Article, Cardiology

Takotsubo cardiomyopathy mid ventricle variant and cardiac arrest: chicken or the egg?

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American Journal of Emergency Medicine

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Takotsubo cardiomyopathy mid ventricle variant and cardiac arrest: chicken or the egg?

Abstract

Takotsubo cardiomyopathy is uncommon emergency con- dition usually precipitated by emotional or physical stress and is characterized by near-Normal coronary arteries and regional wall motion abnormalities that extend beyond a single coronary vascular territory. Variants of TTC include classic Apical ballooning syndrome and less commonly, mid, basal, and biventricular variants. Cardiac arrest is an uncommon complication of TTC. In the convalescence phase of TTC, prolonged QTc interval may cause cardiac arrest, but the reason for cardiac arrest in the acute phase when QTc interval is normal is unclear. We report 3 cases of mid ventricular TTC, with out- of-hospital cardiac arrest as the presenting feature. All 3 patients had normal QTc interval and were found to have normal coronary arteries on cardiac catheterization at presentation. Mid ventricular TTC was confirmed on contrast left ventriculography and echocardiography. Cardiac arrest myocarditis was ruled out by myocardial biopsy in 2 deceased patients and by cardiac magnetic resonance imaging in the one who survived.

Takotsubo cardiomyopathy (TTC) is a cardiac emergency usually precipitated by acute emotional or physical stress [1-3]. Takotsubo cardiomyopathy presents clinically similar to acute coronary syndrome but has regional wall motion abnormalities extending beyond a single coronary vascular territory with no coronary plaque. Takotsubo cardiomyopathy episodes are occasionally associated with cardiac arrest, shock-like state, ventricular fibrilla- tion, or Ventricular tachycardia [1]. Two well-known variants of the TTC involve the midsection or basal segment of the Left ventricle [4]. We reported 3 cases of out-of-hospital cardiac arrest (Table) that had LV appearance similar to mid ventricular variant of TTC.

A 47-year-old woman with no cardiac risk factors had cardiac arrest after visiting her sick partner in the hospital and was found in asystole. Cardiopulmonary resuscitation (CPR) was started, and after achieving spontaneous circulation, ST elevation was noted in the anterolateral leads of electrocardiogram (ECG). Patient needed intubation for low Glasgow Coma Scale and adrenaline infusion for low blood pressure. Coronary angiography showed healthy coronary arteries. Contrast left ventriculography revealed mid ventricle ballooning and akinesis. Resting hemody- namics was pulmonary wedge pressure 28 mm Hg and mean arterial pressure 50 mm Hg. An intraaortic balloon pump was inserted via the left femoral artery, and active cooling was started in intensive care unit. Serial cardiac biomarkers showed increased troponin T (peak value, 555 ng/L). Electrocardiogram showed global T-wave inversion and QTc interval prolongation (baseline, 463 milliseconds; 48 hours after the cardiac arrest, 567

milliseconds). The patient did not make Neurologic recovery and was declared brain dead (hypoxic brain injury) 96 hours after the admission. Cardiac biopsy excluded infiltrative cardiac condition or myocarditis.

A 71-year-old woman found unconscious at home was noted in asystole. Spontaneous circulation was achieved after 18 minutes of CPR and 1-mg adrenaline, but patient did not regain consciousness. She was intubated and transferred to the hospital on an adrenaline infusion. Electrocardiogram showed sinus tachycardia with anterolateral T-wave inversion. transthoracic echocardiogram showed apical hypokinesis and left ventriculo- graphy confirmed mid ventricular dilatation and akinesis (Figs. 1 and 2). Coronary angiography revealed healthy coronary arteries. Pulmonary capillary wedge pressure was 17 mm Hg, and mean pulmonary artery pressure, 28 mm Hg. An intraaortic balloon pump was inserted because of refractory hypotension, and active cooling was started. Gradual rise in troponin T was noted during subsequent days (peak, 524 ng/L). A computed tomography of brain performed for low Glasgow Coma Scale showed extensive subarachnoid hemorrhage with associated intraventricular exten- sion and 5 x 5 mm right anterior cerebral artery aneurysm. Conservative management was decided by neurosurgeons, but patient died after 5 days.

