Surprise Attack!: de Winter Aches and Pains

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© Springer Nature Switzerland AG 2020
C. G. Kaide, C. E. San Miguel (eds.)Case Studies in Emergency Medicinehttps://doi.org/10.1007/978-3-030-22445-5_12



12. ECG Surprise Attack!: de Winter Aches and Pains



Nicholas S. Fern1   and Amal Mattu2  


(1)
The Queen’s Medical Center, Honolulu, HI, USA

(2)
Department of Emergency Medicine, University of Maryland School of Medicine, Baltimore, MD, USA

 



 

Nicholas S. Fern


 

Amal Mattu (Corresponding author)

Email: amalmattu@comcast.net


Keywords

deWinter EKG STEMI equivalent Chest pain


Case 1


Pertinent History


A 42-year-old African-American male presents to the ED at 0415. He reports that 3 hours ago, he was awakened from sleep by worsening central chest pain radiating to his left arm. He feels significantly short of breath at rest and has been profusely diaphoretic. He denies nausea, vomiting, or recent illness. The patient specifically denies a history of heart attack or venous thromboembolism. He reports that yesterday he was shovelling snow in the driveway and was forced to stop multiple times because of chest pain and extreme fatigue. The patient reports his only medical history is hypertension and hypercholesterolemia but admits that he has not seen a doctor in many years.



PMH






  • Hypertension



  • Hypercholesterolemia



  • Meds: Hydrochlorothiazide, amlodipine, atorvastatin



SH






  • Never-smoker, no drug use



  • Drinks 8–12 oz beer several times per week



FH






  • Extensive family history of Diabetes Type II.



  • Father had myocardial infarction at age 50; older brother had myocardial infarction at age 48.


Pertinent Physical Exam






  • BP 164/94, Pulse 82, Temp 98.9 °F (37.2 °C), RR 22, SpO2 94% on RA



  • BMI 32


Except as noted below, the findings of the complete physical exam are within normal limits.



  • General: AAM sitting up in bed clutching his chest, distressed, and profusely diaphoretic.



  • Cardiovascular: Nontachycardic with regular rhythm, normal heart sounds without murmur. No JVD present. No costochondral tenderness. Pulses 2+ all extremities.



  • Respiratory: Moderate respiratory distress. Increased respiratory rate. Speaking in sentences. Clear breath sounds bilaterally.



  • Extremity: Distal pulses intact to DP/PT 2+ bilaterally. No pitting edema.


Pertinent Diagnostic Testing






  • CBC, CMP, PT/INR, PTT – All unremarkable



  • Troponin I: 7.56 ng/mL (Reference Range <=0.06 ng/mL)



  • Portable Chest X-Ray (CXR): Lungs are clear. No atelectasis. Costophrenic angles sharp. Widened mediastinum. Mildly tortuous aorta with moderate calcifications.



  • 12 Lead Electrocardiogram (ECG):



DeWinter EKG



../images/463721_1_En_12_Chapter/463721_1_En_12_Figa_HTML.png


Sinus rhythm, rate 82, poor R-wave progression, slight ST-segment elevation in aVR, upsloping ST-segment depressions with hyperacute T-waves in the anterior precordial leads, consistent with the de Winter T-wave pattern.


ECG Used with Permission, courtesy of Dr. Ammar Ismail.


ED Management



Plan


The patient is placed on cardiac monitoring, and a second large bore IV is placed. The patient is administered 324 mg chewable aspirin and 400 mcg sublingual nitroglycerin (NTG) every 5 minutes for 3 doses with minimal improvement in his chest pain. His blood pressure is 124/82 after the third NTG. In consideration of his presentation and ECG, cardiology is paged for emergent cardiac catheterization.


Updates on ED Course


(0435) The cardiology fellow returns the page: She is initially hesitant to activate the cath lab team without clear ST-segment elevation (STE). You explain that the patient’s ECG findings and presentation are consistent with the de Winter ECG pattern, and although diagnostic STE may or may not develop, you are concerned for an acutely unstable proximal left anterior descending coronary artery (LAD) occlusion. The patient has not responded to multiple rounds of NTG, despite a reduction in blood pressure and still has severe pain and appears acutely unwell. After a brief discussion with her attending, cardiology then agrees to emergent catheterization.


Learning Points



Priming Questions





  1. 1.

    What coronary lesion(s) are typical culprits in patients presenting with the de Winter pattern?


     

  2. 2.

    Do patients with the de Winter pattern progress to having overt ST-segment elevation myocardial infarction (STEMI) on serial ECGs?


     

  3. 3.

    Who is the patient population that generally presents with the de Winter complex and how do these patients differ from our common MI presentations?


     

  4. 4.

