The Bleeding Heart

David Didlake, NRP, APRN, ACNP-BC


Peer review provided by Dr. Steve Smith


A 55 y/o Male presents to a freestanding urgent care center with chest discomfort, left arm pain, nausea, and diaphoresis. He reports to staff that for the past two months, approximately, he has experienced intermittent dyspnea on exertion when walking the dog, particularly when scaling an incline. He admits to a mostly sedentary lifestyle, however denies any smoking, orthopnea, paroxysmal nocturnal dyspnea, or peripheral edema. His father and brother both died of myocardial infarction at ages 61 and 45, respectively.

Here is the time-zero ECG (0939 hours).

There is appreciable STE aVR with near-global STD that appropriately maximizes in Leads II and V5, and thus suggesting a circumstance of generic, diffusely populated, circumferential subendocardial ischemia versus occlusive coronary thrombus. [1]

The issue of supply-demand mismatch at the subendocardial level can be attributed to many external factors that exacerbate the shortcomings of suboptimal coronary flow (e.g. pre-existing, stable atherosclerosis) amidst any state of global duress – to include hypertension, hypoxia, tachycardia, hypotension, sepsis, and GI bleed, for example. There may even be significant overlap between these factors.

The patient was found to be hypertensive and treated accordingly. Although the blood pressure resolved, his pain, however, did not. It persisted with episodic waxing / waning. No ECG’s were recorded during this time. The poorly mitigated symptoms concerned the providers enough to arrange transfer to a PCI center. Below is the patient’s ECG just prior to transfer, and during a phase of symptom resolution (1154 hours).

There is attenuated aVR STE along with mostly resolved STD. However, a more significant finding has emerged – Pattern A Wellens reperfusion T waves in V3-V5 to suggest that the patient’s conundrum all along was occlusive coronary thrombus. The distribution of findings is consistent with the LAD, of which is now open with improved TIMI flow.

The ECG’s were sent to the PCI center, and the providers in the respective ED identified the T wave characteristics mentioned above. STEMI was activated and the patient went to Cath on arrival. Advanced multi-vessel disease was found with stents deployed to the mid-LCx (80% stenosis), D1 (90% stensosis), and the pLAD (95% stenosis). Of these, the pLAD was determined to be the acute culprit.

Next-day Echo demonstrated 55% LVEF, mild concentric LVH, Grade I diastolic dysfunction, and minimal anterior wall motion abnormality. Peak Troponin I 2.397 ng/mL. Below is the ECG at 0649 hours.

There is evolution from Wellens Pattern A to Pattern B, now inclusive of V6.

As discussed, subendocardial ischemia is a consequence of global supply-demand mismatch that ameliorates upon addressing, and mitigating, the underlying cause.

Subendocardial ischemia pattern on the ECG:

  • STE aVR with, or without, STE V1

  • Global STD that is maximal in Leads II / V5

Strategies and tactics include serial ECG’s with emphasis on re-evaluation after one, or multiple, external factors (listed above) have been addressed accordingly. Does the ECG normalize? Or, is there persistent ischemic presentation, especially with unremitting symptoms? It’s judicious, then, to arrange for coronary angiogram.

Coronary occlusion, however, might be present concurrently with subendocardial ischemia on the time-zero ECG, or evolve into such. In this case, the problem is not purely a consequence of external factors (e.g. elevated BP), but rather directly correlated with coronary obstruction and stymied TIMI flow. What patterns, then, exist for which we should surveil when the ECG masquerades as generic supply-demand mismatch?

There are four patterns that readily come to mind, but I should emphasize that those addressed here are not the only times in which OMI bleeds through the characteristic ECG signatures of subendocardial ischemia. Each and every ECG, especially in a clinical presentation consistent with Acute Coronary Syndrome, absolutely requires scrutiny. The purpose here is to detail the patterns which, I believe, tend to “leap off” the page. Dedicated followers of the Smith ECG Blog know that the STD of true subendocardial ischemia does not localize, yet some of the examples listed below demonstrate the opposite, and were subsequently labeled “diffuse ischemia” or “generic subendocardial changes” as a diagnosis of convenience.

Aslanger Pattern

Amidst otherwise characteristic subendocardial ischemia on the ECG there is also:

  • Inferior STE isolated to Lead III

  • STD in any of V4-V6 (but not in V2) with a positive, or terminally positive, T wave

  • ST segment in V1 > V2

From LITFL Blog

The basic concept is a far rightward injury vector that combines the STE of aVR and Lead III. [2]

deWinter Pattern

aVR STE could very well be trivial in this unique circumstance. deWinter often deceives the casual eye masquerading as “generic ischemia” because of the near-global STD. But what makes this pattern unique, and demonstrably separates it from true subendocardial ischemia, is the following:

  • Dramatic upsloping of the STD across the precordium (and limb leads, if implicated)

  • Hyperacute T waves

deWinter pattern is both static and persistent up to the point of invasive procedure, and associated with considerable loss of myocardium despite successful PCI [3].

Max STD V2-V4

The maximal STD vector of subendocardial ischemia is directed to Leads II and V5. But when shifted to any of Leads V2-V4, this suggests an injury vector directed posteriorly [4].

