A 62-year-old white woman was admitted to the emergency department with sudden onset of chest pain and dyspnea, immediately after she had witnessed her husband’s death.

From her past history, the only remarkable event was a transient ischemic attack 6 years prior; she suffered from high blood pressure and depression and was under therapy with lisinopril 20 mg, amlodipine 5 mg, indapamide 2.5 mg, acetylsalicylic acid 150 mg, dipyridamole 75 mg, trimetazidine 35 mg, amitriptyline 10 mg, alprazolam 0.25 mg, paroxetine 20 mg and simvastatin 20 mg.

At presentation she was hemodynamically stable (blood pressure—BP—130/70 mmHg, heart rate 100 bpm, oxygen saturation of 92%, with oxygen delivery 24%), her cardiac auscultation was unremarkable and her pulmonary auscultation revealed rales in the lower third bilaterally.

The blood analysis showed elevated troponin I (0.34 ng/ml, normal range < 0.2 ng/ml) and myoglobin (214 ng/ml, normal range between 9 - 82 ng/ml); the creatinine kinase (CK) and CK-MB isoenzyme were only slightly above normal range (167 U/L and 4 ng/ml, normal range < 145 U/L and 3.6 ng/ml, respectively).

Her chest X-ray revealed an enlarged cardiothoracic index, with bilateral basal infiltrates, suggestive of interstitial edema (Figure 1 (a)).

The ECG showed sinus rhythm, 101 bpm, normal QRS axis, with inferior ST depression and lateral ST elevation, inferior to 1 mm. (Figure 2(a)).

She developed hypotension (BP 70/45 mmHg), with good response to volume. The ECG was repeated and pointed out to anterior and lateral ST elevation (still inferior to 1 mm), inferior ST depression and T Wave inversion, changes more prominent than before (Figure 2(b)).

A transthoracic echocardiogram was performed, showing mid ventricular and apical hypokinesis with apical ballooning, and preserved contraction of the basal segments.

At this time TC was suspected. The patient underwent cardiac catheterization with left ventriculography, which demonstrated unobstructed coronary arteries (Figure 3), with spiral morphology, and a normal dimensioned LV, with antero-lateral, apical and infero-apical akinesis, with global function preserved (ejection fraction—EF—52%) (Figure 4).

She was then admitted to the coronary intensive care unit. The peak troponin I concentration was 1.88 ng/ml, with rapid descending profile. The ECG repeated three days later pointed out diffuse T wave inversion, and prolonged QT (0.6 sec, heart rate 60 bpm) (Figure 2(c)). She was discharged after five days under therapy with acetylsalicylic acid, clopidogrel and atorvastatin. Four weeks later she was observed at a follow up appointment; she had abandoned all therapeutics at this point.

She was readmitted to the emergency department five weeks later with headache, chest pain and dysarthric; the

neurological exam and head CT excluded a cerebrovascular event; serial cardiac enzymes determination were negative; the ECG showed sinus rhythm, 80 bpm, with antero-lateral T wave inversion (Figure 2(d)); the chest X-ray no longer showed bilateral infiltrates and the cardiothoracic index was smaller (Figure 1(b)). The echocardiogram was repeated, showing complete resolution of the hypokinesis observed before. Her complaints were attributed to anxiety.

TC was confirmed.

A 84-year-old white woman presented to the emergency department with dyspnea, diaphoresis and pallor, without chest pain, beginning a few hours after she had been transfused with two units of packed red blood cells.

Her medical history included cerebrovascular disease, stroke with left hemiparesis, congestive heart failure and chronic anemia. She was under therapy with triflusal 300 mg, amiodarone 200 mg, enalapril 5 mg, iron polymaltose complex, sertraline 50 mg, mirtazapine 15 mg, lorazepam 1 mg, omeprazole 20 mg and multivitamin complex.

On physical exam, she was normotensive, apyretic, with a mitral systolic murmur (II/VI) and bilateral rales.

Her cardiac enzymes were increased: troponin I of 1.37 ng/ml, myoglobin of 220 ng/ml and CK MB of 6.8 ng/ml; her creatinine level was also raised (2.18 mg/dl, with normal range between 0.55 and 1.02 mg/dl). The peak troponin I concentration was 1.94 ng/ml, five hours after admission.

The ECG revealed sinus rhythm, 87 bpm, with nonspecific lateral ST changes (Figure 5(a)). Nine hours after admission, she became hypotensive (BP 67/47 mmHg), with partial response to volume. Intravenous administration of dopamine was started at 5 mg/Kg/min and she was admitted to the internal medicine ward.

After thirty six hours she maintained hypotension, despite dopamine perfusion at 10 mg/Kg/min. The ECG revealed diffuse ST segment elevation (Figure 5(b)) and cardiac catheterization was performed, revealing unobstructed coronary arteries (Figure 6). The next day, she underwent transthoracic echocardiogram, showing hypokinesis of the mid-apical segments of the lateral wall and apical segment of the remaining walls, with hyperkinesis of the basal segments, with ejection fraction of 50%; a left intraventricular pressure gradient wasn’t found; there was moderate mitral valve regurgitation and severe tricuspid regurgitation present. The ECG was repeated, showing sinus rhythm, 81 bpm, with non-specific antero-lateral ST changes and prolonged QT (0.6 sec, heart rate 81 bpm) (Figure 5(c)).

TC was suspected.

Dopamine was discontinued. As she presented refractory

hypotension in the context of cardiogenic shock, intravenous perfusion of dobutamine was initiated, with good response.

She was discharged after six days under therapy with triflusal and atorvastatin, and readmitted two days after with health care associated pneumonia; she had no complains of chest pain during the latter. The ECG repeated after 17 days still showed T wave inversion (Figure 5(d)). A control echocardiogram showed complete resolution of the regional wall motion abnormalities. TC was confirmed.