Electrocardiographic patterns of acute coronary occlusion that do not meet STEMI criteria

How can you identify patients who need an immediate trip to the cath lab if they do not meet STEMI criteria? 

We're all familiar with the guideline based metric for door to balloon time of 90 minutes or less for ACS patients who meet criteria for ST segment elevation MI. STEMI is a surrogate for acute epicardial coronary occlusion and therefore the need for immediate reperfusion therapy. In this paradigm, ACS cases that do not meet STEMI criteria are designated as non-ST segment elevation myocardial infarction (NSTEMI). Less well appreciated, however, is that up to 30% of ACS cases not meeting STEMI criteria actually have acute coronary occlusion. Because these occlusions tend to go unrecognized and are not under the CMS “quality” metric of door to balloon time, these are patients with acute coronary occlusions who are often deprived of timely reperfusion. Multiple studies indicate that such patients have a higher mortality even compared to STEMI patients who do get timely reperfusion. Most of these patients can be recognized electrocardiographically as they generally fall into several patterns listed below. However, these can be subtle and require a certain degree of electrocardiographic interpretation skill.

Hyperacute T waves:  these are upright T waves of high amplitude and increased width such that they have an increased area under the curve. They may be the earliest signs of coronary occlusion and may be present without ST segment elevation

DeWinter T waves: these are hyperacute T waves preceded by J point ST segment depression. This pattern is diagnostic of acute LAD occlusion although not meeting STEMI criteria.

Wellens syndrome:  this is a pattern of anterior precordial T wave inversion that occurs after resolution of chest pain. It indicates a proximal LAD occlusion that has recently reperfused. Such patients have a very high incidence of catastrophic anterior STEMI within the coming two weeks and do not respond to medical management.

Precordial swirl pattern:. this is a pattern of ST elevation in V1 and V2 combined with lateral precordial ST segment depression. The ST segment elevation may be subtle and not meet STEMI criteria. This is indicative of proximal LAD occlusion.

South African flag sign: this is a combination of ST elevation in Leeds 1 and AVL and depression in lead 3. There is concomitant ST segment elevation in V2. The pattern is indicative of acute diagonal branch occlusion.

Aslanger pattern:. this is a variant of inferior MI but the ST segment elevation is in lead 3 only. It is accompanied by ST segment depression in any of V4-6. There is also subtle ST elevation in  V1 greater than V2, not enough to meet STEMI criteria. This is indicative of inferior MI, usually circumflex occlusion but occasionally RCA occlusion. It is seen in patients with multivessel disease and is indicative of a large infant.

Terminal QRS distortion:. this is generally seen in LAD occlusions and is manifested by disappearance of the S wave in the anterior precordial leads. It is often accompanied by hyperacute T waves and occasionally may occur before ST segment elevation is seen and therefore not meet STEMI criteria.

Subtle anterior ST segment elevation not meeting STEMI criteria: this pattern can be confused with either normal variant anterior ST elevation, particularly in males, or benign early repolarization. There are a couple of formulas that involve the QT interval, the R&S wave amplitude and the degree of ST elevation in V3 which have good test characteristics for differentiation between early anterior STEMI and these normal variants.

Posterior infarction: because we generally do not employ posterior leads this is a mirror image of posterior current of injury and is seen as ST segment depression in V1-4. It does not meet STEMI criteria and is often missed.

Sgarbossa criteria in left bundle branch block and right ventricular pacing: this consists of concordant ST segment changes. Remember that in left bundle branch block and RV pacing ST segment changes should normally be discordant from the major portion of the QRS. 

Northern OMI pattern: this pattern consists of ST segment elevation in aVL and aVR  accompanied by by T wave inversion in those same leads, and ST segment depression in other leads. It is often indicative of occlusion at the takeoff of the diagonal branch.  It does not meet STEMI criteria.

Right bundle branch block, with or without left anterior fascicle block, not known to be old:  in the context of suspected acute myocardial ischemia, this finding indicates proximal LAD occlusion and a very large infarct with high mortality and high risk of acute complications including pulmonary edema, cardiogenic shock, septal rupture and complete heart block with asystole.  The downward secondary ST segment forces in the anterior leads (due to the RBBB) may obscure the ST elevation and thus fail to meet STEMI criteria.  Moreover, the RBBB itself may be a distractor from what is really going on.

Inferior infarction with only minimal STE not meeting STEMI criteria with reciprocal aVL depression as the principal abnormality.

These patterns are detailed in the paper linked below:

ECG Patterns of Occlusion Myocardial Infarction: A Narrative Review

Tables and Graphics from the paper are displayed here.

