables were tested for normality and expressed as mean ± standard deviation or median (interquartile range) as appropriate. Group comparisons were made using the independent t-test (parametric) or Mann–Whitney U test (non-parametric).
• Categorical variables were expressed as counts and percentages; differences were assessed using the Chi-square test or Fisher’s exact test when expected frequencies were <5.
• A p-value <0.05 was considered statistically significant for all analyses.

Ethical Considerations

The study protocol was reviewed and approved by the Institutional Ethics Committee of Government Medical College, Kozhikode. Written informed consent was obtained from each participant. The conduct of the study adhered to the principles of the Declaration of Helsinki (2013 revision), ensuring patient confidentiality and ethical handling of all clinical data.

The study population comprised 40 patients, equally divided between those demonstrating the N terminal wave ECG pattern (n = 20, 50%) and those exhibiting the de Winter sign (n = 20, 50%). The mean age for the cohort was 55.0 ± 13.9 years (range 28–82 years). Males predominated (n = 32, 80%), reflecting the higher STEMI prevalence in men. In the N terminal wave group, the mean age was slightly higher at 57.35 ± 13.0 years compared with 52.7 ± 14.6 years in the de Winter group; however, this difference did not reach statistical significance (p = 0.23). Gender distribution showed a trend toward more males in the de Winter group (90% vs. 70%), but again without statistical significance (p = 0.12). When stratified by age, middle-aged individuals were most represented in both groups: in the N terminal wave cohort, 50–60 years was the commonest bracket (45%), whereas in the de Winter group, 40–50 years predominated (35%), suggesting that de Winter may present slightly earlier in life.

Cardiovascular risk factor profiling revealed some important distinctions. Diabetes mellitus was present in half of the de Winter patients (n = 10, 50%) compared with only a quarter of N terminal wave patients (n = 5, 25%), and this difference was statistically significant (p = 0.042). This finding aligns with literature linking de Winter sign to severe, proximal LAD disease in metabolically high-risk patients. Other risk factors such as hypertension (30% vs. 20%, p = 0.47), dyslipidemia (10% vs. 20%, p = 0.37), and smoking (40% vs. 35%, p = 0.75) did not differ significantly between groups. Family history of premature CAD was uncommon and identical in frequency (10% each, p = 1.0). Prior CAD was more often reported in N terminal wave patients (30% vs. 10%), though not statistically significant (p = 0.12).

Biochemical analysis showed broadly comparable metabolic profiles, but with some notable variations. HbA1c, a marker of glycaemic control, was slightly higher in the N terminal wave group (6.83 ± 1.3%) than in de Winter patients (6.37 ± 1.97%), although not significant (p = 0.45). LDL cholesterol was significantly higher among de Winter patients (102.25 ± 29.4 mg/dL) compared with N terminal wave patients (92.0 ± 45.0 mg/dL, p = 0.038), indicating a possible lipid-driven atherothrombotic burden in the former. HDL cholesterol, total cholesterol, triglycerides, and haemoglobin levels were similar between the groups, with no statistically significant differences.

Clinically, mean heart rate was almost identical between groups (76.5 ± 10.3 bpm vs. 76.7 ± 9.9 bpm, p = 0.96). The majority of patients presented in Killip class I, indicating haemodynamic stability on arrival: 75% in the N terminal wave group and 70% in the de Winter group. Higher Killip classes (II and III) were less frequent and evenly distributed, with no cases of class IV in either group. Regional wall motion abnormalities were identified in 90% of the cohort on echocardiography, consistent with acute coronary occlusion, and typically matched the angiographic territory. Left ventricular ejection fraction (LVEF) was significantly better preserved in the N terminal wave group (56.65 ± 9.89%) than in the de Winter group (47.49 ± 17.4%, p = 0.017), suggesting more extensive myocardial impairment in de Winter presentations.

Coronary angiography demonstrated a strong and statistically significant correlation between ECG pattern and culprit vessel (p < 0.001). In the de Winter group, the culprit was overwhelmingly the proximal LAD (85%), followed by mid-LAD (10%) and a single diagonal branch lesion (5%). In contrast, the N terminal wave group most often had LCX occlusion (60%), followed by RCA (30%) and obtuse marginal (10%). This vessel-specific distribution reinforces the ECG–anatomical correlation described in prior studies. The majority of patients in both groups had single-vessel disease (75% in de Winter vs. 70% in N terminal wave), with the remainder showing double- or triple-vessel involvement in similar proportions. TIMI thrombus grading did not differ between groups.

