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DeWinter Pattern

Editor: Jose P. Braga Updated: 8/7/2023 11:29:20 PM

Introduction

Ischemic heart disease (IHD) is a major cause of morbidity and mortality.[1] Although there have been significant improvements in the overall management of patients suffering from acute coronary syndromes (ACS), this entity is still associated with a relevant clinical burden.[2][3] A timely diagnosis is of the utmost importance, in order to allow prompt initiation of adequate therapy (both medical and interventional).[2][3] In this context, the electrocardiogram (ECG) has a central role in the diagnostic process, allowing (in association with an appropriate clinical presentation) an adequate presumptive working diagnosis and treatment allocation.[2][4][5]

Though differentiation between ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) is pivotal, over the years, several electrocardiographic patterns associated with an increased risk of cardiovascular (CV) events have been described.[2][3][4][6]

The De Winter pattern, first described in detail in 2008 and consisting of specific changes in the ECG, has been associated with an acute presentation of a left anterior descending (LAD) artery occlusion.[4][7][8] As such, this pattern should be recognized by those involved in the management of ACS patients.

Etiology

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Etiology

The De Winter pattern is associated with occlusion of the coronary arteries, most often the LAD, though cases involving other coronary arteries (such as the right coronary artery and the circumflex artery, whether isolated or in association) have also been described.[7][9][10][11][12][13]

Most cases reported occlusion due to atherosclerotic disease (in line with other presentations of myocardial infarction),[4][12][4][7] though this pattern has also been described as due to a thromboembolic event.[13] It has also been noted in the absence of an acute epicardial occlusion (after a percutaneous coronary intervention), this being hypothesized as associated with impaired microvascular perfusion.[12]

Epidemiology

The De Winter pattern is an infrequent presentation, with different case series reporting it to occur in 2% to 3.4% of anterior myocardial infarction patients.[7][10][14][15] As this pattern relates to a particular presentation of an ACS, risk factors are those associated with IHD in general (namely increased age, smoking, dyslipidemia, hypertension, diabetes mellitus, and overweight status/obesity).[1][2][3][14] Notably, in some series, male patients were more likely to present with this typical pattern,[10][15] whereas some authors also report that these individuals tend to be younger than those who present with an anterior STEMI.[14][15]

Pathophysiology

Though the specific pathophysiology associated with the De Winter pattern is still not fully ascertained, several potential mechanisms have been proposed. One which has garnered substantial interest relates to subendocardial ischemia, with ensuing subendocardial (as compared to subepicardial) action potentials at a hyperacute stage of the event (before transmural ischemia becomes predominant).[8][14][16][17] Another potential explanation for this phenomenon consists of the presence of collateral circulation.[17][18] This latter hypothesis, however, does not appear to fully explain reports of this presentation in patients without adequate collateral circulation.[7][8][14] Other proposed mechanistic pathways include anatomical variants in the Purkinje fibers, as well as myocardial metabolism downregulation.[7][11][16] A contemporary cardiac magnetic resonance imaging study by Zorzi et al. has also provided important data, highlighting the potential interplay of several mechanisms (such as differential expression of action potentials as well as a possible contribution of collateral circulation) for the occurrence of the De Winter pattern.[17]

History and Physical

Given that the De Winter pattern is generally associated with an ACS, patients present with features consistent with this diagnosis such as oppressive acute chest pain and shortness of breath.[2][4][8][11][18]

Findings on physical examination vary as detailed in the Killip classification.[2] As this pattern is often associated with a hyperacute stage of myocardial infarction (MI), physical examination can be unremarkable, except for the presence of diaphoresis and ongoing discomfort associated with acute symptomatology in the setting of an ACS.[8][11][13][17][18]

Evaluation

The ECG findings consistent with this pattern, as proposed in the seminal article by De Winter et al., consist of an ST-segment upsloping depression at the J point of 1 to 3 mm in leads V1 to V6, associated with tall and symmetrical (positive) T waves.[7] Additionally, most individuals present ST-segment elevation (1 to 2 mm) in lead aVR.[7] Other possible findings include loss of R wave progression in the precordial leads, as well as normal duration (or only slightly widened) QRS complexes.[7]