The STEMI/NSTEMI classification: great tool for coders, horrible tool for clinicians

Several times recently on wards I have mentioned a research study under review presenting data that in patients with acute coronary syndrome, the final chart diagnosis of STEMI versus NSTEMI correlated more closely with whether they made it to the cath lab in time to satisfy the applicable metric (120 minutes door to balloon time) than it did the ECG findings. The paper was finally published and I am presenting it here:

Door-to-Balloon Time Outperforms ST-Segment Elevation in Predicting the STEMI vs. NSTEMI Final Diagnosis

This is an observational study drawn from a large database of patients who underwent coronary angiography in an acute setting. 410 patients found to have acute coronary syndrome met the eligibility criteria for the analysis.  The findings, from the abstract of the paper:

Results: Among 410 angiographed AMI patients (mean age 63 ± 13; 71% male), 165 (40.2%) received an FDx-STEMI and 245 (59.8%) an FDx-NSTEMI. D2B time showed 94% agreement with FDx (160/165 FDx-STEMI treated less than 120 min; 225/245 FDx-NSTEMI treated greater than  120 min), exceeding concordance for STE (82%; p less than 0.001) and TIMI 0-1 flow (75%; p less than 0.001). FDx and STE diverged in 75 patients (18%): 60 rapidly treated STE-negative cases were labelled STEMI, whereas 15 delayed STE-positive cases were labelled NSTEMI. In regression analysis, D2B less than 120 min remained the sole independent predictor of discordance (adjusted OR 6.7, 95% CI 3.5–13.8). Conclusions: In this registry, the cath-lab label “STEMI” showed the strongest correlation with meeting a 120 min benchmark, exceeding correlations for STE or angiographic occlusion. These findings suggest that quality-metric compliance, rather than electrocardiographic or anatomic criteria, predominantly drives final diagnosis.

Here is a graphic that summarizes the findings:

Or, better yet, this cartoon (not from the paper):

The authors elaborate in the discussion section:

Our multivariable analysis asked a specific question: what factors explain the 18% of encounters in which the cath-lab label contradicts the patient’s ECG? Overall, door-to-balloon time less than 120 min was far more concordant with the final cath-lab diagnosis than either guideline ST-segment elevation or angiographic TIMI 0-1 occlusion (94% vs. 82% vs. 74%). This observation answers our prespecified question and underscores that, in routine practice, the label applied in the cath report aligns most closely with the treatment timeline recorded in the electronic chart. This suggests that the designation of STEMI is not always a reflection of the original diagnostic framework, but rather a retrospective label influenced by procedural outcomes and time benchmarks.

The authors believe the findings are generalizable, reflecting trends across the U.S.

They conclude, at the end of the paper:

In this retrospective analysis, time to treatment showed the strongest association. in final diagnosis of STEMI vs. NSTEMI, more important than both STEMI millimeter “criteria” and the presence or absence of total coronary occlusion. This has implications for research and quality improvement.

By the way, the 2025 guidelines for acute coronary syndrome are now published. (They’re fairly new, although they've been online since February of this year). You can access them here:

2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes

There's a growing and now overwhelming body of literature calling for a replacement of the STEMI/NSTEMI paradigm. Despite that, the new guidelines, unfortunately, stick with the existing classification scheme and do not mention the emerging OMI/NOMI concept. There is passing mention in the body of the guideline of a couple of electrocardiographic patterns that are diagnostic of acute coronary occlusion but do not meet STEMI criteria (DeWinter pattern and hyperacute T waves). Because the classification remains in current guidelines this will unfortunately drive MKSAP and ABIM board exam questions for some time to come. So you need to know them while recognizing their deficiencies. In this respect the guideline is 10 years or more out of date. In multiple other content areas there is a world of good information and it is worth the read. 

Why this inertia? One big reason is that the STEMI/NSTEMI paradigm is so entrenched in the administrative and coding world. In addition, a reasonably intelligent junior high student can be trained to use a ruler or count a little boxes and measure the degree and direction of ST segment displacement. The new paradigm requires actual skill in electricardiography. I think the cartoon below illustrates the problem well:

Tonicity, osmolality, effective and ineffective Osmoles

Consider these questions that may arise in the assessment of patients with hyponatremia:

In patients with hyperglycemia, is correction of the serum sodium necessary?  Is the corrected serum sodium a valid indication of the risk for neurologic complications, or should one use the uncorrected sodium?

High blood alcohol levels may be associated with an elevated osmolality even in the presence of hyponatremia. Does this impact how we should interpret the serum sodium level? 