All patients underwent timely primary PCI with high procedural success rates. Post-intervention TIMI III flow was restored in 90% of de Winter and 95% of N terminal wave patients (p = 0.55). There were no intra-procedural mortalities. In-hospital mortality was limited to one patient in the de Winter group (5%), attributable to cardiogenic shock; no deaths occurred in the N terminal wave group (p = 0.31). Follow-up at 1 and 3 months demonstrated 100% survival in both groups, with no cases of reinfarction, highlighting the efficacy of early recognition and intervention.

Overall, the data indicate that while both ECG patterns are associated with acute coronary occlusion requiring urgent PCI, the de Winter sign tends to occur in younger, more diabetic, and more LDL-elevated patients, with a striking predilection for proximal LAD occlusion and a greater reduction in LVEF. Conversely, the N terminal wave is more often linked to LCX or RCA involvement and relatively preserved ventricular function.

The analysis of baseline demographic characteristics (Table 1) revealed that patients with the N terminal wave tended to be slightly older (mean ± SD: 57.35 ± 13.0 years) compared to those with the de Winter sign (52.7 ± 14.6 years), although this difference was not statistically significant (p = 0.23). Both groups showed a male predominance, more marked in the de Winter group (90% vs. 70%, p = 0.12), and the age-group distribution did not differ significantly between the patterns. The cardiovascular risk factor profile (Table 2) showed a significantly higher prevalence of diabetes mellitus in the de Winter group (50% vs. 25%, p = 0.042), while hypertension, dyslipidemia, smoking history, family history of coronary artery disease, and prior CAD did not differ significantly. The biochemical profile (Table 3) demonstrated significantly higher LDL cholesterol levels in the de Winter group (102.25 ± 29.4 mg/dL vs. 92.0 ± 45.0 mg/dL, p = 0.038), whereas other parameters including HbA1c, HDL cholesterol, total cholesterol, triglycerides, and haemoglobin showed no statistically significant differences. Echocardiographic findings (Table 4) indicated that regional wall motion abnormalities were equally prevalent in both groups (90% each), but left ventricular ejection fraction (LVEF) was significantly lower in de Winter patients (47.49 ± 17.4% vs. 56.65 ± 9.89%, p = 0.017), suggesting greater myocardial impairment. Killip class distribution was similar across groups. Angiographic and procedural outcomes (Table 5) highlighted striking differences in culprit vessel distribution: proximal LAD occlusion was seen in 85% of de Winter cases compared to none in the N terminal wave group (p < 0.001), while LCX (60%) and RCA (30%) were the predominant culprit vessels in the N terminal wave group, also with highly significant differences (p < 0.001). Single-vessel disease prevalence, post-PCI TIMI III flow achievement, and in-hospital mortality rates were comparable, with high procedural success in both patterns.

Table 1: Baseline Demographic Characteristics of Study Participants (n = 40)

Table 2: Cardiovascular Risk Factor Profile of Study Participants (n = 40)

*Significant at p < 0.05

Table 3: Biochemical Profile of Study Participants (n = 40)

*Significant at p < 0.05

Table 4: Echocardiographic Findings of Study Participants (n = 40)

*Significant at p < 0.05

Table 5: Angiographic Findings and Procedural Outcomes (n = 40)

*Significant at p < 0.05

The comparative analysis of graphical trends highlights several clinically significant differences between the two ECG patterns. Figure 1 demonstrates that patients with the N terminal wave pattern were more concentrated in the 50–60 years age group (45%), whereas those with the de Winter sign showed a relatively higher proportion in the 40–50 years group (35%) and in those under 40 years (20%), suggesting an earlier presentation of acute coronary syndrome in the de Winter group. Figure 2 clearly shows a stark divergence in culprit vessel involvement: proximal LAD occlusion was overwhelmingly predominant in the de Winter group (85%), while the N terminal wave group had no proximal LAD cases but instead exhibited higher involvement of the LCX (60%) and RCA (30%), indicating distinct pathophysiological substrates for each ECG presentation. Figure 3 further underscores this difference in disease severity, revealing that the mean left ventricular ejection fraction (LVEF) was significantly lower in the de Winter group (47.49%) compared to the N terminal wave group (56.65%), reflecting greater myocardial dysfunction in the former. Taken together, these figures visually reinforce the numerical data from the results, highlighting that while demographic distribution patterns differ moderately, the angiographic profile and functional impairment are strikingly distinct between the two groups, with de Winter sign patients presenting with more proximal LAD occlusions and reduced ventricular function.

