Open Access Case

Report DOI: 10.7759/cureus.36056

Classic Unprovoked Takotsubo Syndrome: A Case

Report
Review began 03/04/2023
Abhirami Shankar 1 , Narayanaiyengar Devaraj 2
Review ended 03/08/2023
Published 03/13/2023 1. Internal Medicine, West Anaheim Medical Center, Anaheim, USA 2. Cardiology, West Anaheim Medical Center,
© Copyright 2023 Anaheim, USA
Shankar et al. This is an open access
article distributed under the terms of the Corresponding author: Abhirami Shankar, ashankar@sgu.edu
Creative Commons Attribution License CC-
BY 4.0., which permits unrestricted use,
distribution, and reproduction in any
medium, provided the original author and
source are credited. Abstract
Although Takotsubo syndrome (TS) has been long recognized, it is now more frequently identified as a cause
of stress-induced cardiac injury since its first description in the 1990s. While most cases are transient, many
patients can have acute and long-term effects including persistent or worsening heart failure, arrhythmia,
cardiac thrombi, outflow tract obstruction, ventricular wall rupture, and cardiogenic shock. Medical
optimization is necessary to prevent cardiac remodeling and disease recurrence and manage associated
heart failure. The choice of medications may vary from patient to patient based on the inciting factor or the
most probable cause. Anticoagulation can be added for a small period of time if there is a concern for
thrombus formation from akinesia/dyskinesia. Most patients achieve early recovery and resolution of
symptoms and those with persistent manifestations can be managed medically.

Categories: Cardiology, Internal Medicine, Other

Keywords: chf, heart failure, troponin, myocardial infarction, acs, nstemi, stemi, coronary, cardiomyopathy,
takotsubo

Introduction
Takotsubo syndrome (TS) is a cardiac disorder that can cause transient wall motion abnormalities (WMA),
and hypokinesia/dyskinesia/akinesia of segments of the heart, which determines the “type” of Takotsubo
cardiomyopathy (apical, focal, etc.) [1]. The classic form causes apical ballooning with WMA in mid and
apical regions [1]. TS can be primary or secondary based on whether it is the cause of initial presenting
symptoms, a result of hospitalization or surgery, or caused by another disease like thyrotoxicosis [1].
Generally, it is considered transient with favorable long-term outcomes. However, patients still need to be
on medical therapy depending on the cause and clinical course.

Case Presentation
A 58-year-old female presented due to a first-time episode of dull retrosternal chest pain, tightness, and
pressure with exertion and at rest, rated 10/10 in intensity, radiating to the back in the left interscapular
region since that morning lasting about 1.5 hours. She endorsed profuse diaphoresis, dyspnea,
lightheadedness, and palpitations but denied syncope and loss of consciousness. She had experienced a
similar episode many years ago but had never consulted a cardiologist. She was compliant with her
medications including losartan 25 mg daily and levothyroxine 88 mcg daily. She denied vaping or alcohol
and illicit drug use. Her smoking status was unknown (she possibly smoked a few cigarettes daily for 10
years). The physical exam was unremarkable except for mild chest tenderness.

The patient's past medical and surgical history included hypertension, hyperlipidemia, hypothyroidism, and
meningioma s/p craniotomy ~8 years ago. She denied any history of acute coronary syndrome/myocardial
infarction (ACS/MI), congestive heart failure (CHF), heart murmur, rheumatic fever, arrhythmia, heart block,
and anxiety. In pertinent family history, her father had experienced a stroke. Differential diagnoses included
non-ST-elevation myocardial infarction (NSTEMI), pulmonary embolism, aortic dissection, pneumothorax,
pericarditis, pericardial tamponade, esophageal rupture, pneumonia, pleurisy, gastroesophageal reflux
disease (GERD), and musculoskeletal chest pain. Her heart score was 5. Chest X-ray was unremarkable
except for mild cephalization (Figure 1).

