Patient is informed of her husband's death: is it OMI or it stress cardiomyopathy?

Written by Willy Frick

Disclaimer at the outset: Some aspects of this case are not completely clear to me, and approach being unknowable. I've presented the case as best I understand it, but I can see good arguments for other interpretations.

A woman in her late 60s presented after a car crash. Her husband was driving and she was a passenger. They were hit at high speed. She sustained a large scalp hematoma along with several rib and vertebral fractures, but with CT scanning of chest/abdomen/pelvis/C-T-L-spine and head, no life threatening injuries were found. She complained of pain from her injuries. Her first ECG is shown.

Overall bland. Normal sinus rhythm with non-specific ST abnormality. After this ECG was obtained, the ER physician received word that the patient's husband had died in the crash. He told the patient this horrible news. Within ten minutes, she developed bradycardia, hypotension, and ST changes on monitor. Here is an image showing a few excerpted segments with time stamps:

If you wish to see the transition, I've included a video as I scroll through the telemetry. The changes start to become apparent about 25 seconds into the video.

Repeat ECG was obtained immediately, just 24 minutes after the prior ECG:

Given the context, my top differential diagnosis would be stress cardiomyopathy AKA takotsubo. But that is a diagnosis of exclusion, and OMI must obviously be ruled out with this dramatic ECG. If this were OMI, I would favor proximal RCA culprit (since that commonly produces inferolateral changes and occasionally produces anterior HATW from RV infarct), but LAD is also possible. The other point in favor of RCA is junctional rhythm. Bradycardia and heart block are very common in RCA OMI.

The emergency physician immediately activated the cath lab. In lab, patients are monitored on continuous abbreviated ECG with 5 electrodes. During ballooning, we often see immediate hyperacute T waves. After stent deployment, we often see improvement in the ST-T within seconds or minutes. The patient's ECG at the beginning of the case is shown below.

1:45, case start

To orient you to this screen, the top is obviously ECG waveforms. You can see the lead labels on the left, I, II, aVF, and V (a single precordial lead) in descending order. The bottom half of the screen shows the arterial pressure. Right now it is not hooked up, so it just shows a noisy waveform close to zero.

For a more detailed discussion of the this patient's angiography and angiography in general, please refer to my angiography guide. The patient's left sided arteries had only mild disease. The RCA film is shown below. You will see the following:

First, filling of the RCA and posterolateral system. Second, a freeze frame when the whole vessel is opacified, but no PDA is yet seen. Third, a slow motion segment showing delayed, brisk filling of the PDA due to dislodgment of a thrombus from contrast injection and distal embolization. Fourth, the same clip repeated at normal speed.

This LAO cranial angiogram shows at least three findings, annotated below:

• An ostial lesion (red arrow), more on this below.

• A distal RCA lesion (blue arrow),

• Delayed brisk filling of an initially occluded PDA due to a thrombus dislodged during injection which embolized distally. The yellow arrow points to the stump of the PDA before the thrombus embolizes allowing contrast to fill the vessel.

Although the ostial lesion may not appear very impressive angiographically, there is reason to believe it is severe, due to an observation in the cath lab called "pressure damping." This requires a little explanation. The arterial pressure waveform is transduced using the coronary catheter. Normally, the diameter of the coronary artery ostium is much greater than the diameter of the catheter so that catheter engagement does not significantly impair antegrade coronary perfusion. But in the case of an ostial lesion, there is little or no space between the outside of the catheter and the wall of the coronary artery. This prevents antegrade flow into the coronary artery during catheter engagement, and as a result the transduced pressure drops significantly below systemic arterial pressure.

Here is the ECG and arterial waveform during RCA angiography. Note the pressure on the arterial line, estimated at 45/25 mm Hg.

1:51, diagnostic RCA angiography

At this point, the patient very clearly has a diagnosis of OMI, especially since we visualized embolism within the PDA. But is the coronary pathology enough to explain the persistent ECG changes? Here is the final angiogram following placement of a stent in the ostial RCA.

2:04 PM, post stent deployment

You can see that even after complete restoration of flow, the ECG still looks terrible, V most of all. It is possible there is microvascular dysfunction producing residual transmural ischemia. But this is most common when there is prolonged ischemia, and this patient had the fastest reperfusion imaginable! In my opinion, the more likely explanation is that the ST-T changes are primarily driven by stress cardiomyopathy.

At this point, with TIMI 3 flow in all vessels, the interventional cardiologist performed right heart catheterization. The patient's wedge pressure was 18 mm Hg with normal cardiac output and index by estimated Fick. After completing the right heart catheterization, the patient had worsening ST segments on EKG. The catheter was out of the body and the arteriotomy had been closed, so there is no pressure waveform.

