Echo Case: A 71 Year-Old Woman Presenting with Abdominal Pain and Dyspnea

Authors: Kan Liu MD, PhD, Debanik Chaudhuri, MD, Arunpreet Kahlon, MD

State University of New York, Upstate Medical University, Syracuse, NY

Corresponding author:

Kan Liu MD, PhD

Heart and Vascular Center
State University of New York
Upstate Medical University
Syracuse, NY 13202
Tel: 315-464-4535; 315-464-1931 (office)

Author contributions: K.L., D.C. and A.K. had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis, including and especially any adverse effects. K.L., D.C. and A.K. helped write the manuscript.

Figure 1. A CT imaging of the abdomen reveals ischemic bowel perforation secondary to incarcerated hernia.

A 71-year-old woman presented with sudden abnormal pain and vomiting. She underwent CT imaging study of the abdomen, which revealed ischemic bowel perforation secondary to an incarcerated hernia (Figure 1A and B). An emergent surgery for acute abdomen was planned.

However, she suddenly became dyspenic and hypotensive (systolic blood pressure 70 mm Hg). In addition to diffuserebound abdominal tenderness and cold extremities, there were noteworthy crackles in bilateral lung bases. A III/VI systolic murmur was heard at left upper sternal border. Therefore, a chest radiograph was performed and showed diffuse bilateral infiltrates, consistent with pulmonary edema (Figure 2A). A simultaneous electrocardiogram (ECG) revealed ST segment myocardial infarction (STEMI) pattern (Figure 2B). Other laboratory data were notable for a white blood cell10.5 K/ul, lactic acid 2.2 mmol/L, creatine 1.9 mg/dL, creatinine kinase–MB 31.40 ng/mL, and cardiac troponin T 1.46 ng/mL.

Figure 2. A: A portable chest radiograph shows bilateral hilar fullness/haziness, diffuse infiltrates  and pleural effusion. B: An electrocardiogram shows ST segment elevation myocardial infarction pattern.

The surgery was held due to the concern of significantly increased operative mortality in the presence of untreated STEMI. Transthoracic echocardiography (TTE) was performed (Videos 1-4).

Question:

On the basis of Videos 1-4, and the patient’s clinical presentation/laboratory data, which of the following is the next best step in management:

1. Thrombolytic therapy
2. Cardiac cauterization with percutaneous coronary intervention
3. Urgent surgery for ischemic bowel perforation
4. Conservative medical management

Discussion

Combined with clinical pictures, severe ventricular dysfunction with only minimal elevations in cardiac enzymes is consistent with apical ballooning syndrome (or Tako-tsubo syndrome, TTS).  This diagnosis avoided potentially harmful treatments for STEMI, and allowed life-saving surgery to be performed timely. Therefore, Option C is right. Bowel perforation/bleeding contradict not only thrombolytic therapy, but also anti-platelet/anti-coagulation required for cardiac catheterization / percutaneous coronary intervention. Both Option A and B are wrong.  Medical management can’t treat acute abdomen or prevent hypovolumic/septic shock. Optional D is wrong

While the changes on the ECG were concerning for an acute myocardial infarction, there were important discriminating features of the case to allow another diagnosis: 1. despite ST segment elevation, reciprocal ECG change was lack (Figure 2B); 2. the degree of cardiac enzyme elevation was too low for the degree of LV dysfunction shown by the echocardiogram;  3. the pattern of the ventricular contractile dysfunction in the echocardiogram (Video1-3) was beyond the myocardial territory of any single coronary artery. In addition, apical (hypokinetic) and basal (hyperkinetic) segments exhibited a discordant contractile pattern (Figure 3A and 3B).  These findings support the diagnosis of TTS. TTS also caused a dynamic left ventricular outflow tract (LVOT) obstruction, generating the systolic murmur and resulting in hypotension (Figure 3C and 3D, and Video 4). Of note, catecholamine inotropes/pressors are harmful since they can worsen LVOT obstruction and hemodynamic instability.  After we applied prompt fluid resuscitation and intravenous phenylephyrine infusion, this patient became hemodynamically stable, and received exploratory laparotomy/small bowel excision successfully. The ECG and echocardiographic abnormalities spontaneously normalized in 3 weeks.

