Download Early Postoperative Tako-Tsubo-Like Left Ventricular Dysfunction

Case Report
Early Postoperative Tako-Tsubo-Like Left Ventricular
Dysfunction: Transient Left Ventricular Apical
Ballooning Syndrome
Claude Lentschener*
Olivier Vignaux†
Christian Spaulding‡
We diagnosed transient left ventricular apical wall motion abnormalities after
surgery in a patient presenting with a clinical and electrocardiographic picture of
acute myocardial infarction in the absence of significant coronary disease. These
angiographic, clinical, and electrocardiographic features satisfied the criteria of the
recently described tako-tsubo-like left ventricular dysfunction.
(Anesth Analg 2006;103:580 –2)
Philippe Bonnichon§
Paul Legmann†
Yves Ozier*
T
ako-tsubo-like left ventricular dysfunction is characterized by the acute onset of transient left ventricular apical wall motion abnormalities in patients presenting with a clinical and electrocardiographic (ECG)
picture of acute myocardial infarction in the absence
of significant coronary disease (1,2). This phenomenon
has recently been referred to as “transient left ventricular apical ballooning syndrome” (1,2). The term
“tako-tsubo” was initially used because the morphological feature of early left end-systolic ventriculogram reveals a balloon-shaped, short-necked, round
flask resembling a tako-tsubo, a device used to trap
octopuses in Japan (3). We now describe such a case,
diagnosed in the early postoperative period after an
uneventful thyroidectomy.
CASE REPORT
A 53-yr-old, 105-kg, 163-cm woman underwent uneventful elective total thyroidectomy. A multinodular goiter had
caused neck discomfort. Preoperative endocrinology assessment had shown euthyroidism. Hypertension had been
diagnosed 6 yr ago. Oral medications included bisoprolol,
spironolactone, and levothyrox. There was no history of
chest pain, functional limitation, or smoking habit. Physical
examination revealed an arterial blood pressure of 130/75
From the Departments of *Anesthesia and Critical Care, †Radiology, ‡Cardiology, §Surgery, Université Paris-Descartes, Faculté
de Médecine, Assistance Publique—Hôpitaux de Paris, Hôpital
Cochin, Paris, France.
Accepted for publication April 20, 2006.
Address correspondence and reprint requests to Claude
Lentschener, MD, Department of Anesthesia and Critical Care,
Hôpital Cochin, 27 rue du Faubourg Saint Jacques, 75679 Paris
Cedex 14, France. Address e-mail to claude.lentschener@ cch.aphp.fr.
Copyright © 2006 International Anesthesia Research Society
DOI: 10.1213/01.ane.0000226091.19987.c6
580
mm Hg, a heart rate of 55 bpm, clear lungs, and normal heart
sounds. Preoperative laboratory tests were within normal
ranges. The ECG and the chest radiograph were unremarkable. Surgery was conducted under standard general anesthesia and proceeded uneventfully. Toward the end of the
procedure, 2 g of propacetamol and 20 mg of nefopam were
administered IV. No additional drugs, including analgesics
or antiemetics, were required in the postanesthesia care unit.
Two hours after the end of surgery, the patient was transferred to the ward. Systematic oral propacetamol and subcutaneous morphine, as required, were prescribed for postoperative analgesia.
On the 16th postoperative hour, the patient experienced a
midline, constrictive, mild chest pain radiating to the back.
ECG revealed T-wave inversion in I, II, VL, VF, V2, V3, V4,
V5, and V6 leads (Fig. 1). On physical examination, the
patient seemed well. Her heart and lungs showed no abnormalities. Her arterial blood pressure was 120/70 mm Hg,
and her heart rate was 65 bpm. A complete blood count and
measurements of serum electrolytes (including calcium),
urea nitrogen, creatinine, and arterial oxygen saturation
were within normal ranges. Her troponin I level was
0.23 ng/mL (normal, ⬍0.01 ng/mL). A chest radiograph
showed no acute cardiopulmonary disease, no infiltrates,
and normal tissue density. Echocardiography showed hypokinesis of the left ventricular apex. The left ventricular
ejection fraction was 40%. A presumptive diagnosis of acute
anterior wall myocardial infarction was made. Urgent coronary angiography was performed. The angiography revealed no evidence of coronary artery stenosis (Fig. 2). A
coronary spasm provocation test by intracoronary infusion
of methylergometrine (Methergin, Novartis Pharma Laboratory, Rueil Malmaison, France) did not induce coronary
spasm. Contrast left ventriculography demonstrated
marked akinesis of the mid and distal segments of all walls
(Fig. 3). Cardiac magnetic resonance imaging (CMR) (Echospeed Excite 1.5 T, GEMS, Milwaukee, WI) was performed 3
days after the onset of the symptoms. Functional steadystate free precession gradient echo and delayed GadoliniumDOTA-contrast-enhanced sequences exhibited akinesis of
the apex with hyperkinesis of the base without an area of
Vol. 103, No. 3, September 2006
Figure 1. Twelve-lead electrocardiogram (ECG) obtained 6
hours after the onset of chest pain. Sinus rhythm with
T-wave inversion in leads I, II, VL, VF, V2, V3, V4, V5, and
V6.
hyper-enhancement, consistent with stunned viable myocardium (Fig. 4) (4,5). These CMR, angiographic, clinical, and
ECG features satisfied the criteria of the recently described
tako-tsubo-like left ventricular dysfunction (1,2). Treatment
included aspirin, ␤-adrenergic blockade, and an
angiotensin-converting enzyme inhibitor. Twenty-four
hours later, there was complete resolution of the chest pain,
and the troponin I level was within the normal range. The
patient remained clinically and hemodynamically stable
during her 4-day hospitalization in the cardiology unit.
