Neurosurgery Department, University General Hospital of Alicante, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Alicante, Spain
Takotsubo cardiomyopathy, also known as transient apical ballooning syndrome, apical ballooning cardiomyopathy, stress-induced cardiomyopathy, Gebrochenes-Herz-Syndrom, is a type of non-ischemic cardiomyopathy in which there is a sudden temporary weakening of the myocardium.
Because this weakening can be triggered by emotional stress, such as the death of a loved one, a break-up, or constant anxiety, it is also known as broken-heart syndrome.
There are two major types of takotsubo cardiomyopathy: the classical type with left ventricular apical ballooning and a type with midventricular ballooning. Both types show different electrocardiographic patterns at presentation.
A sudden surgical pain stimulus combined with insufficient analgesia are hypothesized to probably cause a catecholamine surge in Takotsubo cardiomyopathy 1).
High circulating levels of catecholamines seem to cause catecholamine-induced microvascular spasms with subsequent myocardial dysfunction and stunning 2).
However, elevated blood catecholamine levels are not always present 3).
The clinical presentation is similar to that of an acute myocardial infarction.
Symptoms are acute substernal chest pain, dyspnea, syncope, shock, or electrocardiographic abnormalities. In contrast to these clinically impressive symptoms, further diagnostics cannot confirm a coronary syndrome with the signs of coronary occlusion and ischemic lesions. The onset of Takotsubo can be triggered by emotional stress or constant anxiety and unexpected catastrophic conditions 4) 5)
Clinicians should suspect takotsubo cardiomyopathy in patients with subarachnoid haemorrhage who have an ECG abnormality. Echocardiography is needed to detect the distinctive regional wall motion abnormality. 6).
Takotsubo is characterized by ST segment elevations especially in the anterior precordial leads, deep T wave inversions or abnormal Q waves 7).
Classical electrocardiographic findings of the acute and subacute phases of takotsubo cardiomyopathy are descibed by Bonnemeier 8).
Stress-induced cardiomyopathy may mimic myocardial infarction and is an important condition to recognize in patients with underlying stress states, particularly neurologic injuries 9).
There are no controlled data to define an optimal medical regimen, but it seems reasonable to treat these patients with standard medications for left ventricular systolic dysfunction. These include ACE inhibitors, β-blockers and diuretics to prevent volume overload. However, because the condition may recur, on-going adrenergic blockade with β-blockers is suggested. Consequently, Takotsubo is a transient disorder managed with the resolution of physical or emotional stress and supportive therapy. Due to the personal needs in case of elective neurosurgery and the possibility of neurogenic mechanisms in triggering of Takotsubo, surgical interventions and perioperative care should be realized under stress-free conditions as far as possible 10).
Neurosurgeons treating SAH must take into account the various general treatment strategy options on a case by case basis after prompt recognition 11).
Despite its severity in the acute phase, takotsubo cardiomyopathy is self-limiting and its management is conservative 12).
Treatment methods in Takotsubo cardiomyopathy that use extracorporeal circulatory support and medications that do not rely on β-receptor stimulation and preemptive blockade of β receptors or calcium channels before brain death may be relevant to donor care 13).
Stress cardiomyopathy is a well-recognized cause of acute heart failure, lethal ventricular arrhythmias, and ventricular rupture.
Patients who survive the acute episode typically recover to normal ventricular function within four weeks. The prognosis is determined by the acute complications of Takotsubo. Despite the severity of the acute illness, Takotsubo is a transient disorder manageable with supportive therapy 14).
In some the condition proves fatal. Seizure-associated takotsubo cardiomyopathy may cause sudden unexplained death in epilepsy (SUDEP), and EEG measurements should be carefully checked for seizure patients 15).
A case of a 53 year-old female with a spinal neurinoma and surgery-associated Takotsubo cardiomyopathy is demonstrated. The patient developed typical signs of a myocardial infarction with circulation depression and ST elevation, but normal cardiac enzymes at the end of surgery. Cardiac catheterization and levocardiography confirmed the absence of any critical coronary disease but the presence of a typical apical ballooning and midventricular hypokinesis. The patient recovered completely under supportive conservative and cardiological therapy, showing regular left ventricular pump function 16).