2:34 PM, following right heart catheterization

She then went into atrial fibrillation with complete heart block and junctional escape rhythm prompting placement of transvenous pacemaker.

2:38, atrial fibrillation with complete heart block

Given her hemodynamic instability, the cardiologist placed an Impella and prepared to repeat angiography. In the midst of this, she went into VF. Several 200 J shocks did not terminate the VF, so a second defibrillator was applied for double sequential defibrillation with 400 J. The patient developed electrical storm with recurrent VF. During the resuscitation, she received amiodarone 450 mg IV, lidocaine 100 mg IV, and magnesium 6 g IV. She was defibrillated perhaps 25 times.

Angiography was technically challenging as the patient was receiving CPR, but the cardiologist suspected acute stent thrombosis and initiated cangrelor, although no repeat angiography was able to be obtained. Unfortunately, even with Impella in place and when the patient was in rate controlled AF, she remained pulseless.

3:07 PM, slow atrial fibrillation with electromechanical dissociation

At this time, the patient's family terminated resuscitation efforts and the patient was pronounced dead.

Case discussion:

This is a tragic case. The patient survived the car crash, but upon learning of her husband's death, she deteriorated. Despite almost immediate revascularization, she had persistent dramatic ST-T abnormalities. The cardiologist thought she had stent thrombosis which is possible, but I do not necessarily think is sufficient to explain her complete hemodynamic collapse.

Just a few weeks ago, I took care of a patient who had ostial RCA OMI (TIMI 0 at cath) and his only complaint was syncope! He had no chest pain, dyspnea, or any other anginal equivalent, and his vital signs were normal. 

In my opinion, the ECG changes and hemodynamic collapse seem out of proportion to the observed/suspected coronary pathology. Additionally, the timing is highly suggestive of stress induced etiology. Takotsubo characteristically occurs in women in their 60s. It is now well recognized that acute MI can precipitate takotsubo. Here is a case report and review of the literature. The authors describe a case with some features in common with our patient -- a stressful event followed by a stress cardiomyopathy/acute myocardial infarction overlap syndrome. No LVgram was done in this patient's case, but even that could be challenging to interpret if the patient had one of the recognized phenotypes other than classical apical ballooning (e.g. midventricular, basal, focal).

In my review of the literature, there are many articles which purport to demonstrate an acutely increased risk of plaque rupture from emotional stress, but I could not find any credible case reports that were not at least as likely to be takotsubo. Please message me on Bluesky or Twitter if you know of any such case reports. Here is some of what I found:

• A case report which describes stress induced acute MI but is much more likely to be takotsubo in my opinion (including characteristic ECG changes)
• A review article which asserts the role of emotional stress in plaque rupture, and cites the above case report as well as a few population studies that are hard to draw firm conclusions from
• Another review article with similar citations
• A case control study ostensibly showing increased risk of MI following death of a loved one, but without angiographic data and the authors even acknowledge that takotsubo could have been present
• An autopsy study claiming a role for stress in sudden cardiac death from coronary disease, but not clearly proving it
• These authors describe a case of takotsubo syndrome complicated by suspected LV thrombus and cardioembolic OMI

Ultimately, most of this discussion is clinically irrelevant. The patient certainly had OMI and received treatment for it. There is no specific treatment for stress cardiomyopathy, only supportive treatment. Was her outcome to be expected for ostial RCA OMI? Or was it out of proportion, perhaps worsened by the sympathetic surge? We will never know for certain.

In addition to profound acute heart failure, the patient suffered from electrical storm. After completing the ACS algorithm with amiodarone and lidocaine, there are diminishing returns on further treatments. If the patient can be temporized with VA ECMO, consider propranolol or stellate ganglion blockade. Both treat sympathetic surge which is a driver of electrical storm.

Learning points:

• Takotsubo and OMI can co-exist

• If max output on the defibrillator doesn't terminate VT, add another defibrillator

• If amiodarone, lidocaine, and magnesium are ineffective at suppressing VT/VF, consider VA ECMO or propranolol

References:

Angulo‐Llanos, R., Sanz‐Ruiz, R., Solis, J., & Fernández‐Avilés, F. (2013). Acute myocardial infarction: an uncommon complication of takotsubo cardiomyopathy. Catheterization and Cardiovascular Interventions, 82(6), 909–913. https://doi.org/10.1002/ccd.24846 

Bai, J., Xiang, W., Kong, L.-Y., Zhao, L.-T., Liu, F., Liu, L.-F., Tang, Z., & Zhang, P. (2022). Acute myocardial infarction complicated with takotsubo syndrome in an elderly patient: case report and literature review. Journal of Geriatric Cardiology, 19(6). https://doi.org/10.11909/j.issn.1671-5411.2022.06.007 

