Takotsubo Cardiomyopathy as a Sequela of Elective Direct-Current Cardioversion for Atrial Fibrillation

Takotsubo cardiomyopathy (TC) is characterized by the clinical appearance of an acute myocardial infarction and by left ventricular (LV) apical ballooning in a patient who has no obstructive coronary artery disease.¹ Patients typically present after a precipitating physical or emotional stressor. However, the mechanism by which these stimuli lead to cardiac decompensation is unclear—proposed factors include catecholamine excess and coronary vasospasm.² We present the case of a patient whose TC was precipitated by elective direct-current (DC) cardioversion for atrial fibrillation.

Case Report

In January 2012, a 67-year-old woman was admitted to our hospital after a syncopal episode. She had been cooking breakfast and was able to catch herself before falling. During the event, her shirt caught on fire, but she was not burned. She reported no palpitations or chest pain; however, she had experienced dizziness and diaphoresis minutes after the event.

The patient's medical history included paroxysmal atrial fibrillation and hypertension, treated with spironolactone and metoprolol succinate. Two years before the patient's current presentation, a computed tomographic angiogram had revealed normal coronary arteries. Her metoprolol succinate dose had recently been increased from 12.5 mg/d to 50 mg/d, and her warfarin therapy had recently been discontinued because of hematuria in the presence of a supratherapeutic international normalized ratio.

Upon the patient's presentation, examination revealed an irregular pulse of 126 beats/min and a blood pressure of 106/72 mmHg. An electrocardiogram showed atrial fibrillation and low voltage (Fig. 1A). Laboratory values, including cardiac troponin I levels, were within normal limits. Echocardiograms showed normal LV function, normal wall motion, and a mildly dilated left atrium.

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The decision was made to establish sinus rhythm by means of DC cardioversion. The patient was sedated with propofol, and electrical cardioversion via biphasic energy at 200 J was performed, with a resultant rhythm of sinus bradycardia at 30 beats/min. After cardioversion, the patient was hypotensive and lethargic, despite the correction of the bradycardia with atropine and epinephrine. She was intubated for respiratory protection and was given norepinephrine, vasopressin, and dobutamine for hemodynamic support.

Serial electrocardiograms revealed sinus rhythm with low voltage, diffuse T-wave inversions, and a prolonged QT interval (Fig. 1B). Echocardiograms revealed an LV ejection fraction of less than 0.15. Contraction in only the basal segments of the LV and akinesis in the remaining segments resulted in a ballooning appearance (Fig. 2). The patient's troponin I level peaked at 3.39 ng/mL the next day. Swan-Ganz catheter readings revealed a cardiac index of 1.3 L/min via the thermo-dilution method. The patient's central mixed venous saturation was 45%. The diagnosis was TC with clinical cardiogenic shock.

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The patient underwent hemodynamic support and intravenous diuresis for several days. Six days after the cardioversion, she sustained one minute of monomorphic ventricular tachycardia with associated hypotension, and electrical cardioversion was performed to re-establish sinus rhythm. By hospital day 9, she no longer needed hemodynamic support and was extubated. Her rhythm returned to atrial fibrillation with rapid ventricular response, with intermittent periods of relative bradycardia and associated pauses (the longest, 3 sec). On day 11, a single-lead permanent pacemaker was implanted, and the patient's cardiac rhythm remained atrial fibrillation. An echocardiogram on that day showed improvement in LV systolic function (ejection fraction, 0.35–0.40). Warfarin and β-blocker therapy was resumed before her discharge from the hospital on day 17. An echocardiogram 2 weeks later showed normal LV function and wall motion (Fig. 3). She was doing well and had returned to her baseline functional status.

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Discussion

Our patient's clinical presentation of sudden LV failure and cardiogenic shock, along with characteristic echocardiographic findings and her subsequent complete recovery, support the diagnosis of TC. Although patients with this clinical course often undergo cardiac catheterization for the evaluation of coronary artery disease, coronary angiograms were not obtained in this patient, in view of the normal evaluation 2 years earlier and the clinical findings.

Takotsubo cardiomyopathy has occurred after numerous precipitating events,¹ including DC cardioversion.^3,4 However, this case differs from previous reports (in which the patients presented with symptoms 10–24 hr after the procedure) in that our patient immediately experienced LV dysfunction and cardiogenic shock—which suggests a more direct pathophysiologic link between electrical cardioversion and TC.

The relevant medical literature provides some insight into how cardioversion might lead to the TC clinical complex. Although the precipitating events vary widely, there is often an association between TC and an elevated catecholamine level.^1,2,5,6 Intense psycho-emotional precipitants that have been associated with TC presumably induce a catecholamine surge. However, the mechanism by which catecholamine excess leads to TC is poorly defined. Results of animal studies suggest that high levels of serum epinephrine directly signal myocardial depression, with an apical preference because of a natural gradient of myocardial catecholamine receptors from base to apex.⁶ Other postulated mechanisms include coronary vasospasm, which has been documented in several cases of TC,^7–9 as well as the effect of myocardial bridging.¹⁰ It is unknown whether these mechanisms are the end result of catecholamine excess or are independent causes. Perhaps TC is a heterogeneous disorder with several plausible mechanisms, or perhaps it is the result of several precipitants interacting closely.

In our patient, catecholamine stimulation during cardioversion might have played a role in the development of TC and cardiogenic shock; however, the cardioversion itself also might have had an effect. Takotsubo cardiomyopathy has been reported consequent to various forms of electrical stimulation: electrical cardioversion,^3,4 electroconvulsive therapy,^11,12 and electrocution caused by lightning strike.¹³ To our knowledge, no one has investigated whether electri cal stimulation has a direct role in the development of the cardiomyopathy, or whether the cardiomyopathy is merely the result of catecholamine overload.

Although TC is usually self-limited, this case illustrates additional sequelae that can arise in the disease. In general, the sequelae are similar to those in myocardial infarction. Our patient had a fairly rapid and complete recovery, which is also typical of most TC cases. Whereas early reactions can lead to early death, long-term mortality rates tend to be low and appear to be unrelated to LV dysfunction at its most severe.^14,15 It is important to remember that TC can recur years later, although this is unusual.^16,17

This is not the first report of TC precipitated by DC cardioversion; however, it differs from previous reports in that the procedure was immediately followed by a clinical TC syndrome. This does not rule out other causes of TC, particularly medications that were administered during the procedure; however, a growing body of evidence indicates that electrical stimulation and catecholaminergic stimulus contribute to the pathogenesis of this disorder. Our patient experienced severe sequelae (including LV failure, cardiogenic shock, and ventricular tachycardia) and made a complete recovery, both clinically and echocardiographically. This case underscores the need for further investigation of the effect of myocardial electrical stimulation on the development of TC.