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Ultrasound For The Win! – 57F with Chest Pain and Dyspnea #US4TW

Welcome to another ultrasound-based case, part of the “Ultrasound For The Win!” (#US4TW) Case Series. In this case series, we focus on a real clinical case where point-of-care ultrasound changed the management of a patient’s care or aided in the diagnosis. In this case, a 57-year-old woman presents with chest pain and dyspnea.

Learning Objectives

  1. List a differential diagnosis for a patient presenting with chest pain and shortness of breath.
  2. Discuss the role point-of-care ultrasound plays in differentiating acute chest pain.
  3. Discuss the prevalence, diagnostic criteria, common sonographic findings, and management of Takotsubo syndrome.

Case Presentation

A 57-year-old woman presents to the Emergency Department (ED) with a 2 day history of retrosternal chest pain and progressive dyspnea present at rest and worsening on exertion. She reports orthopnea, pre-syncope, and palpitations. She denies fever, cough, or history of venous thromboembolism. She is not currently on any medications. Her only past medical history is mitral valve prolapse with normal systolic function on transthoracic echo (TTE) 2 months prior. Her review of systems is otherwise non-contributory. She is physically active, exercises daily on a treadmill, and works as a registered nurse.

On physical examination, you find a well-appearing woman in no acute distress. Her cardiovascular exam reveals normal heart sounds with no audible murmurs on auscultation, strong pulses in her lower extremities with no edema. The respiratory exam reveals good air entry bilaterally and fine bi-basilar crackles. Her abdominal exam is unremarkable.

Vital Signs

  • BP 110/65 mmHg
  • P 85 bpm
  • RR 20 breaths/min
  • O2 95% on room air
  • T 36.4 C

Differential Diagnosis

  • Acute Coronary Syndrome (STEMI/NSTEMI/Unstable Angina)
  • Anxiety
  • Aortic Dissection
  • Arrhythmia
  • Cardiomyopathy
  • Congestive Heart Failure
  • Costochondritis
  • Gastroesophageal reflux disease
  • Pericarditis/Myocarditis
  • Pneumomediastinum
  • Pneumonia
  • Pneumothorax
  • Pulmonary Embolism
  • Takotsubo Syndrome
  • Valvular heart disease

Laboratory Investigations

  • WBC 11.8 x 10^9 cells/L
  • Hemoglobin 13.6 gm/dL
  • BUN 10.6 mmol/dL
  • Creatinine 0.77 mg/dL
  • Creatine Kinase 192 U/L
  • Troponin-I 10,611 ng/L
  • VBG – pH 7.41 pCO2 42 mmHg HCO3 26 mmol/L
  • Lactate 1.6 mg/dL

Electrocardiogram (ECG)

Figure 1. Electrocardiogram, non-diagnostic. Normal sinus rhythm at 87. Normal axis and intervals. Nonspecific anterolateral repolarization abnormalities and delayed R-wave progression suggesting possible age-indeterminate anterior infarct. No ST-elevation myocardial infarction (STEMI).

Case Evolution

The cardiac monitor alarms and premature ventricular contractions (PVCs) are noted on the cardiac monitor. The ED nurse later alerts you to a tracing showing 2 runs of non-sustained ventricular tachycardia. She now has an increasing O2 requirement and her blood pressure declines to 80/50 mmHg.

Point-of-Care Ultrasound

Given your concern for her rapid deterioration, you perform a point-of-care ultrasound (POCUS) echocardiogram:

Figure 2. Parasternal Long Axis. The parasternal long axis view (PSL) reveals a left ventricle with a hyperdynamic base, mid anteroseptal and mid inferolateral akinesis and apical ballooning.

Figure 3. Parasternal Short Axis. The parasternal short axis (PSS) view, taken at the level of the papillary muscles, demonstrates circumferential hypokinesis/akinesis of the LV.

Figure 4. Apical 4 Chamber. The apical four-chamber (A4C) view shows akinesis/hypokinesis of the mid inferoseptal, anterolateral, and apical segments. The base appears hyperdynamic. Right ventricular size and systolic function are grossly normal. No pericardial effusion is seen.

