• David Didlake

Something Winter This Way Comes

David Didlake

Acute Care Nurse Practitioner

Firefighter / Paramedic

@DidlakeDW


A 50 y/o Male was taking his dog for a leisurely stroll through the park when he suddenly experienced new onset chest discomfort. He waited for it to subside, but after 30 minutes of persistence he called 911.


EMS personnel found him seated on a bench, uncomfortable, but without gross distress. There was no obvious pallor, diaphoresis, or dyspnea, and he denied any prior episodes of vomiting. He described the pain as “nagging,” and equally not exacerbated by any kind of movement. A pertinent medical history remarkable for HTN was disclosed, which was well controlled on Rx Olmesartan. Otherwise, no admission of CAD, HLD, or family history of sudden cardiac death.


A 12 Lead ECG was recorded:



This is pathognomonic for classic deWinter T waves, indicative of LAD occlusion. The specific ST/T pattern was not fully appreciated by the attending EMS personnel, yet alarming enough to convince the patient to be seen in the Emergency Department despite his intentions of seeking evaluation on his own accord through his respective family physician.


The patient verbalized spontaneous improvement just before 324mg ASA administration. A second 12 Lead ECG was recorded:



This is a testament to the dynamic nature of coronary thrombosis and thrombolysis. Here the ST segments are not so deep, nor are the T waves so wide and bulky, because of improved coronary flow at the level of the occlusion. But the lesion is still active! This is demonstrated by lingering Hyperacute T waves in V2-V5 (i.e. hyperacute in their own rite despite attenuated ST segments).


MICU transport was unremarkable. The patient’s vital signs remained stable, and he was equally comfortable, even verbalizing that his pain had mostly resolved. The nearest PCI center was a stone’s throw from the incident location, so overall transport duration was minimal. However, upon entry into the respective hospital campus, the patient experienced restoration of pain and displayed an uncomfortable grimace.


A third, and final, EMS 12 Lead ECG was recorded:



The precordial ST segments (even Leads I/aVL, as well) have reverted to a dramatically depressed state. These sunken J-points make a rapid, crescendo rise into large, fat, and bulky T waves. Again, pathogonomic signature markers of deWinter LAD occlusion!


The ST changes went overlooked by both the ED physician and the on-call cardiologist, and the patient was subsequently admitted to telemetry. However, when the Troponin I returned 8.4 ng/mL during the night – in the presence of unmitigated pain – cardiology decided to take him to the Cath Lab.



The red arrow shows a 90% LAD occlusion at the D1 branch.



One stent was deployed with restorative TIMI-0 flow.


A more detailed discussion on the deWinter ECG can be found here (with peer review by Dr. Steve Smith).


https://www.ems12lead.com/post/the-dewinter-debacle


deWinter first reported his unique characteristics of LAD occlusion in 2008, and since the respective ECG changes do not fit the conventional STEMI paradigm (as he even stated – “instead of signature ST-segment elevation” ….) it has been subsequently deemed a STEMI-equivalent. He described:

  • 1-3 mm upsloping STD at the J-point in V1-V6

  • Tall, symmetrical T waves in affected leads

  • QRS complexes not usually wide, or only slightly widened

  • Potential loss of precordial R-wave progression

  • 1-2 mm STE aVR in most patients

N Engl J Med (2008); 359, 19


It was found that the deWinter pattern was both static and persistent up to the point of invasive procedure, and associated with considerable loss of myocardium despite successful PCI, although a specific window of time for salvageable heart muscle after onset was not elucidated in the original publication.


Accurate identification is absolutely necessary as this pattern can be easily misinterpreted for something less nefarious: for example, generic “subendocardial ischemia.” deWinter characteristics have been presented elsewhere in the literature:


Letter to the Editor: deWinter sign – A STEMI Equivalent

  • STD 1mm at the J-point

  • Tall, symmetrical T waves in the precordial leads

  • 0.5-1 mm STE aVR

Indian Heart Journal (2018); 70,758-766


Case Report: deWinter Pattern – An Unusual but Very Important Electrocardiographic Sign to Recognize

  • Loss of R waves in precordial leads

  • Upsloping STD at J-point greather than 1mm

  • Tall, positive, and symmetrical T waves

Canadian Cardiovascular Society (2019); CJC Open Vol 2, 1 22-25


Case Report: deWinter Syndrome – An Easily Ignored but Life-threatening Disease

  • 1-3 mm upsloping STD at the J-point in precordial leads

  • Persistent hyperacute T wave

  • Does not always progress into classic STEMI

  • Slight aVR STE

J South Med Univ (2020); 40(7), 919-921


Editorial Comment: Electrocardiographic Diagnosis of Life-threatening STEMI Equivalents – When Every Minute Counts

  • Isolated Posterior STEMI

  • Wellens Syndrome

  • Hyperacute T waves

  • “Shark Fin” Sign

  • deWinter Syndrome

  • Upsloping STD >1mm at the J-point

  • Tall, symmetrical T waves in precordial leads

JACC: Case Reports (2019); Vol 1, No 4


It has been demonstrated in previous posts that deWinter is often overlooked due to periodic absence of ST elevation in aVR. It was present only minimally in this case, and I can’t say with certainty if said unimpressive manifestation had any decision making influence during ED admission.


deWinter continues to rear its ugly face, and although the ST depression itself is grossly apparent to the naked eye, it’s the hyperacute T waves that unequivocally categorize this specific ECG pattern as deadly.


About Me

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I am the Battalion Chief of EMS for Hilton Head Island Fire Rescue and obsessed with all things process improvement, system performance, human factors, crew resource management, and evidence-based performance measures for time-sensitive diagnoses.

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