    If you truly believe that a patient needs emergent or urgent cardiac catheterization, how can the cath lab be activated without the patient meeting the traditional “STEMI criteria” (i.e., STE in contiguous leads)?


     

Introduction/Background





  1. 1.

    The de Winter ECG pattern is an electrocardiographic pattern found in some patients presenting with ischemic chest pain [1]. The pattern is associated with acute proximal LAD occlusion lacking anterior STE on ECG and places the patient at considerable risk for progression to an extensive anterior wall myocardial infarction (MI) [1–3].



    • Many authors contend that the obstructing plaque is often acutely unstable, and therefore, the pattern should be considered a STEMI equivalent and managed emergently [3–9].



    • The de Winter pattern is yet to be included as an indication for emergent reperfusion therapy (i.e., emergent catheterization or administration of fibrinolytics) in the current management guidelines of major cardiovascular societies [10–12] despite increasing literature affirming its association with significant acute coronary disease.


     

  2. 2.

    The ECG pattern was originally described by de Winter and colleagues in 2008 as: “…1- to 3-mm upsloping ST-segment depression at the J point in leads V1 to V6 that continued into tall, positive symmetrical T waves. The QRS complexes were usually not widened or were only slightly widened, and in some there was a loss of precordial R-wave progression. In most patients there was a 1- to 2-mm ST-elevation in lead aVR” [13]. This pattern has since been refined to the following [2]:


     


The de Winter EKG Pattern






  • Upsloping ST-segment depression (STD) >1 mm at the J point in the precordial leads



  • Continuation of the STD into tall, prominent, symmetric T waves in the precordial leads



  • STE (0.5–2 mm) in lead aVR



  • The absence of other, anatomically oriented, STE





  1. 3.

    There is some debate over the dynamic versus static nature of the de Winter pattern.



    • In the original two articles, the pattern was defined as “static,” persisting from initial presentation until the preprocedural ECG and angiography (30–60 minutes). In all cases, the pattern resolved after reperfusion [1, 13].



    • Other authors [4, 14–17] have proposed a dynamic pattern with conversion between traditional de Winter findings and overt STE resulting from ebb and flow between complete coronary occlusion and spontaneous reperfusion.



    • Zhao and colleagues [14] proposed a 2-category division of both static and dynamic, reflecting the possibility that the underlying plaque can be unstable.


     

  2. 4.

    In the original 2008 series, de Winter and colleagues drew from their primary database of percutaneous coronary interventions identifying 30 patients (2.0%) showing the de Winter pattern among 1532 patients with anterior wall MI [13].



    • In a 2009, a larger cohort from the same database showed identical incidence of the de Winter pattern, 2% (35 patients) of 1890 patients who had undergone primary percutaneous intervention (PCI) of the LAD. Meanwhile, the remaining 1855 LAD patients (98%) all exhibited precordial STE [1].


     

Physiology/Pathophysiology





  1. 1.

    The de Winter pattern has proven association with LAD occlusion on coronary angiography, specifically the proximal LAD [1].



    • Despite being pathognomonic of LAD occlusion, no cases involve occlusion of its supplying left main coronary artery (LMCA). Most cases (67%) exhibit isolated LAD disease [1].



    • Roughly half of patients were found to have a wraparound LAD, which is associated with a greater region of ischemia [1].


     


Coronary Anatomy



../images/463721_1_En_12_Chapter/463721_1_En_12_Figb_HTML.png


By Coronary.pdf: Patrick J. Lynch, medical illustratorderivative work: [CC BY-SA 3.0 (https://​creativecommons.​org/​licenses/​by-sa/​3.​0)], via Wikimedia Commons





  1. 2.

    The question arises as to why an anterior infarction may present with this unconventional pattern in 2% of cases while the remaining 98% present with the more typical precordial STE.



    • The electrophysiological explanation for J-point depression and prominent T-waves initially proposed by de Winter et al. [13] suggested the presence of endocardial conduction delay resulting from one of two mechanisms:



      • An anatomical variant of the Purkinje fibers.



      • Ischemia diminishing cardiomyocyte ATP resulting in failure of activation of sarcolemmal ATP-sensitive potassium (KATP) channels [13], supported by work with KATP knockout mice in which ligation of the LAD fails to produce STE [18].



    • Sala et al. theorize that the de Winter ST–T complex is created by a delay in subendocardial repolarization with a change in transmembrane action potential shape [16].



    • Verouden et al. suggest that “the area of transmural ischemia (is) very large, such that no injury currents (are) generated towards the precordial leads but only directed upwards to standard lead aVR” [1].



    • Montero-Cabezas propose the absence of STE is secondary to an incomplete occlusion of the LAD [15].


     

Making the Diagnosis


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Mar 15, 2021 | Posted by in EMERGENCY MEDICINE | Comments Off on Surprise Attack!: de Winter Aches and Pains

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