Dislocated spine, damaged heart: Takotsubo cardiomyopathy following acute cervical spine injury

INTRODUCTION

Takotsubo cardiomyopathy (TCM), also known as stress-induced cardiomyopathy or “broken heart syndrome,”^[1,2] was first described in 1991 by Dote et al.^[3] It is a form of reversible cardiomyopathy characterized by transient dysfunction of the left-ventricle (LV) classically consisting of apical and mid-ventricular hypokinesia with relative sparing of the basal segment.^[1,2] It may mimic an acute myocardial infarction.^[1] In neurological disease, it has been described following aneurysmal subarachnoid hemorrhage (SAH), strokes, traumatic brain injuries, and seizures.^[2]

CASE REPORT

A 65-year-old lady presented 12 h following a road traffic accident with complete loss of power and sensation in all four limbs with loss of sphincter function since the time of injury. At admission, she was conscious but hypotensive, had bradycardia, and breathing difficulty. Arterial blood gas showed acidosis and hypoxia, and she was intubated, ventilated, and started on ionotropes. A magnetic resonance imaging study showed fracture dislocation of C6 on C7 while a computed tomography scan of the brain showed no intracranial injury.

Electrocardiogram (ECG) showed bradycardia and T wave abnormalities. A two-dimensional echocardiogram showed akinetic apical anterior septum, LV apex, and apical anterior wall. Ballooning of the LV apex was seen [Figure 1 and Supplementary Video 1]. There was moderate LV systolic dysfunction with an ejection fraction of 40%. Doppler study at the level of the mitral valve showed the wave form of early diastolic filling (E wave) to be smaller than that caused by atrial contraction (A wave) [Figure 2].

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Figure 1:

Apical four-chamber view on echocardiogram showing right atrium (RA), right ventricle (RV), left atrium (LA), and left ventricle (LV). Apical akinetic ballooning of the left ventricle is shown by the red star.

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Figure 2:

Doppler at the level of mitral valve showing early diastolic filling wave (e) is less than the wave caused by late filling due to atrial contraction (a). In a normal patient, E will be greater than A.

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Quantitative troponin T levels were >800, and NTproBNP (N-terminal prohormone of brain natriuretic peptide) was 3480 pg/mL. Antiplatelets and low-molecular-weight heparin were started. A coronary angiogram revealed no evidence of any coronary artery disease. Supportive care was continued, and over the next few days, the hemodynamic and ventilatory parameters improved, and by the 6^th day, she was weaned off the ventilator, and ionotropes were stopped. A repeat echocardiogram at 10 days showed no regional wall motion abnormality, and EF improved to 60%. Following this, she underwent cervical spinal fixation [Figure 3].

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Figure 3:

Preoperative (a) X-rays (lateral view) showing C6 on C7 dislocation and (b) T2 sagittal magnetic resonance imaging showing disruption of the C6-C7 disc space with dislocation of C6 on C7. Intraoperative X-rays (c and d) showing reduction of dislocation and C6-C7 fixation with placement of polyaxial screws in the lateral mass in the superior vertebra and pedicle screws in the inferior vertebra.

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DISCUSSION

The term Takotsubo comes from a Japanese word for a fishing pot used to trap octopus as the ballooning of the LV apex resembles the former.^[1] Various theories have been put forward to explain the cause of the cardiac dysfunction including spasm of the epicardial coronary vessels, microvascular dysfunction in these arteries, and LV outlet obstruction.^[3,4] The currently accepted theory is the “catecholamine surge theory” where a stressful triggering event (mental or physical) causes excessive release of epinephrine and norepinephrine which causes cardiac myocyte injury.^[3]

While TCM following aneurysmal SAH is well described, we came across only 7 cases in the literature where this syndrome has been described in spinal pathologies.^[5-11] Of these, one was following a spinal arteriovenous malformation bleed, one occurred 3 days following lumbar spinal surgery, one occurred during positioning a patient for dorsal kyphoplasty, two occurred in patients with chronic spinal cord injury, and one each after surgery for a spinal nerve sheath tumor and a cervical epidural steroid injection. These are summarized in Table 1. There was no case report of such an event following an acute cervical spinal cord injury.

We speculate that there may be two reasons for the scarcity of reports of TCM following spinal injury – (a) hypotension is often attributed to the cord trauma and other causes are overlooked and (b) the decreased sympathetic outflow that occurs after high cervical injury might itself mitigate against the development of TCM.

In our patient, TCM causing hypotension occurred immediately after the spinal fracture dislocation. This is different from situations where hypotension is due to decreased sympathetic tone of the vasculature following spinal cord injury, which the literature describes as usually peaking around the 4^th day following injury.^[12] The mortality rate of TCM is said to be only 1.1%^[6] and it usually resolves completely over 3 weeks.^[13] Our patient too had a rapid improvement with supportive care. Awareness of this entity and the fact that the cardiac dysfunction is reversible with a very low mortality is important since the prognosis may not be as grim as the initial picture suggests.

While initially there was a doubt in this case as to whether TCM or an acute myocardial infarction was responsible for the hemodynamic instability, the classic appearance of the left ventricle and later rapid resolution of wall motion abnormalities on echocardiogram as well as lack of any demonstrable coronary vascular pathology on angiogram all pointed to a diagnosis of TCM. Further, our case fulfilled the revised Mayo criteria^[13] for the diagnosis of TCM as she had a precipitating physical stressor in the setting of trauma as a trigger, had regional wall motion abnormality, had only modest elevation of troponin levels in the setting of ECG changes, and had a normal coronary circulation. The other mimics of TCM can be rapidly ruled out by the classic picture of echocardiogram, cardiac enzyme studies, and the time frame over which hypotension develops.

CONCLUSION

In patients with complete spinal injuries following cervical spine trauma who present with hypotension, poor hemodynamic parameters, ECG changes, and low ejection fraction, a diagnosis of TCM must be kept in mind and best possible supportive care continued as the outcome may not be as bleak as it appears when the patient is initially evaluated.