From Smith ECG Blog

LCx occlusion

There is aVR STE with broad STD, appreciable in both Leads II and V5. However, the maximal STD in this case is V3.

STE “spread” to V2, V3, or aVL

STD vectors that are maximal in Leads II and V5 necessarily beget STE in aVR, which may also be accompanied by STE in V1 as this lead follows the same direction as aVR. It has been my experience that when STE is inclusive of V2 / V3 (assuming proper lead placement) one should take pause; but most certainly when the STE is spread to aVL as this implies a more directly superior ST axis and is worrisome for high pLAD (even ostial) occlusion.

Some of the examples below do not meet purist ECG criteria for subendocardial ischemia (e.g. gross aVR STE) but were categorized as such due to near-global STD.

Example #1

Broad STD with only minimal aVR STE

Subtle STE aVL and Lead I (both with HATW’s)

This was an OM occlusion, initially dismissed because of “non-specific ischemia” of STD found in most leads. What ultimately propelled emergent Cath was the sudden rhythm change:

Example #2

Broad STD (maximal in II / V5) with aVR STE

It has been mentioned that STE V1 is a typical finding in generic subendocardial ischemia, but here there is spread to V2 and aVL. Moreover, there is RBBB, so the STE V1 is abnormal because it is concordant STE (which also applies to V2 and aVL). Furthermore, this RBBB is accompanied by LAFB – a particularly hazardous sign of pLAD occlusion [5].

Example #3

Broad STD

Even though demonstrable aVR STE is lacking, this ECG was dismissed as “global subendocardial ischemia” because of STD in most leads. Close inspection will show, however, that said STD is maximal in Leads III and V3 (contrary to the expected maximal STD in II and V5 of true subendocardial ischemia). The reason for this maximal STD vector is the subtle STE in Leads I and aVL, each equipped with HATW’s. This was another OM occlusion.

Example #4


There is subtle STE aVR with broad STD. But there is also concordant STE V1 that is spread to leads V2, V3, and V4. Patient was found to have an ostial occlusion of the LAD and expired during attempted PCI.

In Review

Time-zero ECG patterns that suggest acute occlusive coronary obstruction, amidst true subendocardial ischemia – or, otherwise broad STD – include, but are not limited to:

  • Aslanger Pattern

  • deWinter Pattern

  • Max STD V2-V4

  • STE “spread” to V2, V3, but most worrisome in aVL

Let’s backtrack to the original ECG in today’s case and surveil it for any of the above listed criteria. Remember, this was recorded during active pain.

There is no appreciable patterns of Aslanger, or deWinter. The broad STD is appropriately maximal in Leads II / V5 (and not in any of Leads V1 – V4). The distribution of STE appears confined to aVR and V1. Thus, the ECG seems devoid of any occlusive evidence bleeding through the characteristic trademark signatures of subendocardial ischemia.

One finding, however, does catch my eye. And I should emphasize that it’s more atypical than truly diagnostic. The J-points of V2 and aVL are both baseline. Granted, neither possesses a HATW; but it does seem odd, and equally out of place, given the principle of global STD in true subendocardial ischemia. It’s possible that the baseline ST of aVL and V2 are the ischemic equivalents of STE (when they should both be depressed on pure technicality).

Such an oddity, at the very least, should encourage serial ECG’s. There’s a chance that the findings in aVL and V2 may have evolved into gross STE, or HATW’s, based on the knowledge that the patient’s pain persisted (despite waxing / waning intervals) and was ultimately found to have an LAD occlusion. I can’t say this with certainty because the follow-up ECG was recorded hours later, and furthermore during a phase of reperfusion.

It’s possible that the J-point peculiarities of aVL and V2 are the result of ST vector cancellation, in which the ST segments here could have been elevated but were relegated to baseline manifestation due to conflicts of interest from neighboring ischemic zones (varying intensities of subendocardial, sub-epicardial, and transmural currents of injury) in the presence of multi-vessel disease.

Conjecture aside, I believe the lesson here, ultimately, is serial ECG’s. Such aggressive investigation was particularly warranted in this case because of symptoms compatible with ACS, as well as an equally frightening revelation of family history.

Readers interested in a more robust discussion of STD vectors, and their implications in OMI, are encouraged to read this phenomenal post at the Smith ECG Blog.

[1] Mirand, D. F, et al. (2018). New insights into the use of the 12 Lead Electrocardiogram for diagnosing Acute Myocardial Infarction in the emergency department. Canadian Journal of Cardiology, 34; 132-145.

[2] Aslanger, E., et al. (2020). A new electrocardiographic pattern indicating inferior myocardial infarction. Journal of Electrocardiology, 61; 41-46.

[3] deWinter, R. J., et al. (2008). A new ECG sign of proximal LAD occlusion. New England Journal of Medicine, 359; 2071-2073.

[4] Meyers, H. P, et al. (2021). Ischemic ST-segment depression maximal in V1-V4 (versus V5-V6) of any amplitude is specific for occlusion myocardial infarction (versus non-occlusive ischemia). Journal of the American Heart Association, 10; 1-14.

[5] Surawicz, B. & Knilans, T. K. (2008). Chou’s Electrocardiography in Clinical Practice (6th ed). Chapter 5: Right Bundle Branch Block (pg. 95-107). Elsevier-Saunders: Philadelphia, PA.

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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