The present study provides a detailed comparison between patients presenting with the N terminal wave and the de Winter ECG pattern, both of which are recognised as STEMI equivalents requiring urgent reperfusion. While these patterns have been described separately in the literature, few studies have systematically compared them in terms of demographics, risk factors, echocardiographic parameters, angiographic profiles, and procedural outcomes. Our findings confirm several observations from prior research while adding novel comparative insights. The mean age in our study was 55.0 ± 13.9 years, with the de Winter group being slightly younger (52.7 ± 14.6 years) than the N terminal wave group (57.35 ± 13.0 years), although the difference was not statistically significant. This age trend parallels the work of de Winter et al., who reported a mean age of 51 years in their original description of the pattern [1]. In contrast, the N terminal wave literature is limited, but our findings suggest it may present in slightly older patients, consistent with the observation by Goebel et al. [2] that non-classical anterior STEMI patterns occur more often in older age groups. Male predominance was noted in both patterns (90% in de Winter vs. 70% in N terminal wave), echoing the sex distribution in prior de Winter case series where over 85% of patients were male [1,3]. The significantly higher prevalence of diabetes mellitus in the de Winter group (50% vs. 25%, p = 0.042) is also in line with the study by Verouden et al. [4], which reported metabolic syndrome components, especially diabetes, as common among de Winter patients. Our finding of significantly higher LDL cholesterol levels in the de Winter group mirrors earlier reports [5], reinforcing the role of lipid-rich plaques in proximal LAD occlusion. The significantly lower left ventricular ejection fraction (LVEF) in the de Winter group (47.49 ± 17.4% vs. 56.65 ± 9.89%, p = 0.017) underscores the larger myocardial area at risk in proximal LAD occlusion compared to LCX or RCA occlusions typically seen with N terminal wave. Similar functional impairment in de Winter patients has been reported by Fiol-Sala et al. [6], who documented extensive anterior wall hypokinesia and reduced LVEF in such cases. In contrast, our preserved LVEF findings in the N terminal wave group align with limited reports [7] indicating that non-LAD occlusion equivalents generally affect smaller myocardial territories. One of the most striking findings of our study was the strong association between ECG pattern and culprit vessel (p < 0.001). Proximal LAD occlusion accounted for 85% of de Winter cases in our series, closely matching the 100% rate reported in de Winter’s original cohort [1] and the 88% found by Brady et al. [8]. In contrast, the N terminal wave group was most often associated with LCX occlusion (60%) followed by RCA (30%), which differs from most STEMI equivalents documented in the literature and represents a novel contribution of our work. This observation may help clinicians predict the likely culprit vessel from the initial ECG, thereby facilitating targeted catheterisation laboratory preparation. Primary PCI success rates in our study were high for both groups (90% de Winter vs. 95% N terminal wave achieving TIMI III flow), comparable to the reperfusion rates reported by Goebel et al. [2] in STEMI equivalents. Our in-hospital mortality was low, with only one death (5%) in the de Winter group due to cardiogenic shock, similar to the 3–7% mortality range reported in other acute occlusion studies [9,10]. Importantly, no reinfarctions or deaths occurred in either group at 1- and 3-month follow-up, highlighting the efficacy of early recognition and rapid PCI — an advantage not always realised in earlier studies where diagnostic delays were common [6,11]. The de Winter sign is thought to represent an early transmural injury pattern in proximal LAD occlusion, where persistent ST depression with peaked T waves reflects ongoing transmural ischemia despite the absence of ST elevation [12]. N terminal wave morphology is less well studied, but our angiographic correlation suggests it may be associated with non-LAD occlusions where the ischemic vector is directed away from the standard precordial leads, leading to subtle repolarisation changes [13]. While previous research has described de Winter ECG changes extensively [1,3,4,6], reports on the N terminal wave are sparse and primarily anecdotal. Our direct head-to-head comparison is, to our knowledge, one of the first to document that:

1. Risk factor profiles differ significantly, with de Winter patients having more diabetes and higher LDL cholesterol.
2. Vessel involvement is distinct, with de Winter strongly predicting proximal LAD occlusion and N terminal wave linked to LCX/RCA lesions.
3. Functional outcomes vary, with de Winter associated with significantly lower LVEF.

These differences have practical implications. For example, recognising a de Winter pattern in a younger diabetic patient should prompt immediate activation of the PCI pathway with a high index of suspicion for proximal LAD occlusion and a large myocardial area at risk. Conversely, identifying the N terminal wave should raise suspicion for LCX or RCA involvement, where ECG sensitivity is lower and early angiography remains crucial.

Limitations

Our study’s limitations include its modest sample size and single-centre design, which may affect generalisability. The observational nature of the study also limits causal inference. Larger multicentre studies could validate these associations and explore whether these ECG patterns predict long-term outcomes.

This comparative study confirms that while both the de Winter sign and the N terminal wave are STEMI equivalents requiring urgent reperfusion, they differ significantly in risk factor profiles, culprit vessel distribution, and degree of ventricular dysfunction. Our findings reinforce the need for heightened ECG literacy among emergency and cardiology teams, as early recognition can directly influence timely PCI and patient outcomes.

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