An ALS crew is dispatched for a 60-year-old male in cardiac arrest. On arrival, the crew finds the patient apneic, pulseless and cool to the touch with obvious signs of death.
The patient’s wife is visibly distraught and unable to present a detailed history to the crew. The patient is confirmed asystolic on the monitor and the crew pronounces him dead on arrival. The crew leaves the scene and returns to service.
Shortly after returning to service, the crew is dispatched to the same address, this time for a 60-year-old female complaining of chest pain. It’s the wife of the decedent.
On arrival, the crew finds the woman in obvious distress over the loss of her husband. She describes suffering a sudden onset of crushing chest pain. The pain was retrosternal and did not radiate. She describes the pain as pressure-like, rating it a 5 on a scale from 1—10.
The woman denies feeling any associated shortness of breath, nausea, vomiting, abdominal pain, lightheadedness, dizziness, fevers and recent illness.
Her past medical history is significant for back pain, arthritis and diabetes. Physical exam reveals an emotionally distraught 60-year-old female.
The crew next performs a complete cardiac workup on the patient. Her initial vitals are a pulse of 100, blood pressure 190/100 mmHg, oxygen saturation of 93% on room air, and her respiration rate is 24 and non-labored. Her lungs are clear to auscultation bilaterally. There’s no jugular vein distension or peripheral edema noted.
The patient is given 324 mg of aspirin. A 12-lead ECG is obtained (Figure 1); it reveals anterio-lateral ST-segment elevation. (See Figure 1.)
Figure 1: 12-lead ECG showing anterio-lateral ST-segment elevation
Two large-bore IVs are placed, followed by administration of a spray of nitroglycerin, which provides minimal relief.
As per protocol, the catheterization lab is activated and the crew initiates transport without delay to the hospital. During transport, two more sprays of nitroglycerin are administered, and the patient’s vitals remain stable.
On arrival to the ED, the patient is briefly evaluated and is then taken quickly for left heart catheterization.
Heart catheterization reveals clear and open coronary circulation with moderate left ventricular dysfunction with left ventricular wall motion abnormalities. A transthoracic echocardiogram reveals an ejection fraction of 55—74% and apical ballooning.
The patient is diagnosed with takotsubo cardiomyopathy and subsequently transferred to the cardiac care unit (CCU).
After a three-day uncomplicated stay in the CCU, the patient is well enough to be discharged home with a prescription for metoprolol and lisinopril.
Discussion
Takotsubo cardiomyopathy, also called “broken heart syndrome” or “stress-induced cardiomyopathy,” was first studied in Japan in 1991. The word “takotsubo,” which means octopus trap, was used by the Japanese to describe the cardiac anomaly seen in the disease, as it resembled the pot used to collect octopus.1
Despite thousands of cases reported since the early 1990s, there’s still no clear and decisive cause to this condition. Some of the more common speculations include stress hormones, microvascular spasm, focal myocarditis and cellular level muscle changes.2
In the United States, the disease is more common in females with roughly a 9:1 female to male ratio.3 The clinical presentation is characteristically similar to that of acute coronary syndrome, and there’s typically a significant stressful event that precedes the onset of symptoms.
12-lead ECG is often consistent with an anterior MI, while cardiac enzymes can be slightly elevated and return to normal quickly. Diagnosis of takotsubo cardiomyopathy can be made with heart catheterization and transthoracic echocardiography. Coronary angiography is performed to rule out acute coronary syndrome. Most patients will have a loss of motion at the apex and an apical ballooning pattern–the visible sign behind the syndrome’s name, because the enlarged left ventricle takes on the shape of the octopus pot.4,5 (See Figure 2.)
There are no evidence-based guidelines for the treatment of takotsubo cardiomyopathy. Treatment is usually supportive, with physicians often ordering standard heart failure medications such as beta-blockers, ACE inhibitors and diuretics. Aspirin may also be given to patients who also have atherosclerosis.6
About 10—15% of people who’ve experienced takotsubo cardiomyopathy will have another episode, and, for those affected a second time, the stressful event can be completely different.
Conclusion
Prehospital providers must always remember to do a full cardiac assessment for patients with unexplained causes of chest pain. Takotsubo cardiomyopathy is a rare cardiac anomaly, but affected patients may be at risk for development of dysthymia or heart failure,6 and require prompt medical attention.
References
1. Bielecka-Dabrowa A1, Mikhailidis DP, Hannam S, et al. Takotsubo cardiomyopathy: The current state of knowledge. Int J Cardiol. 2010;142(2):120—125.
2. Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s emergency medicine: Concepts and clinical practice, 8th edition. Elsevier/Saunders: Philadelphia, 2014.
3. Dorfman TA, Iskandrian AE. Takotsubo cardiomyopathy: State-of-the-art review. J Nucl Cardiol. 2009;16(1):122—134.
4. Komamura K, Fukui M, Iwasaku T. Takotsubo cardiomyopathy: Pathophysiology, diagnosis and treatment. World J Cardiol. 2014;6(7):602—609.
5. Castillo Rivera AM1, Ruiz-Bailén M, Rucabado Aguilar L. Takotsubo cardiomyopathy–A clinical review. Med Sci Monit. 2011;17(6):RA135—RA147.
6. Takotsubo cardiomyopathy. (n.d.) British Heart Foundation. Retrieved March 16, 2018, from www.bhf.org.uk/heart-health/conditions/cardiomyopathy/takotsubo-cardiomyopathy.
