OMI Equivalents and Special Syndromes DE_WINTER

De Winter Pattern (OMI Equivalent)

Guillermo Nimubona Castrillo
Graduate in Medicine · AI Consultant
Editorial track:

Technical model documentation. Not reviewed by a cardiology specialist.

Last technical review:

Also known as: de Winter Pattern (OMI Equivalent) · patron de de Winter · de Winter · ondas T de de Winter · sindrome de de Winter · de Winter pattern · de Winter T waves · equivalente de SCACEST · de Winter STEMI equivalent

What this page documents

This page documents bioelectrical waveform synthesis and vascular topology for the De Winter electrocardiographic pattern (DE_WINTER), categorized in the simulator as an acute coronary occlusion (OMI) equivalent. Mathematical constants for J-point depression, precordial T-wave morphology, and its localization to the proximal left anterior descending artery are detailed. This text represents technical documentation of the MioAtlas computational model and must not be used as clinical decision criteria for real patients.

Model parameters

The electrocardiographic signal generator (src/ecg/wavegen.ts) and coronary phenotype catalog (src/coronaries/catalog.ts) parameterize the De Winter pattern using the following values:

Parameter Engine value Unit Computational morphometric description
compatibleSites LMCA, LAD_VERY_PROX, LAD_PROX, LAD_MID — Compatible arterial territories: left main trunk and very proximal, proximal, or mid left anterior descending artery.
defaultSeverity SUBTOTAL — Critical subtotal luminal stenosis with insufficient residual microflow to perfuse the anterior myocardium.
J-point depression (V2-V3) -0.24 to -0.26 mV (2.4 to 2.6 mm) J-point depression in anteroseptal precordial leads with continuous upsloping ST segment.
J-point depression (V4-V6) -0.14 to -0.22 mV (1.4 to 2.2 mm) J-point depression in lateral precordial leads (V4 through V6).
effectiveTAmp (V1-V6) +1.15 mV (11.5 mm) Maximum positive amplitude of hyperacute, tall, symmetrical, peaked precordial T waves.
tSigma 0.040 s Standard deviation of the repolarization Gaussian bell curve defining the peaked T-wave morphology.
maxStDev (aVR) +0.10 mV (1.0 mm) Concordant ST-segment elevation in unipolar lead aVR (0.5 to 1.0 mm).
stUpslopeWindow 0.265 – 0.440 phase tau Temporal cardiac cycle window where ST segment directly upslopes from the J point into the T-wave peak.

Source of each parameter value

The implemented bioelectrical parameters originate from the following foundational publications:

  1. Original description of the electrocardiographic pattern: The combination of 1 to 3 mm J-point depression with upsloping ST segments into tall, peaked, symmetrical precordial T waves and reciprocal aVR elevation was first described by de Winter et al. (2008).
  2. Classification and nomenclature of transmural vs subendocardial ischemia: Definitions of injury currents and acute occlusion equivalents adhere to AHA/ACCF/HRS standards in Wagner et al. (2009).
  3. Morphology and duration of T wave and ST-T complex: Temporal dispersion and symmetrical amplitude parameters of ventricular repolarization are based on recommendations from Rautaharju et al. (2009).
  4. LAD segmentation and anatomical correlation: Compromised myocardial territories (segments 1, 2, 7, 8, 13, and 14) correspond to the 17-segment model of Cerqueira et al. (2002).

How it is modeled

In the simulator, selecting the DE_WINTER phenotype modifies transfer functions for the ST segment and T wave across all precordial leads (V1 to V6). Rather than modeling transmural injury as classic convex ST elevation, the algorithm applies negative displacement at the onset of the ST segment (J point) calibrated to -0.25 mV in V2 and V3.

An ascending linear ramp elevates potential along the ST interval, connecting without an isoelectric plateau into a narrow Gaussian repolarization curve (tSigma = 0.040) of high amplitude (effectiveTAmp = 1.15 mV). Simultaneously, lead aVR receives a direct positive current (+0.10 mV) reflecting basal subendocardial ischemia in the ventricular outflow tract.

What is NOT reproduced

The software incorporates mathematical simplifications designed to maximize real-time 3D rendering speed and robustness:

  • Spontaneous temporal evolution to STEMI: In clinical practice, the De Winter pattern is dynamic and can rapidly evolve within minutes to classic ST elevation upon complete thrombotic occlusion; the simulator maintains the selected steady-state parameterization.
  • Cardiac biomarker kinetics: High-sensitivity troponin curves and hourly release dynamics are not computed.
  • Plaque histology and intracoronary thrombosis: The 3D mesh illustrates macrovascular stenosis severity without modeling fibrous cap rupture, platelet aggregation, or distal microembolization (OCT/IVUS).
  • Hemodynamic instability and malignant ventricular arrhythmias: Primary ventricular fibrillation during the hyperacute phase is not spontaneously induced.

Interactive variants

You can verify model responses across different sites of the coronary tree and alternative phenotypes via these links:

To explore other phenotypes and OMI equivalents in the 3D simulator:

Related clinical comparisons

Sources and bibliographic references

  1. de Winter RJ, Verouden NJ, Wellens HJJ, Wilde AAM (2008). "A new ECG sign of proximal LAD occlusion". N Engl J Med.
  2. Wagner GS, Macfarlane P, Wellens H, et al. (2009). "Recommendations for the standardization and interpretation of the electrocardiogram: Part VI: Acute ischemia/infarction". Circulation.
  3. Rautaharju PM, Surawicz B, Gettes LS, et al. (2009). "Recommendations for the standardization and interpretation of the electrocardiogram: Part IV: The ST segment, T and U waves, and the QT interval". Circulation.
  4. Cerqueira MD, Weissman NJ, Dilsizian V, et al. (2002). "Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart". Circulation.