How does one interpret serum sodium in the face of extreme hypertriglyceridemia?

The answers to these types of questions depend on an understanding of the concepts of tonicity, osmolality, effective osmoles, and ineffective osmoles. These advanced concepts are covered in the JAMA Internal Medicine review linked here: 

Hyponatremia, Hyposmolality, and Hypotonicity:  Tables and Fables


Below is table 2 from the article which summarizes the key concepts.

What is beer potomania and what is the associated mechanism of hyponatremia?

 
This topic was reviewed in an article linked here: 

Beer Potomania—An Unusual Cause of Hyponatremia


General considerations

Beer potomania is an unusual syndrome of hyponatremia in patients with heavy alcohol consumption (usually beer) and very little solute intake. 

Mechanism of hyponatremia

Beer itself has sufficient caloric content for patients to subsist, with little additional food source, for an extended time. All of the solute in beer (ethanol) is metabolized, leaving only free water. Even when the vasopressin axis and renal tubular function are normal (leading, in the context of hyponatremia, to maximal urinary dilution, less than or equal to 100 mOsm per liter) these patients cannot normally excrete a free water load or maintain water balance. This is because, given the limits on the capacity of the kidneys to dilute the urine, free water clearance is dependent on the amount of solute delivered to the distal nephron.   For example, a person consuming a normal diet might be able to deliver 1,000 mOsm per day to the nephron. Assuming maximum urinary diluting capacity (50 mOsm/L) such a person would be capable of a daily excretion of 20 L free water per day. Put another way, that person could drink 20 L in a day's time, maintain neutral water balance, and not become hyponatremic., On the other hand, in beer potomania, solute intake, if any, is very low. Let's say for example a person has a daily solute intake of 150 mOsm.  Assuming normal diluting capacity such an individual would be limited to 3 L daily free water excretion. Considering that a six pack of beer contains just over 2 L, that person would have difficulty maintaining water balance.

Additional points to consider

Tea and toast syndrome can be considered the physiological equivalent of beer potomania. A review of tea and toast syndrome is linked here: 

Tea and Toast Syndrome: A Case Report

Beer potomania is a relatively uncommon cause of hyponatremia in alcoholism. In patients hospitalized with alcoholism volume depletion is probably the most common cause followed by acute anti-diuresis due to stress related vasopressin secretion.

Beer potomania may not always present in pure form. There may be concomitant other disturbances in water balance. 

Among hyponatremic patients, those with beer potomania are at particularly high risk for osmotic demyelination syndrome. This complication has been reported in as many as 18% of patients with beer potomania. In such patients who are hospitalized, the mere provision of solute, whether via IV fluids or diet, is likely to restore some degree of free water clearance capacity and result in a brisk water diuresis.

What are the mechanisms of hyponatremia in alcohol use disorder?

 Based on my literature search, several mechanisms are at play.

Probably the most common is volume depletion, which prevails in many patients admitted to the hospital with acute alcoholism. It is due to low intake and GI losses. Hypovolemia is a non-osmotic signal for vasopressin (ADH) release. Accordingly, vasopressin is secreted regardless of sodium level. 

Another important cause is stress related vasopressin release, an acute form of the syndrome of inappropriate antidiuresis (SIAD). 

Less common but nonetheless important is beer potomania. It is possible to sustain one's caloric intake solely on beer for extended periods of time. All of the solute in beer (ethanol)  is metabolized. So, in effect, drinking beer is drinking free water.   Because patients who subsist on beer for their major source of calories are taking in little or no solute they are unable to excrete sufficient urine volume to maintain free water balance. In pure beer potomania the collecting duct and the vasopressin axis are functioning properly. Therefore, due to the presence of hyponatremia, the urine is maximally dilute. Urine osmolalities of 80 to 100 are seen.

Finally, since alcoholism rarely results in extreme hypertriglyceridemia, pseudohyponatremia is possible. This is not seen unless triglyceride levels are1500 or greater. 

This topic was reviewed in the November 2000 issue of Alcohol and Acoholism. 

Mechanisms of Hyponatremia in Alcohol Patients

This table from the article lists the causes and number of patients in their small study population.

This was a small number of patients and may not be representative sample. Stress related inappropriate antidiuresis was not mentioned in this article but is probably an important mechanism. Two conditions found among the patients in the series, one of each, were cerebral salt wasting and the reset osmostat syndrome. These may have been incidental and not directly related to alcoholism.

In addition, an important article in The New England Journal of Medicine reviewed alcohol related electrolyte disturbances in general. 