Figure 5. Apical 4 Chamber view of the heart with Takotsubo Syndrome. (RV = Right Ventricle, RA = Right Atrium, LV = Left Ventricle, LA = Left Atrium)

Figure 6. Apical 3 Chamber. Apical left ventricular ballooning again is seen on the apical 3-chamber (A3C) views with regional wall motion abnormalities as described above.

Figure 7. Inferior Vena Cava. The inferior vena cava is plethoric with minimal respiratory variation.

Conclusions from POCUS

The following was concluded from the point-of-care cardiac views:

  • There was severe left ventricular systolic dysfunction.
  • There were regional wall motion abnormalities involving most mid and apical segments of the left ventricle.
  • The base of the left ventricle was hyperdynamic.
  • There was no pericardial effusion to suggest pericarditis or cardiac tamponade.
  • The right ventricle was normal in size and function arguing against a submassive or larger pulmonary embolus as a cause for her clinical deterioration.

Acute Coronary Syndrome (ACS) with resultant LV aneurysm is the most likely and most important diagnosis to pursue based on the history obtained. Although the left ventricular regional wall motion abnormalities (RWMA) involved could have been the result of ACS, a single culprit artery would be unlikely to cause several areas of hypokinesis as the regions involved are perfused from multiple arteries. Instead, the pattern of RWMA is more characteristic of the “apical ballooning” present in Takotsubo syndrome (TTS).

Figure 8. Takotsubo Syndrome takes its name from the Japanese Octopus Trap

TTS is an acute life-threatening transient cardiomyopathy characterized by a temporary wall motion abnormality of the left ventricle. It is named after the Japanese Octopus Trap [Fig. 8]. Presenting symptoms can include acute chest pain, dyspnea, or syncope. An ECG may present with ST-changes matching a STEMI or NSTEMI, making it indistinguishable from ACS at first glance1. It is often associated with an acute emotional or physical stressor, however about one-third of patients present without evidence of an identifiable preceding stressful event.2 The 2018 International Takotsubo Diagnostic Criteria (InterTAK Diagnostic Criteria) are shown in Table 1.3

Table 1. 2018 International Takotsubo Diagnostic Criteria (InterTAK Diagnostic Criteria)3

1. Patients show transienta left ventricular dysfunction (hypokinesia, akinesia, or dyskinesia) presenting as apical ballooning or midventricular, basal, or focal wall motion abnormalities. Right ventricular involvement can be present. Besides these regional wall motion patterns, transitions between all types can exist. The regional wall motion abnormality usually extends beyond a single epicardial vascular distribution; however, rare cases can exist where the regional wall motion abnormality is present in the subtended myocardial territory of a single coronary artery (focal TTS).b
2. An emotional, physical, or combined trigger can precede the Takotsubo syndrome event, but this is not obligatory.
3. Neurologic disorders (e.g. subarachnoid haemorrhage, stroke/transient ischaemic attack, or seizures) as well as pheochromocytoma may serve as triggers for Takotsubo syndrome.
4. New ECG abnormalities are present (ST-segment elevation, ST-segment depression, T-wave inversion, and QTc prolongation); however, rare cases exist without any ECG changes.
5. Levels of cardiac biomarkers (troponin and creatine kinase) are moderately elevated in most cases; significant elevation of brain natriuretic peptide is common.
6. Significant coronary artery disease is not a contradiction in Takotsubo syndrome.
7. Patients have no evidence of infectious myocarditis.b
8. Postmenopausal women are predominantly affected.

aWall motion abnormalities may remain for a prolonged period of time or documentation of recovery may not be possible. For example, death before evidence of recovery is captured.

bCardiac magnetic resonance imaging is recommended to exclude infectious myocarditis and diagnosis confirmation of Takotsubo syndrome.

Disposition & Case Conclusion

Although TTS is suspected, its diagnosis is felt to be a diagnosis of exclusion and requires that ACS be ruled out.2 Therefore, the case was discussed with the on-call cardiologist and the point-of-care ultrasound clips were presented. Based on the findings, an urgent coronary angiogram was performed which demonstrated normal coronary anatomy and an absence of culprit plaque deposits, ruling out ACS as a probable cause.