How to cite this article

Shankar A, Devaraj N (March 13, 2023) Classic Unprovoked Takotsubo Syndrome: A Case Report. Cureus 15(3): e36056. DOI
10.7759/cureus.36056
 FIGURE 1: Chest X-ray showing a normal cardiac silhouette
Some calcification is present in the right hilar region (orange arrow) and aortic knob. There is a slight prominence
of vascular markings (blue arrows)

Vitals showed a temperature of 97.7 °F, a heart rate of 64 beats per minute, and a respiratory rate of 15
breaths per minute. Her blood pressure was 112/76 mmHg. Labs were significant for elevated ALT (~39),
leukocytosis (~11.2K), low thyroid stimulating hormone (TSH)/free T4 (~0.182/0.61), and elevated
triglycerides (~258). UDS, coagulation panel, electrolytes, D-dimer, and SARS tests were unremarkable. HS
troponin trend was as follows: admission: 207→2794→1478→; day of cath: 573→2148→1974→; POD 1:
1199→712→642→; POD 2: 616→544. Figure 2 shows the EKG on admission.

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 FIGURE 2: EKG on admission: sinus bradycardia
HR 57, no ST elevation, no ectopy. Small r-wave in V1 and V2, abnormal T/T-wave variation anterior leads, small
q-wave in I

EKG: electrocardiogram

The patient was given fluids, aspirin, and nitroglycerin and admitted to telemetry. Cardiology was consulted.
The patient’s chest pain initially subsided with the above but recurred as dull chest pressure. She was
otherwise hemodynamically stable. Troponin was elevated and repeat EKG showed T-wave inversions not
present on the initial EKG (Figures 2, 3). A full dose of Lovenox was initiated. Echo (Table 1) showed WMA.
She had cardiac catheterization with fluoroscopy supervision of the left heart and coronaries (Table 2) for
NSTEMI, which showed Takotsubo cardiomyopathy (Figure 4).

2023 Shankar et al. Cureus 15(3): e36056. DOI 10.7759/cureus.36056 3 of 6

 Location Findings

Normal size. Systolic function is relatively preserved. Hypertensive heart disease. Significant regional wall motion
Left
abnormalities are noted (severe hypokinesis of distal septum and apex). The left ventricular diastolic function is normal.
ventricle
LVEF is 50-55%

Right
Normal size. Systolic function is normal. RVSP 13 mmHg
ventricle

Left and
Normal size
right atria

Aortic valve Trileaflet. Mild valve sclerosis. No regurgitation. AoV peak Vel. 115.2 cm/s. AO peak Gr. 5.3 mmHg

Mild annular calcification. Mild regurgitation. MV E Vel. 79.7 cm/s. MV peak Gr. 26 mmHg. MV DECEL time 144 ms. MV A
Mitral valve
Vel. 66.5 cm/s. E/A ratio 1.2

Tricuspid
Normal structure. Trace regurgitation. TR peak Vel. 90 cm/s. RAP estimate 10 mmHg. TR peak Gr. 3 mmHg
valve

Pulmonic
Normal structure. Mild regurgitation. PV peak Vel. 67.5 cm/s. PV peak Gr. 2 mmHg
valve

Great
The aortic root is of normal size. IVC is normal in size and collapses ~50% with inspiration
vessels

Pericardium No pericardial/pleural effusion

TABLE 1: Echocardiogram findings prior to cardiac cath

LVEF: left ventricular ejection fraction; RVSP: right ventricular systolic pressure; AoV: aortic valve; Vel: velocity; AO: aortic; Gr: gradient; MV: mitral valve;
TR: tricuspid; RAP: right atrial pressure; PV: pulmonic valve; IVC: inferior vena cava

FIGURE 3: EKG on the day of cath: sinus bradycardia with T-wave

inversion across the precordial leads, lead I and aVL
Findings are consistent with anterolateral ischemia and/or nontransmural injury

EKG: electrocardiogram

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 FIGURE 4: Cardiac catheterization image showing Takotsubo heart
(white arrow and outline). Type: apical ballooning with “nipple sign”
(red arrow)

Region Angiographic findings

Left ventricular cineangiogram performed in 30 degrees right Apical hypokinetic and akinetic area consistent with Takotsubo
anterior oblique projection cardiomyopathy

Left main coronary artery Widely patent

Left anterior descending coronary artery Transapical vessel, widely patent with no arteriosclerotic changes

Circumflex artery Non-dominant vessel, widely patent with no arteriosclerotic changes

Right coronary artery Large dominant vessel, widely patent with no arteriosclerotic changes

Patent common iliac and common femoral artery. The catheter entry point
Right iliofemoral angiography
is well above the bifurcation

