Tako-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.
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 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 steady-state free precession gradient echo and delayed Gadolinium-DOTA-contrast-enhanced sequences exhibited akinesis of the apex with hyperkinesis of the base without an area of 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, β-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.
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 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 gadolinium-chelate, 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 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).
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