An intra-operative left ventriculogram confirmed apical ballooning and severe left ventricular dysfunction (Ejection Fraction ~20%). Considering TTS does not have culprit lesions on angiography to explain observed RWMAs the patient was given a diagnosis of TTS.

Takotsubo syndrome is estimated to represent approximately 1–3% of all and 5–6% of female patients presenting with suspected ACS4–6. Based on the published literature, about 90% of TTS patients are women and about 80% are older than 50 years.1,7

There are no evidence-based guidelines for treating TTS, however the use of angiotensin converting enzyme inhibitors (ACE inhibitors) or Angiotensin II Receptor Blockers (ARBs) was associated with improved survival at 1-year follow-up.1 Patients who survive the initial event have a second event in approximately 5% of cases, mostly occurring 3  weeks to 3.8  years after the first event; However, ACE inhibitors or ARBs are associated with lowering the recurrence rate.8

The patient was started on vasopressors and inotropes in the ED for cardiogenic shock and transferred to the catheterization lab. After angiography she was monitored in the hospital, and her symptoms improved over the course of 1 week. She was then discharged with a prescription for an ACE inhibitor and beta blocker.

Take Home Points

  1. Takotsubo syndrome is an acute, life-threatening, and transient cardiomyopathy of the left ventricle which often presents very similar to and indistinguishable from ACS.
  2. ACS must be ruled out before a diagnosis of TTS can be made.
  3. POCUS can be a very useful tool to differentiate between TTS and ACS and can help direct the appropriate management.
1.
Templin C, Ghadri J, Diekmann J, et al. Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy. N Engl J Med. 2015;373(10):929-938. [PubMed]
2.
Gianni M, Dentali F, Grandi A, Sumner G, Hiralal R, Lonn E. Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review. Eur Heart J. 2006;27(13):1523-1529. [PubMed]
3.
Ghadri J, Wittstein I, Prasad A, et al. International Expert Consensus Document on Takotsubo Syndrome (Part I): Clinical Characteristics, Diagnostic Criteria, and Pathophysiology. Eur Heart J. 2018;39(22):2032-2046. [PubMed]
4.
Redfors B, Vedad R, Angerås O, et al. Mortality in takotsubo syndrome is similar to mortality in myocardial infarction – A report from the SWEDEHEART registry. Int J Cardiol. 2015;185:282-289. [PubMed]
5.
Bybee K, Prasad A, Barsness G, et al. Clinical characteristics and thrombolysis in myocardial infarction frame counts in women with transient left ventricular apical ballooning syndrome. Am J Cardiol. 2004;94(3):343-346. [PubMed]
6.
Prasad A, Dangas G, Srinivasan M, et al. Incidence and angiographic characteristics of patients with apical ballooning syndrome (takotsubo/stress cardiomyopathy) in the HORIZONS-AMI trial: an analysis from a multicenter, international study of ST-elevation myocardial infarction. Catheter Cardiovasc Interv. 2014;83(3):343-348. [PubMed]
7.
Schneider B, Athanasiadis A, Stöllberger C, et al. Gender differences in the manifestation of tako-tsubo cardiomyopathy. Int J Cardiol. 2013;166(3):584-588. [PubMed]
8.
Sharkey S, Windenburg D, Lesser J, et al. Natural history and expansive clinical profile of stress (tako-tsubo) cardiomyopathy. J Am Coll Cardiol. 2010;55(4):333-341. [PubMed]
John MacIsaac, BSc. Hons, MD Candidate (2019)

John MacIsaac, BSc. Hons, MD Candidate (2019)

Faculty of Medicine
University of Ottawa
John MacIsaac, BSc. Hons, MD Candidate (2019)

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George N. Mastoras, MD, FRCPC

George N. Mastoras, MD, FRCPC

Department of Emergency Medicine
University of Ottawa
The Ottawa Hospital
George N. Mastoras, MD, FRCPC

Latest posts by George N. Mastoras, MD, FRCPC (see all)

Jeffrey Shih, MD, RDMS
Director, Emergency Ultrasound Fellowship Program
The Scarborough Hospital;
Lecturer
University of Toronto;
Editor, Ultrasound for the Win Series
Academic Life in Emergency Medicine