Bentzon, J. F., Otsuka, F., Virmani, R., & Falk, E. (2014). Mechanisms of plaque formation and rupture. Circulation Research, 114(12), 1852–1866. https://doi.org/10.1161/circresaha.114.302721 

Chatzidou, S., Kontogiannis, C., Tsilimigras, D. I., Georgiopoulos, G., Kosmopoulos, M., Papadopoulou, E., Vasilopoulos, G., & Rokas, S. (2018). Propranolol versus Metoprolol for treatment of electrical storm in patients with implantable cardioverter-defibrillator. Journal of the American College of Cardiology, 71(17), 1897–1906. https://doi.org/10.1016/j.jacc.2018.02.056 

Cheskes, S., Verbeek, P. R., Drennan, I. R., McLeod, S. L., Turner, L., Pinto, R., Feldman, M., Davis, M., Vaillancourt, C., Morrison, L. J., Dorian, P., & Scales, D. C. (2022). Defibrillation strategies for refractory ventricular fibrillation. New England Journal of Medicine, 387(21), 1947–1956. https://doi.org/10.1056/nejmoa2207304 

Falk, E., Shah, P. K., & Fuster, V. (1995). Coronary plaque disruption. Circulation, 92(3), 657–671. https://doi.org/10.1161/01.cir.92.3.657 

Gelernt, M. D., & Hochman, J. S. (1992). Acute myocardial infarction triggered by emotional stress. The American Journal of Cardiology, 69(17), 1512–1513. https://doi.org/10.1016/0002-9149(92)90918-o 

Ghadri, J.-R., Wittstein, I. S., Prasad, A., Sharkey, S., Dote, K., Akashi, Y. J., Cammann, V. L., Crea, F., Galiuto, L., Desmet, W., Yoshida, T., Manfredini, R., Eitel, I., Kosuge, M., Nef, H. M., Deshmukh, A., Lerman, A., Bossone, E., Citro, R., … Templin, C. (2018). International expert consensus document on takotsubo syndrome (part I): Clinical characteristics, diagnostic criteria, and pathophysiology. European Heart Journal, 39(22), 2032–2046. https://doi.org/10.1093/eurheartj/ehy076 

Jentzer, J. C., Noseworthy, P. A., Kashou, A. H., May, A. M., Chrispin, J., Kabra, R., Arps, K., Blumer, V., Tisdale, J. E., & Solomon, M. A. (2023). Multidisciplinary critical care management of electrical storm. Journal of the American College of Cardiology, 81(22), 2189–2206. https://doi.org/10.1016/j.jacc.2023.03.424 

Mostofsky, E., Maclure, M., Sherwood, J. B., Tofler, G. H., Muller, J. E., & Mittleman, M. A. (2012). Risk of acute myocardial infarction after the death of a significant person in one’s life. Circulation, 125(3), 491–496. https://doi.org/10.1161/circulationaha.111.061770 

Myers, A., & Dewar, H. A. (1975). Circumstances attending 100 sudden deaths from coronary artery disease with coroner’s necropsies. Heart, 37(11), 1133–1143. https://doi.org/10.1136/hrt.37.11.1133 

Park, J., Choi, K. H., Lee, J. M., Kim, H. K., Hwang, D., Rhee, T., Kim, J., Park, T. K., Yang, J. H., Song, Y. B., Choi, J., Hahn, J., Choi, S., Koo, B., Chae, S. C., Cho, M. C., Kim, C. J., Kim, J. H., Jeong, M. H., … Kim, H. (2019). Prognostic implications of Door‐to‐balloon time and onset‐to‐door time on mortality in patients with st‐segment–elevation myocardial infarction treated with primary percutaneous coronary intervention. Journal of the American Heart Association, 8(9). https://doi.org/10.1161/jaha.119.012188 

Singh, T., Khan, H., Gamble, D. T., Scally, C., Newby, D. E., & Dawson, D. (2022). Takotsubo syndrome: Pathophysiology, emerging concepts, and clinical implications. Circulation, 145(13), 1002–1019. https://doi.org/10.1161/circulationaha.121.055854

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MY Comment, by KEN GRAUER, MD (3/8/2025):

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If you Google, “Broken Heart Syndrome” — you will immediately see reference to many pages of “Patient Education” news briefs and informationals, in which the questions addressed are, “Can You Really Die of a Broken Heart?” — and if so, “How Can this Happen?”.

• The answer is YES, you can die of "Broken Heart Syndrome" — as becomes tragically evident in today’s case presented by Dr. Frick.