A 68-year-old woman was admitted for symptomatic seizure. She had a history of cerebral infarction in the right fronto-temporal lobes, and was medicated for the symptomatic seizure with valproic acid. Her electrocardiogram(EEG)showed ST-segment elevation in leads II, III, aVF, and V2-V6. Emergency coronary angiography showed normal coronary arteries, however, left ventriculography showed apical ballooning in the systolic phase. She had no chest pain or dyspnea, and takotsubo cardiomyopathy was diagnosed due to ECG abnormality 17).
A 67-year-old woman was admitted with aneurysmal subarachnoid haemorrhage and a 12-lead ECG showed ST segment elevation. Transthoracic echocardiography confirmed akinesis of the left ventricular mid-apical segment, with an ejection fraction of 26%, features characteristic of takotsubo cardiomyopathy. Five days later, we identified thrombus in the apex of the left ventricle. Sixteen days after onset, the thrombus had disappeared and wall motion improved (ejection fraction 58%) without evidence of cardioembolism 18).
A 90-year-old woman presented with aneurysmal subarachnoid hemorrhage (SAH) corresponding to Hunt and Hess grade II. Acute congestive heart failure and pulmonary edema developed following uneventful surgical clipping. Serial electrocardiography and echocardiography led to a diagnosis of neurogenic stress cardiomyopathy (NSC), also known as tako-tsubo cardiomyopathy. The outcome was favorable after supportive therapy with respiratory management and diuretic administration 19).
The first case of neurogenic stunned myocardium presenting with heart left ventricle noncompaction requiring intensive care in the perioperative period of tension tumor-induced hydrocephalus.
A 12-yr-old female with intracranial astrocytoma and hypertensive hydrocephalus presented with severe heart dysfunction and life-threatening ventricular ectopies intraoperatively. A severe heart failure developed requiring hemodynamic and ventilatory support for 10 days. Echocardiography showed a transient noncompaction aspect of the left ventricular wall, further confirmed by a cardiac magnetic resonance image. The noncompaction aspect lasted until 15 days postadmission, as was the case for the QT interval prolongation; no life-threatening ectopies were demonstrated on the subsequent Holter electrocardiogram monitoring.
This report describes a unique presentation of myocardial stunning in association with an intracranial illness, namely, a hypertensive hydrocephalus complicating an intracranial neoplasm 20).
A 65-year-old female with subarachnoid hemorrhage (SAH) developed takotsubo cardiomyopathy induced by dobutamine infusion for vasospasm 9 days after onset of SAH. She underwent neck clipping of the ruptured cerebral aneurysm on day 1. Course after surgery was uneventful, but she developed motor aphasia on day 9. Hypertensive therapy was carried out under the diagnosis of symptomatic vasospasm. Half an hour after initiation of dobutamine infusion at 6 microg/kg/min, sudden symptoms of takotsubo cardiomyopathy developed. Fortunately, her symptoms recovered in a few days with supportive therapy without any consequences. Takotsubo cardiomyopathy is one pattern of cardiac dysfunction occasionally encountered after SAH. Possible mechanisms of this disorder include epicardial catecholamine cardiotoxicity. Therefore, generally, cardiac function is worst at the early stage of SAH, when sympathetic activity is highest, and recovers thereafter. Dobutamine infusion seems to have triggered the takotsubo cardiomyopathy in the present patient even 9 days after onset of SAH. Inotropic agents including dobutamine are often used during the course of SAH, and since takotsubo cardiomyopathy can occur in patients with SAH, this complication must be considered21).
Gologorsky and Gologorsky present the case of a 43 year-old female that developed the signs of Taksotsubo intraoperatively during lumbar interbody fusion 22).
A 66-year-old woman presented with subarachnoid hemorrhage(SAH) caused by a ruptured aneurysm of the left middle cerebral artery. Electrocardiography (ECG) disclosed abnormalities resembling acute myocardial infarction. She underwent neck clipping of the aneurysm uneventfully. Sixteen days after admission, ECG again disclosed abnormalities resembling acute myocardial infarction, and echocardiography suggested heart failure. Coronary angiography showed no abnormalities, but left ventriculography showed severe hypokinesia in the apex of the heart consistent with so-called ampulla (takotsubo) cardiomyopathy. The heart failure was treated with catecholamines and her heart function gradually recovered. Ampulla (takotsubo) cardiomyopathy associated with SAH requires careful management of heart function 23).