TABLE 2: Angiography findings

The patient was discharged in stable condition and advised to follow up with the cardiologist as an
outpatient. She was discharged home on aspirin, atorvastatin, lisinopril, and metoprolol succinate. She was
subsequently readmitted for orthopnea and midsternal, non-radiating, reproducible pleuritic chest pain. Her
troponin remained elevated and was likely secondary to demand ischemia, periprocedural myocardial injury,
and LV dysfunction. Repeat limited Echo showed EF of ~55% but with no significant WMA as seen on the
previous Echo. Cardiologist readjusted her medications with the addition of isosorbide mononitrate,
furosemide, and spironolactone to address LV failure and to reverse remodeling, given her symptomatic

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 presentation although EF was preserved. The patient’s symptoms resolved and she was discharged when
stable. She has not had any further ER visits or readmissions to this hospital since.

Discussion
Management of TS mainly involves supportive therapy. Approach to acute management can be based on the
suspected underlying cause, although this is difficult to achieve as patients presenting are usually worked up
for other diseases such as acute MI, and the diagnosis is not made until after catheterization and left
ventriculogram. Therapy corresponding to pathophysiology would mean beta-blockers in suspected
autonomic hyperactivity, nitrates or calcium channel blockers in coronary vasospasm, etc. [2]. Heart failure
can occur, especially in patients aged >70 years, and those with LVEF <40% and physical stressors [2]. Mild
cases (stable vitals, minimal troponin leak, no cardiogenic shock) can be treated with classic heart failure
guideline-directed therapy including ACE-I/ARB/ARNI, beta-blockers, mineralocorticoid receptor
antagonists, and/or another diuretic. Some studies in the literature recommend initial treatment with the
above along with dual antiplatelet therapy, anticoagulation, and statins [3]. If patients are asymptomatic and
hemodynamically stable, pharmacotherapy should be carefully chosen to avoid inflicting iatrogenic harm on
an otherwise naturally recovering process [2].

Short-course anticoagulation can be added especially if there is a concern for thrombus formation related to
cardiac akinesia/dyskinesia with ballooning [2]. Patients with large areas of hypo/akinesia and/or LVEF <30%
need to be observed more closely for heart failure, atrial/ventricular arrhythmias, cardiac thrombi, and
cardiogenic shock [2]. Management of shock depends on the presence of left ventricular outflow tract
obstruction (LVOTO); if LVOTO is present, inotropic agents are contraindicated and medications to increase
diastolic filling time, such as IV metoprolol, esmolol, or landiolol, are recommended [2-3]. Arrhythmias due
to QTc prolongation are also seen, but no prophylactic treatment is indicated for the same [4]. However,
administering magnesium helps with acute phase TS-associated ventricular tachycardia with long QTc [4].

Conclusions
Although TS is seen as a benign transient condition, it can lead to many acute complications. Some of these
complications include acute heart failure, LVOTO, RV involvement, mitral regurgitation, arrhythmias,
cardiac thrombus formation, pericardial effusion, ventricular wall rupture, and cardiogenic shock.
Depending on the clinical analysis, hemodynamic stability, Echo findings, suspected diagnosis, and
underlying pathophysiology, therapy needs to be tailored to individual patients. Mortality usually occurs due
to refractory shock or fatal arrhythmias such as ventricular fibrillation. Data on long-term prognosis is
limited; while most patients recover within a few weeks, there have been reports on subsets of patients who
experience persistent symptoms such as exertional dyspnea, palpitations, and angina. Beta-blockers can
exacerbate bradyarrhythmia or AV blocks, and hence they need to be used with caution. Inotropic agents can
help in cardiogenic shock but are contraindicated in LVOTO. Thus, medical optimization is important to
prevent future recurrence and long-term complications of the disease.

Additional Information
Disclosures
Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In
compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services
info: All authors have declared that no financial support was received from any organization for the
submitted work. Financial relationships: All authors have declared that they have no financial
relationships at present or within the previous three years with any organizations that might have an
interest in the submitted work. Other relationships: All authors have declared that there are no other
relationships or activities that could appear to have influenced the submitted work.

References
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3. Sattar Y, Siew KS, Connerney M, Ullah W, Alraies MC: Management of Takotsubo syndrome: a
comprehensive review. Cureus. 2020, 12:e6556. 10.7759/cureus.6556
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heart failure. Circulation. 2008, 118:2754-62. 10.1161/CIRCULATIONAHA.108.767012

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