Neurology India Medknow Publications on behalf of the Neurological Society of India ISSN: 0028-3886 EISSN: 1998-4022 Vol. 59, Num. 2, 2011, pp. 304-306

Neurology India, Vol. 59, No. 2, March-April, 2011, pp. 304-306

Letter to Editor

Cardiac dysfuntion after acute subarachnoid hemorrhage: Neurogenic stress cardiomyopathy or takotsubo cardiomyopathy

Shiv Bagga¹, Yash Paul Sharma¹, Meenu Jain²

¹ Department of Cardiology, Post Graduate Institute of Medical Education & Research, Chandigarh, India
² Department of Obstetrics and Gynaecology, Government Medical College & Hospital, Chandigarh, India

Correspondence Address: Shiv Bagga, Department of Cardiology, Post Graduate Institute of Medical Education & Research, Chandigarh, India, shivbagga@gmail.com

Date of Submission: 26-Dec-2010
Date of Decision: 26-Dec-2010
Date of Acceptance: 28-Dec-2010

Code Number: ni11086

PMID: 21483145

DOI: 10.4103/0028-3886.79161

Sir,

Takotsubo cardiomyopathy (TC) is a novel cardiomyopathy associated with transient left ventricular (LV) dysfunction consisting of akinesia predominately of the apex and midventricle with relative sparing of the basal segment, creating a highly characteristic configuration during systole. ^[1] We present a patient with subarachnoid hemorrhage (SAH) complicated by TC and discuss the clinical implications associated with this condition.

A 65-year-old woman with postmenopausal bleeding was referred to the Emergency Department with complaints of mild chest discomfort and headache. There was no history of trauma, and medical history, including cardiovascular risk factors, was unrevealing. An electrocardiogram (ECG) done as part of routine evaluation showed a normal sinus rhythm with ST segment elevation in leads V2 to V5 along with ST depression in inferior leads II, III and aVF [Figure - 1]. Her qualitative troponin was positive and CK-MB levels were raised. Based on these ECG changes and positive cardiac troponin levels, a diagnosis of acute myocardial infarction was made. The patient underwent emergency coronary angiography, which demonstrated normal coronaries. However, contrast left ventriculography demonstrated marked akinesis of the mid- and distal segments of all walls, with compensatory hyperkinesis of the base [Figure - 2]. Transthoracic echocardiography revealed left ventricular wall abnormality, characteristic of TC [Figure - 3]. However, in view of persistent headache, computed tomogram (CT) of brain was done, which revealed subarachnoid hemorrhage. CT angiography revealed ruptured aneurysm of the left posterior communicating artery (PCOM). The patient underwent successful clipping of PCOM aneurysm. The patient was discharged on beta-blocker therapy. Repeat echocardiography 1 month later demonstrated a complete resolution of the regional LV dysfunction.

Reversible cardiac dysfunction is a well-documented complication of SAH. Approximately, 20-30% of patients with SAH manifest a secondary cardiomyopathy and/or regional wall motion abnormality, referred to as neurocardiogenic stunning and "neurogenic stress cardiomyopathy" (NSC). ^[2] The most common wall motion abnormality in NSC is either hypokinesis of the basal and midventricular segments with sparing of the apex or global LV hypokinesis. Most series on TC cardiomyopathy specifically excluded patients with SAH, and the proposed diagnostic criteria for apical ballooning syndrome require the exclusion of head trauma and intracranial bleeding. ^[3] However, in a recent report of consecutive patients with NSC, a third of patients had isolated apical and midventricular LV hypokinesis with sparing of the basal segments, consistent with TC. ^[4] Ako et al. were the first to recognize that TC had similarities with the cardiac dysfunction seen in SAH and proposed a state of massive endogenous catecholamine release as the hypothetical shared mechanism of both conditions. ^[5]

SAH-associated TC as in our case is rarely described in the literature. ^[6],[7],[8] Although TC carries a favorable prognosis, ^[1] this pattern of cardiac dysfunction in a population with SAH is associated with pulmonary edema, prolonged intubation, and cerebral vasospasm which may have implications in managing SAH. ^[4] On the other hand, cardiologists should always consider TC in the differential diagnosis of ECG changes and elevated cardiac biomarkers in patients with SAH. An early echocardiographic evaluation should be considered in all patients with SAH for the appropriate risk stratification and further management.

References

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