A 41-year-old woman collapsed while changing curtains. She was in ventricular fibrillation on ambulance arrival, revived with 4 shocks of 200 J and 3 mg adrenaline, intubated, and brought to the emergency department. Electrocardiogram showed sinus rhythm and anterior leads ST depression; coronary angiogram showed normal coronary

Table

Patient’s summary

Patients

Patient 1

Patient 2

Patient 3

Age (y)

47

73

41

Sex

Female

Female

Female

Cardiac arrest

Asystole

Asystole

Ventricular fibrillation

Variant of TTC

Mid ventricle

Mid ventricle

Mid ventricle

Brain natriuretic peptide

1293

13821

3635

Ejection fraction

45%

40%

57%

Troponin T

555

524

2129

Creatine kinase

100

200

5095

Coronary findings

Normal

Normal

Normal

Metanephrine

230

5610

6340

Normetanephrine

370

3730

2720

Right ventricular

involvement

None

None

None

QTc at presentation

463

495

448

Longest QTc

567

503

538

Time for QTc prolongation

N 48 h

N48 h

N 48 h

0735-6757/$ – see front matter (C) 2013

Fig. 1. Left ventricle during systole.

arteries and severe mid LV hypokinesis consistent with mid ventric- ular variant; while computed tomography head/spine and blood tests were normal. She received therapeutic cooling and was extubated 24 hours later with full neurologic recovery. Following Cardiac magnetic resonance imaging showed resolving TTC and 57% ejection fraction with no right ventricular dysplasia. She had an implantable cardiac defibrillator insertion and started on bisoprolol 2.5 mg and perindopril 5 mg daily before discharge. Echocardiogram performed at 10 days and 3 months showed complete resolution of the hypokinesis with normal ejection fraction.

Takotsubo cardiomyopathy is neither rare nor benign as thought once. Hospital mortality varies between 2% and 2.5% [1,2] with sudden cardiac death being the major cause [5]. malignant ventricular arrhythmias are noted in few with presentation mode in one-third of cases [5]. Although the cardiac arrest in TTC has been reported, the cause is unknown [6]. Prolonged QTc may be possibly linked with

Fig. 2. Left ventricle during diastole.

cardiac arrest in TTC. Madias et al [7] reported 8 TTC patients with cardiac arrest with prolonged QTc interval in 6 who developed arrest after few days. A hypothetical possibility of prolonged QTc interval predisposing TTC patients to cardiac arrest during conva- lescence phase can be made.

Malignant ventricular arrhythmias are common in TTC. In sudden cardiac death, it is possible that the ventricular dysfunction occurs secondary to CPR and sympathomimetic drugs, with an otherwise unrecognized cause. Ventricular ar- rhythmia may be catecholamenergic induced VT or a variant of catecholaminergic polymorphic VT (CPVT), which have been associated with exertion or emotional stress [8-10]. Protective effect of ?-blockers has been reported in atrial and ventricular arrhythmias in TTC [11]. Thus, high baseline adrenaline level may be risk factor for cardiac arrest in TTC. Two of our patients had high metanephrine with an obvious source of metanephrine excess, subarachnoid hemorrhage in one and venlafaxine use in other. High catecholamine can induce VT like CPVT, but whether presence of underlying TTC brings the CPVT threshold lower is unclear and requires further studies.

Kuljit Singh MD Department of Cardiology The Queen Elizabeth Hospital

Woodville West SA 5011, Australia E-mail address: [email protected]

Ajay K. Parsaik MD Department of Neurology and Department of Health Sciences Research Mayo Clinic, Rochester, MN 55905, USA

Christopher J. Zeitz MD, PhD, FRACP

Department of Cardiology The Queen Elizabeth Hospital Woodville West SA 5011, Australia

http://dx.doi.org/10.1016/j.ajem.2012.12.037

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