Figure 3. A: A two dimensional echocardiogram shows apical akinesis (arrowheads) in an apical 2 chamber view. B:  A speckle-tracking echocardiogram depicts a unique distribution pattern of abnormal myocardial contractility in a left ventricular 17-segment (bull’s eye) plot. Impaired peak systolic longitudinal strains are highlighted by digital (normal: < -17%) and color codes (red: normal; pink: impaired; blue: significantly impaired). C. A color Doppler study shows a turbulent flow in left ventricular outflow tract (LVOT, arrowhead) and simultaneous mitral regurgitation (arrow). D. A continuous-wave Doppler study shows an increased gradient across LVOT (arrowhead, the first heart beat) and mitral regurgitation (arrow, the 2nd heart beat).

TTS often mimics the clinical features of acute myocardial infarction (AMI), including STEMI.  Coronary angiography is the only definitive approach to differentiate TTS and AMI (1, 2). Nevertheless, frontline clinicians often face a dilemma when cardiac catheterization and thrombolytic therapy (in case of STEMI) is contradicted, or can potentially cause critical adverse consequences. Under life-threatening conditions, characteristic ECG/non-invasive imaging features can provide valuable diagnostic information to prompt timely decision-making.  Although most TTS episodes have benign course, acute heart failure and hemodynamic instability can occur (3). With basal interventricular septal hypertrophy, hyper-contractility of basilar walls and systolic anterior motion of the anterior leaflet of the mitral valve (MV) can induce dynamic LVOT obstruction, disrupting coaptation of MV and worsening mitral regurgitation (4). Avoiding catecholamine inotropes/pressors (such as dobutamine), maintaining appropriate ventricular preload, and applying alpha-adrenergic agonists (when indicated) might be the most effective therapies during the acute phase of TTS.

Reverberations

1. Tako-tsubo syndrome often mimics clinical and electrocardiographic features of acute anterior myocardial infarction.
2. When cardiac catheterization is contradicted, characteristic non-invasive imaging characteristics can provide valuable diagnostic information to help timely decision-making under life-threatening condition.
3. Dynamic left ventricular outflow tract obstruction and mitral regurgitation play important roles in the development of heart failure and hemodynamic instability during Tako-tsubo syndrome.

 Answer: C.

Video1: A transthoracic echocardiogram (TTE) shows apical akinesis in an apical 2 chamber view.

Video2: A TTE shows apical akinesis in an apical 4 chamber view.

Video3: A TTE shows apical akinesis in a parasternal short axis view.

Video 4: A color Doppler study shows left ventricular outflow tract obstruction and mitral regurgitation.

Video 5: Discussion video.

Reference

1. Lyon AR, Bossone E, Schneider B, Sechtem U, Citro R, Underwood SR, et al. Current state of knowledge on Takotsubo syndrome: a Position Statement from the Taskforce on Takotsubo Syndrome of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2016, 18:8-272.
2. Templin C, Ghadri JR, Diekmann J, Napp LC, Bataiosu DR, Jaguszewski M et al. Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy. N Engl J Med 2015; 373:929-938.
3. Citro R, Rigo F, D’Andrea A, Ciampi Q, Parodi G, Provenza G, et al. Echocardiographic correlates of acute heart failure, cardiogenic shock, and in-hospital mortality in tako-tsubo cardiomyopathy. J Am Coll Cardiol Cardiovasc Imaging 2014, 7:119-129.
4. Liu K, Krone JK. What Truly Causes the Adverse Outcome of Tako-Tsubo Cardiomyopathy? J Am Coll Cardiol: Cardiovasc Imaging. 2014, 7: 742-743.