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Table of Contents    
Year : 2011  |  Volume : 59  |  Issue : 2  |  Page : 304-306

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

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

Date of Submission26-Dec-2010
Date of Decision26-Dec-2010
Date of Acceptance28-Dec-2010
Date of Web Publication7-Apr-2011

Correspondence Address:
Shiv Bagga
Department of Cardiology, Post Graduate Institute of Medical Education & Research, Chandigarh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.79161

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How to cite this article:
Bagga S, Sharma YP, Jain M. Cardiac dysfuntion after acute subarachnoid hemorrhage: Neurogenic stress cardiomyopathy or takotsubo cardiomyopathy. Neurol India 2011;59:304-6

How to cite this URL:
Bagga S, Sharma YP, Jain M. Cardiac dysfuntion after acute subarachnoid hemorrhage: Neurogenic stress cardiomyopathy or takotsubo cardiomyopathy. Neurol India [serial online] 2011 [cited 2020 Feb 27];59:304-6. Available from:


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.
Figure 1: Twelve-lead ECG. Sinus rhythm with 1- to 2-mm ST elevation in leads V2 through V5 with ST depression and T-wave inversion in inferior leads

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Figure 2: Contrast left ventriculogram. (a) End-diastolic and (b) end-systolic frames illustrating marked akinesis of the mid- and distal segments of all LV walls, with compensatory hyperkinesis of the base

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Figure 3: Transthoracic echocardiography showing typical apical ballooning during systole

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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 Top

1.Pernicova I, Garg S, Bourantas CV, Alamgir F, Hoye A. Takotsubo cardiomyopathy: A review of literature. Angiology 2010;61:166-73.  Back to cited text no. 1
2.Banki N, Kopelnik A, Tung P, Lawton MT, Gress D, Drew B, et al. Prospective analysis of prevalence, distribution, and rate of recovery of left ventricular systolic dysfunction in patients with subarachnoid hemorrhage. J Neurosurg 2006;105:15-20.  Back to cited text no. 2
3.Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med 2004;141:858-65.  Back to cited text no. 3
4.Lee VH, Connolly HM, Fulgham JR, Manno EM, Brown RD, Wijdicks EF. Tako-tsubo cardiomyopathy in aneurysmal subarachnoid hemorrhage: An underappreciated ventricular dysfunction. J Neurosurg 2006; 105:264-70.  Back to cited text no. 4
5.Ako J, Sudhir K, Farouque HM, Honda Y, Fitzgerald PJ. Transient left ventricular dysfunction under severe stress: brain-heart relationship revisited. Am J Med 2006;119:10-7.  Back to cited text no. 5
6.Hakeem A, Marks AD, Bhatti S, Chang SM. When the worst headache becomes the worst heartache! Stroke 2007;38:3292-5.  Back to cited text no. 6
7.Konrad FM, Unertl KE, Schroeder TH. Takotsubo cardiomyopathy after cerebral aneurysm rupture. J Neurosurg Anesthesiol 2010;22:181-2.  Back to cited text no. 7
8.Das M, Gonsalves S, Saha A, Ross S, Williams G. Acute subarachnoid haemorrhage as a precipitant for takotsubo cardiomyopathy: a case report and discussion. Int J Cardiol 2009;132:283-5.  Back to cited text no. 8


  [Figure 1], [Figure 2], [Figure 3]

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