The syndrome referred to was first identified in 1990 — and initially named "Takotsubo" CardioMyopathy (TCM) because of the heart's resemblance on a ventriculogram to the shape of the container used by Japanese fishermen to trap octopuses. 

• As shown in Figure-1 — the unusual round bottom and narrow neck design of takotsubo is similar to cath findings that manifest ballooning of the cardiac apex with hypercontraction of the base.
• Additional names for this syndrome followed — including "Stress" Cardiomyopathy (Stress CM) — "Apical Ballooning Syndrome" — and the lay press name of "Broken Heart" Syndrome.
• Many variations regarding the location of cardiac involvement have since been described. Instead of LV dysfunction localized to the apex — the dysfunction may be of the base = "Reverse" Takotsubo, in which case there will not be apical ballooning. Or, there could be mid-ventricular Takotsubo, in which there is poor function (and ballooning) of the mid-LV, with good function at both the base and the apex — and, still other anatomic possibilities (See the June 24, 2014 post — and My Comment in the July 21, 2022 post of Dr. Smith's ECG Blog regarding Takotsubo variant patterns).
• And, as often occurs with “newly described” clinical syndromes — once they appear in the medical literature, the syndrome becomes increasingly recognized (whereas it probably had been present all along at some undefined frequency). Thus, the entity of Stress CM is not "one size fits all" — but instead encompasses a range of anatomic (and therefore electrocardiographic) presentations.
• Although the precise mechanism for this entity remains unclear — the common denominator appears to be sympathetic overdrive (catecholamine excess), with a marked preponderance in post-menopausal women — in which the entity is often precipitated by strong emotional or physical stress. That said — many cases are not that simple, and I found myself both emotionally moved — as well as intellectually fascinated by the sequence of events in today's case.

Figure-1: Collection of actual "octobus traps" (takotsubo) — showing the round bottom and narrow neck that resembles the diagnostic picture seen on the cardiac cath ventriculogram (shown here during end-systole). Note characteristic “ballooning” of the apex and hypercontractility of the base during cardiac cath (Figure excerpted from Grauer K: ECG-2014- Expanded ePub, KG/EKG Press).

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MY Thoughts on Today’s CASE:

Although we do not know details of the relationship between today’s patient (a woman in her late 60s) and her husband — I found it easy to imagine a marriage of many decades duration, in which the patient, while she herself is being treated for severe but not life-threatening injuries — suddenly learns that her life-time partner has died in the auto crash.

• Given the immediate physiologic “chain reaction” of intense autonomic dysfunction that followed on learning of her husband's death (and which ultimately led to this patient’s demise) — I have to wonder WHEN (and How?) to best convey the terrible news that a loved one has just died in the accident that just occurred?
• Clearly — the physiologic “chain reaction” of autonomic dysfunction seen in today’s case does not commonly lead to death of the person learning this news. But if faced with a similar decision in the future — I wonder, if in the interest of the patient's medical condition — it might be better not to immediately convey the death of a loved one in the same accident until the patient was in a more capable state to process what happened. I do not know the answer to this.

With regard to the Physiologic “Chain Reaction” …

• As per Dr. Frick — We do not have all the answers. Cardiac cath apparently showed some ventricular dysfunction, though not the typical findings of Takotsubo CM (hard to do procedures while patients are receiving CPR ...).
• What is known — is that the repeat ECG in today’s case (shown in Figure-2) — suggests profound parasympathetic hyperactivity.

• Whereas the patient's initial ECG shows sinus rhythm and nonspecific ST-T wave abnormalities — just 24 minutes later, there is now profound bradycardia with a junctional escape rhythm (YELLOW arrows highlighting retrograde P waves) — and obvious findings of an acute inferior STEMI.
• Marked inferior lead ST elevation (greater in lead III than in lead II) — with equally marked reciprocal ST depression in lead aVL suggest an RCA "culprit" — though uncharacteristically flat ST segments in V1,V2 (competing RV and posterior wall involvement?) with ST elevation in V3-thru-V6 indicate a complicated picture.

The patient's condition deteriorated. As per Dr. Frick — the ongoing ECG changes in association with hemodynamic collapse seemed out of proportion to the apparent coronary pathology.

• There was indication of parasympathetic overdrive (the acute inferior STEMI with profound bradycardia and junctional escape).
• This was overtaken by a predominance of sympathetic surge (tachycardia, persistent ST elevation — development of electrical "storm" with failure to respond to recurrent defibrillation).
• Perhaps best summed up as a tragic case of extreme autonomic dysfunction precipitated by overwhelming psychologic stress that proved too much for the most intense efforts at treatment.

Figure-2: Comparison between the initial 12-lead ECG in today's case — with the repeat ECG done just 24 minutes later, after the patient learns that her husband has died.