The deWinter Debacle
Updated: Aug 14, 2022
Firefighter / Paramedic
Acute Care Nurse Practitioner
Peer review with commentary by Dr. Stephen Smith
An adult male calls 911 for new onset central chest discomfort (approximately 20 minutes duration at the time of EMS activation) that radiates to the back. Paramedics find him uncomfortable and clammy with 9/10 pain severity. His blood pressure is 162/104. HLD is the only medical history disclosed. This is the time-zero ECG at 2206 hours.
V2-V5 display varying magnitude of STD that upwardly slope into Hyperacute T-waves (HATW).
Leads I/aVL display HATW.
aVF shows scooped out STD with perceptible down-up TW.
Lead III shows STD with prominent TWI that is reciprocal to the HATW in aVL.
Very slight upwardly coved STE aVR.
Dx deWinter OMI.
ASA 324mg was administered. The paramedics identified “ischemia” and transported the patient to the nearest PCI center, where he arrived with lingering complaints and symptoms. This is the receiving ED admission ECG at 2235 hours.
Mostly similar findings.
The STE aVR is becoming slightly more pronounced.
The first 4th generation (not high sensitivity) Troponin I returned undetectable. The attending ED provider was concerned for deWinter pattern and pursued cardiology consultation, but emergent cath was deemed unnecessary because (according to the cardiologist) deWinter requires profound STE in aVR, which the ECG was lacking in his/her estimation. It was determined that the ischemic changes were the result of subendocardial ischemia secondary to mismatches of oxygen supply-demand. The patient was subsequently admitted to the hospital for medical management.
Smith comment: The presence of only minimal STE in aVR should have no bearing on this case. I would add that the presence of HATW alone, without ANY ST depression, is just as alarming as deWinter’s (which has ST depression). When there are HATW, you do not need any STD with reciprocal STE in aVR to make the diagnosis of LAD OMI. It should be noted that, even if one does not recognize the Occlusion MI on this ECG, ischemia that is persistent (continued chest pain) is a hard indication for emergent cath lab activation according to the cardiologists’ own guidelines (American College of Cardiology/American Heart Association Guidelines for the management of Non-ST-Elevation-Myocardial Infarction).
Unfortunately, his pain was never fully mitigated. A second Trop I returned 26 ng/mL at 0130 hours, ultimately peaking at 144 ng/mL (a troponin at this level indicates a massive amount of permanent myocardial loss). This third value compelled Cath investigation where the following was discovered:
LVEDP 27 mmHg
LAD – 95% pLAD ulcerated plaque, balloon with DES (no comment on TIMI flow available)
RCA luminal, dominant
Subsequent to PCI another Trop I returned at 79 ng/mL (although specific time unspecified). A final ECG was recorded at 0957 hours.
QS V1-V2 and rS V3-V6 to suggest transmural infarct of the anterior wall.
Dedicated followers of the Smith ECG Blog probably felt deep anguish watching this story unfold, especially when the need for emergent intervention was apparent at the time-zero 12 Lead. The deWinter pattern was not fully appreciated in the pre-hospital setting, however was modestly entertained by the receiving ED provider. The PCI trajectory was then halted when cardiology determined the ECG trivial, and not convincing for deWinter, due to the lack of a single finding – specifically, compelling STE aVR.
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.
Since then deWinter case reports have been less than ubiquitous but identifiable, no less. Three of these reports, followed by a JACC editorial, are presented here, and in each circumstance the authors issue stern warning to both EMS and ED providers that accurate identification is absolutely necessary as this pattern can be easily misinterpreted for something other than the deadly occlusion it truly is. Of unique interest to this post, it should be noted, is the revisiting of deWinter characteristics / criteria on each occasion to establish precedent for the unique ECG changes in which it presents.
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
Hyperacute T waves
“Shark Fin” Sign
Upsloping STD >1mm at the J-point
Tall, symmetrical T waves in precordial leads
JACC: Case Reports (2019); Vol 1, No 4
What I find striking about this amassed literature is that STE aVR is only intermittently discussed, whereas T wave characteristics are persistently addressed as key changes consistent with the pathological process of OMI. Such a conclusion is uniquely pertinent to today’s case because the PCI trajectory dismantled when a singular, isolated expectation (i.e. STE aVR) was lacking. ECG interpretation, however, is never myopic. It requires broad attention to the entire constellation of behavior and characteristics. Only in this context, after having fully appreciated the bigger picture, can one then scrutinize nuance.
Use this “constellation” approach while assessing the below ECG’s. Each patient presented with chest pain. Each LAD ultimately showed acute ulcerated plaque. And each case encountered delays in immediate PCI secondary to: 1) unnecessary trivial focus on aVR when entertaining the possibility of deWinter STEMI equivalent, or 2) complete misdiagnosis altogether. That said, pay close attention to the fact that STE aVR is only present some of the time while T wave hyperacuity – along with other signatures of reciprocal change or early transmural injury – is present every single time.
Courtesy of @DocNikko
Digitized by #PMCardio
Strict allegiance to rigid parameters can easily dismiss the subtle, or otherwise atypical, manifestations of pathology. The STEMI paradigm, even STEMI-equivalent, plays by a certain set of rules that is continuously mocked by the cellular and electrical changes of acute ischemia. This is why ECG assessment for OMI is superior because, in my estimation, it casts a wide net of constellation first that then funnels down to scrutiny.