Case Presentation by Sarah Michael, DO
Chief Complaint: “My chest has been bothering me.”
History of Present Illness:
A 67-year-old female patient presents to the ED complaining of chest discomfort slowly worsening over the past 10-12 hours. It has been relatively mild but constant since the time of onset. The patient reports a left substernal nonradiating pressure sensation. She has never experienced anything similar in the past and has not taken anything for pain. She is not short of breath, diaphoretic, dizzy, or lightheaded. When questioned further, the patient reports she thinks her symptoms are “due to stress” as she has been hosting several extended family members at her home over the past few days. She drove herself to the ED.
Past Medical History: hypothyroidism, hyperlipidemia
Past Surgical History: none
Medications: simvastatin, levothyroxine
Social: Lives alone. Drinks alcohol infrequently (none recently). No tobacco or drug use.
Family History: Denies significant family history. No family history of early myocardial infarction.
Oxygen saturation 100% RA
General: Alert, oriented, well-appearing Caucasian female, sitting in a chair without distress. She speaks in complete sentences.
Cardiovascular: Regular rate & rhythm. No murmurs. No chest wall tenderness or exacerbation of pain with palpation.
Respiratory: Clear to auscultation bilaterally
GI: Abdomen soft, non-tender, non-distended
Neuro: Alert, oriented, appropriate. Strength 5/5 in all extremities.
Psychiatric: No acute psychiatric decompensation is noted. She is appropriate, lucid and able to formulate and articulate complex thought processes without delusions. No evident anxiety.
A cardiac workup was initiated and the following EKG was obtained.
1. Where does the pathology demonstrated in the EKG localize?
A. right coronary artery
B. left circumflex artery
C. left anterior descending artery
The following bedside echocardiogram was obtained in the ED.
2. On the basis of the echocardiogram, where does the patient’s pathology localize?
A. right ventricle
B. left ventricle
C. mitral valve
3. What is the underlying pathologic mechanism resulting in this clinical picture?
A. catecholamine surge
B. plaque rupture
C. inflammation with PMN infiltration
D. infection of a pletelet-fibrin nidus with circulating bacteria
1. C. Let’s start by agreeing that this is not pericarditis (D). The concavity can be misleading, but recognize that the ST segments are not globally elevated. There is also a giant pathologic Q wave with deeply inverted T wave in III and a fragmented (potential goes up, then down, then up) small voltage QRS in V2. These features are far more consistent with infarct than with pericarditis.
There is ST elevation in V2-V6 consistent with anterolateral infarct. The remaining leads have been mapped on the hexaxial reference figure below.
The infarct predominantly affects the anterolateral aspect with involvement of aVR and III. What vessel supplies all of these regions? A “wraparound” type III LAD, which, when obstructed, can produce ST elevations in any inferior, anterior or lateral leads. Caution is required because an obstruction of this vessel can create a compelling pericarditis mimic. (A) A dominant RCA is unlikely to cause this degree of anterior ST elevation. (B) Similarly, the circumflex (obtuse marginal) artery does not perfuse a large enough percentage of myocardium to cause diffuse ST elevation.
2. B. Takotsubo cardiomyopathy takes it’s name from “Tako-tsubo,” the Japanese word for “octopus pot.” With its wide base and narrow neck, this eartherware structure is an ideal home for unsuspecting cephalopods. It also nicely describes the shape of the LV apex in people afflicted with this condition, which is also called “left ventricular apical ballooning syndrome.” On echocardiogram, you will typically see dilation and hypokinesis of the apex with relative sparing of the base. There is typically not primary involvement of the other chambers or valves. Underlying left ventricular outflow tract obstruction exacerbates the disease.
Takotsubo cardiomyopathy typically presents in times of emotional distress and most commonly occurs in post-menopausal women. The initial presentation is often indistinguishable from STEMI and evidence of inferior, lateral, or anterior localization may be seen. Cardiac catheterization will reveal non-occlusive coronary arteries and apical dilation on left ventriculogram, shown below. Ejection fraction is often moderately to severely reduced and troponin is typically positive.
3. A. There are many names for the condition and in the lay media it is often referred to as “broken heart syndrome” because it presents during times of emotional stress, though the trigger may be relatively minor, as seen in this case. The definitive mechanism has not been elucidated, but there is clearly a catecholamine surge, which when combined with a relative decrease in endothelial NO after menopause, is thought to cause distal coronary artery vasospasm and myocardial ischemia.
(B) Plaque rupture would be expected in the case of obstructive atherosclerotic coronary artery disease. (C) Inflammation and PMN infiltration is typically seen in the setting of acute pericarditis. (D) Infection of a platelet-fibrin nidus is the mechanism by which endocardial vegetations form.
1. Smith, S. Pericarditis, or Anterior STEMI? The QRS proves it. Dr. Smith’s ECG Blog. http://hqmeded-ecg.blogspot.com/2012/08/pericarditis-or-anterior-stemi-qrs.html
2. Merchant, et al. Takotsubo Cardiomyopathy: A Case Series and Review of the Literature. West J EM. 2008 vol. 9 no. 2. http://westjem.com/case-report/takotsubo-cardiomyopathy-a-case-series-and-review-of-the-literature.html
3. Takotsubo Cardiomyopathy. Circulation. December 16/23, 2008 vol. 118 no. 25 2754-2762. http://circ.ahajournals.org/content/118/25/2754/F4.expansion.html