However, it should be acknowledged that strict criteria remain elusive,[10] as elegantly reported in a systematic review by Morris et al. which showed differences in categorization among studies.[9] In this review, upsloping depression of the ST-segment focusing on lead V3 and associated with upright T waves were consistently reported, whereas most individuals also had poor progression of the R wave as well as ST-segment elevation in lead aVR.[9]

Interestingly, albeit initially described as comprising a static pattern,[7][9] (a fact also noted in other series)[15][18], there are reports describing a potential temporal evolution as the ischemic event unfolds.[9][19]

Cardiac biomarkers, specifically high-sensitivity cardiac troponin (hs-cTn) should be assessed, though (as stressed in contemporary guidelines) this should not delay the reperfusion strategy.[2][4] Importantly, and as previously mentioned, this pattern is associated with a hyperacute presentation. As such, hs-cTn can be within the normal range or only mildly elevated upon initial measurement.[8][20] Given the differential diagnosis, assessment of potassium levels can also be of interest though this should also not delay the reperfusion strategy.[7][8][21]

Treatment / Management

In the proper clinical context (compatible with an ACS), the presence of the De Winter pattern should lead to a high degree of suspicion for a LAD artery occlusion.[4][10][18] Emergent consultation with a cardiologist should be undertaken, thus allowing early referral for cardiac catheterization and primary PCI if appropriate, in order to ensure appropriate reperfusion as per STEMI guidelines.[2][3][7][10][18] Additionally, optimized medication including aspirin, a P2Y12 inhibitor, and anticoagulation should be implemented as tailored by the interventional cardiologist.[2][3](A1)

After adequate reperfusion, patients should be admitted to a monitored unit (coronary care unit / intensive cardiac care unit), with subsequent management in terms of therapy and ancillary testing depending on the specific clinical course as detailed in the current guidelines.[2][3][4](A1)

Differential Diagnosis

Though in an appropriate clinical setting, most cases of this pattern comprise an acute occlusion of the LAD artery, it should be highlighted that similar changes in repolarization can be present in other clinical scenarios.

Among these, hyperkalemia should be considered. Importantly, in this entity, a different clinical presentation, as well as the fact that T waves tend to be narrow and peaked (presenting a sharp apex), should be noted.[20][21][22] Moreover, as discussed by Xu et al., tachycardia can also be associated with the upsloping depression of the ST-segment and cTn elevation.[14]

Prognosis

As discussed above, the De Winter pattern is associated with acute occlusion of a coronary artery, most notably the LAD.[7][9] As such, early recognition and treatment allocation are critical, in order to allow adequate reperfusion, thus improving the substantial morbidity and mortality associated with a large anterior MI.[2][23]

Deterrence and Patient Education

As early diagnosis plays a prominent part in the management of individuals with an ACS and given the potential adverse outcomes associated with an acute LAD occlusion, improving patient presentation is of paramount relevance. In this regard, ensuring educational tools in a community for the most common symptoms associated with this pathology is one important strategy.[2][23] In this way, the so-called “patient-delay” can be optimized, thus reducing total ischemic time.[2]

Enhancing Healthcare Team Outcomes

As reviewed in the present article, in an appropriate clinical context, the De Winter pattern is highly suggestive of acute occlusion of the LAD artery.[7][9][10] Given this background, all members involved in the interprofessional care process of individuals presenting with acute chest pain should be able to expertly identify this ECG finding, thus streamlining the diagnostic and therapeutic process of this challenging and high-risk subset of patients.[2][4][10][23]

Media


(Click Image to Enlarge)
Electrocardiogram depicting the De Winter pattern
Electrocardiogram depicting the De Winter pattern
Contributed by EM Vilela, MD

References


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