T-wave inversion normalized progressively in 10 days. At
follow-up 4 weeks later, she was clinically stable with no
recurrence of chest pain, and repeat echocardiography demonstrated complete resolution of the regional systolic dysfunction.
DISCUSSION
Several case reports and review articles have described the features of tako-tsubo-like left ventricular
dysfunction (1–3,6 – 8). Acute myocardial infarction
was initially suspected in most patients (1–3). Transient left-ventricular apical ballooning syndrome is
Figure 2. On coronary angiography (A, right coronary artery;
B, left coronary artery), no coronary artery stenosis was seen.
Figure 3. End-diastolic (A) and end-systolic (B) left ventriculogram showed extensive akinesia of the apical and mid
portions of the left ventricle.
Vol. 103, No. 3, September 2006
Figure 4. Cardiac magnetic resonance (CMR) imaging assessment of myocardial viability three days after the onset of
pain. (A) Four-chamber-view steady-state free precession
gradient echo acquisition (systolic phase) showing balloonshaped apical hypokinesis with relative sparing of the base
of the heart (arrow). (B) Four-chamber-view inversionrecovery gradient echo acquisition 10 min after injection of
gadolinium showing that the akinetic regions seen on ventriculography are dark (no delayed enhancement), consistent with viable myocardium without necrosis.
diagnosed in 0.2%–2.6% of patients admitted to intensive care units with the diagnosis of acute myocardial
ischemia (1,2). Most affected patients are between 62
and 74 years, with a preponderance of women
(1–3,6 – 8). Patients experienced stressful incidents immediately preceding the onset of symptoms and,
anecdotically, during a recent noncardiac surgical
procedure (1–3,6 – 8). ECG findings in the acute phase
revealed ST segment increase or T-wave inversion in
V2-V5 leads and often simultaneously at the inferior
and posterior leads (1–3,6 – 8). Troponin I and troponin
T were positive in all patients assessed (1–3,6 – 8).
However, troponin levels were lower than expected
relative to the degree of left ventricular dysfunction
(1–3,6 – 8). Patients had a decreased left ventricular
ejection fraction (1–3,6 – 8). In the acute phase, the
ventriculogram showed transient left ventricular apical ballooning with apical akinesis and basal hyperkinesis (1–3,6 – 8). Endomyocardial biopsy was performed in a few cases and showed interstitial
inflammatory lymphocytic infiltrates and foci of contraction bands (1,2). Transient life-threatening complications were occasionally reported, including pulmonary edema, cardiogenic shock, paroxysmal atrial
fibrillation, ventricular fibrillation, and left ventricular
thrombosis associated with stroke (1,2). The patient’s
initial prognosis was generally good after appropriate
treatment of acute phase complications (1,2). Late
adverse outcomes have been anecdotically reported
(1,2). After the IV administration of a gadoliniumchelate, delayed enhancement on CMR allows accurate identification of akinetic myocardial segments
without delayed hyper-enhancement that is believed
to be related to reversibly stunned myocardium, as in
the present case (4,5).
Other causes of postoperative left ventricular dysfunction and T-wave inversion are not likely to account for the postoperative left ventricular dysfunction diagnosed in our patient (9 –11). Hypocalcemia
© 2006 International Anesthesia Research Society
581
related to intraoperative parathyroid ischemia or removal, potassium imbalance, and postoperative anemia were excluded by laboratory assessment (10).
Unrelated pericarditis or myocarditis or myocardial
dysfunction resulting from myocardial stunning were
not suggested by the clinical features and were excluded by echocardiography and CMR (4,5,10,11).
Euthyroidism was preoperatively assessed in this patient, thus excluding hyperthyroidism anecdotically
reported as a possible cause of this syndrome (8).
There is still debate concerning the pathophysiology
of this syndrome (1,2,6,12). Coronary spasm cannot
explain the syndrome because pharmacological coronary vasospasm tests induced coronary spasm in only a
few reported patients (1,2,6). Contrast-enhanced echocardiography strongly suggests intact microcirculation
(2,6). Myocardial biopsy has failed to demonstrate specific histopathological alteration (1,2,6). Repeated rest
tomographic myocardial imaging and CMR did not
show features of myocyte injury (1,2,4 – 6). Sympathetic
activity was suggested to play a major role in the
pathophysiology of this syndrome (1,2,6,12). However,
catecholamine levels were found to be normal or only
slightly increased in patients with apical ballooning (6).
Changes in T-wave morphology have been reported to average 19% after anesthesia and noncardiac
surgery (9). Furthermore, left ventricular dysfunction
is a possible occurrence after noncardiac surgery (9).
Whether tako-tsubo-like left ventricular dysfunction
partly accounts for these postoperative events warrants further study (9).
582
Case Report
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