Electrolyte Disturbances in Patients with Chronic Alcohol-Use Disorder

In some patients, multiple mechanisms of hyponatremia may overlap.

Hemophagocytic lymphocystiocytosis and the related disorder macrophage activation syndrome

Hemophagocytic lymphohistiocytosis (HLH) is a syndrome of hyperinflammation. Fever, organomegaly and hyperferritinemia are characteristic. It is an emerging disorder yet widely underdiagnosed and considered a "must not miss” condition due to high mortality.

It is the topic of a New England Journal review, Hemophagocytic Lymphohistiocytosis, published earlier this year.

HLH is subdivided into primary and secondary forms. Primary HLH comprises a group of heritable disorders of immune system regulation. It is mainly a pediatric entity and is therefore not the focus of this discussion. Secondary HLH refers to HLH triggered by another known disease. Infections, autoimmune (rheumatic) disease (especially adult Stills and SLE) as well as neoplasia are the main trigger categories. There are usually underlying susceptibility factors present. Macrophage activation syndrome (MAS) is the subset of HLH triggered by rheumatic disease. While theoretically any infectious agent could be a trigger, certain patterns deserve mention. Active Epstein-Barr infection is most commonly noted among infections. Influenza has been reported as an associated infection. According to the review, COVID is believed to be a rare trigger.  Potential confusion lies in the fact that cytokine storm was a characteristic of severe COVD infection in 2020 and 2021. Of note, in light of a recent case on our wards, ehrlichiosis is a known trigger with, mentioned in the review, reports of as many as 16% of cases of ehrlichiosis being complicated by HLH.

When should it be suspected? Consider it and check ferritin and triglyceride levels in critical illness of uncertain etiology. Think of it particularly in sepsis like critical illness that does not have a clear source or is not responding to treatment as expected. The Hscore (available on MD Calc) his good “test” characteristics. 

What is the treatment approach?

In secondary HLH, in addition to treatment of the underlying disease, immunosuppressive therapy is used and generally centers around high-dose glucocorticoids and etoposide. By this point in the evaluation and treatment sequence expert consultation is necessary. 

How do we categorize pneumothorax?

There have been several cases of pneumothorax on the wards recently. How do we classify them?

This was addressed in a review in the December 2021 issue of Clinics in Chest Medicine entitled Pneumothorax.  The article is behind a paywall but free tull text is available to UAMS residents in Clinical Key.

Here are some of the main points from that review:

Pneumothorax that's not iatrogenic or traumatic is designated spontaneous pneumothorax. This category is further subdivided into primary and secondary spontaneous pneumothorax. Primary spontaneous pneumothorax refers to spontaneous pneumothorax in those patients with no clinically apparent lung disease.  Secondary spontaneous pneumothorax is designated in those patients with known lung disease. Here it gets a little confusing because the British Thoracic Society guidelines categorize all smokers and all patients greater than 50 years of age in the secondary category with or without known underlying lung disease.

Assuming smokers without clinically apparent lung disease are classified as primary, tobacco smoking is the strongest risk factor for primary spontaneous pneumothorax. After an episode of primary spontaneous pneumothorax in smokers, cessation reduces the recurrence rate four fold.

Height and male sex are also risk factors for primary spontaneous pneumothorax. Tall men have increased apical plural stretching. However, when increased height is part of a heritable disorder of connective tissue such as Marfan or certain types of Ehlers Danlos syndrome, associated pneumothoraces are designated as secondary.

Any type of pulmonary disease can be a risk factor for secondary spontaneous pneumothorax but COPD is the main one. Tuberculosis is the most common underlying disorder in endemic areas and was a significant cause historically. Many other infections can be associated with secondary spontaneous pneumothorax. PJP is well known. Bacterial pneumonias that cause necrosis can be associated with secondary spontaneous pneumothorax including staphylococcus, klebsiellla, pseudomonas, and anaerobes.  Covid can cause pneumothorax.  In non mechanically ventilated patients the frequency is around 1%.  Higher rates, not surprisingly, are seen in mechanically ventilated covid patients.

Less common causes of secondary spontaneous pneumothorax are the cystic lung diseases including lymphangioleiomyomatosis, Langerhans cell histiocytosis, and catamenial pneumothorax. Each individual cause is rare but together they account for a significant minority.  There are other examples of these which would be appropriate for a more narrowly focused review.

Recurrence of spontaneous pneumothorax is common across the board.  Prevention strategies are detailed in the article.

Topics for deeper dives:  Cystic lung diseases; tuberous sclerosis comples (a factor in many cases of lymphangioleiomyomatosis).