Transient left ventricular apical ballooning in a patient with cardiac arrest after subarachnoid hemorrhage

Summary

Subarachnoid hemorrhage (SAH) often accompanies cardiac abnormalities. Sudden cardiac arrest is also known to occur after SAH. A 32-year-old woman was admitted to our hospital because of cardiac arrest immediately after the onset of SAH. Return of spontaneous circulation was obtained by conventional advanced cardiovascular life support. After resuscitation, her echocardiogram showed left ventricular apical ballooning, which improved within 7 days. This is the first report presenting both sudden cardiac arrest and transient left ventricular apical ballooning after SAH.

Introduction

Spontaneous subarachnoid hemorrhage (SAH) often accompanies electrocardiographic and/or echocardiographic abnormalities [1]. These cardiac findings are more likely to occur with increasing neurological deficits [1]. On the other hand, cardiac arrest is also known to occur after SAH [2], [3]. About 4% of patients with SAH experience cardiac arrest immediately after the onset [2]. However, the mechanism of cardiac arrest after SAH remains uncertain. One hypothesis is that SAH leads to cardiac arrest directly. The other hypothesis is that myocardial damage is elicited by SAH, and then leads to cardiac arrest. Here, we describe a woman with cardiac arrest after SAH, who presented with transient left ventricular apical ballooning, so-called Takotsubo cardiomyopathy, after resuscitation.

Case report

A 32-year-old woman, without any history of cardiovascular disease, was transferred to our emergency department because of cardiac arrest. Her initial cardiac rhythm, recorded by emergency medical service, showed pulseless electrical activity. Twenty minutes before arrival, she suddenly collapsed with a moan in her house, and her friend started cardiopulmonary resuscitation. Although return of spontaneous circulation (ROSC) was obtained following a 1 mg epinephrine bolus at the emergency department, she was still unconscious with anisocoria. A computed tomography of her head showed extensive SAH (Fig. 1A), and the severity of her clinical presentation was grade 5, as quantified by the World Federation of Neurological Surgeons guidelines. Her 12-lead electrocardiogram after ROSC showed sinus tachycardia with mild ST-segment depression on II, III, aVF, V3, V4, and V5 and ST-segment elevation in aVL (Fig. 2). Akinesis of the left ventricular apex and mid segments with normal contraction of basal segments was found on echocardiography, and the ejection fraction measured by modified Simpson's method was 19% (Fig. 1B and C). These left ventricular wall motion abnormalities resembled Takotsubo cardiomyopathy and could not be explained by a single epicardial coronary artery obstruction. Her chest X-ray showed bilateral pulmonary edema, and creatine kinase on admission was 71 IU/l (normal range <163 IU/l). Serial electrocardiographic and echocardiographic examinations were performed. Although poor R-wave progression in the precordial leads, ST-segment elevation, and T-wave inversion with QT prolongation (corrected QT interval 480 ms) were found without creatine kinase elevation on day 3, all electrocardiographic abnormalities normalized on day 9 (Fig. 2). Takotsubo-like wall motion abnormalities improved with disappearance of pulmonary edema on day 7. However, she died of brain death on day 10.

Figure 1.

Computed tomography (A), and echocardiogram of end systole (B) and end diastole (C) of the presented patient. Extensive subarachnoid hemorrhage with bilateral intraventricular hemorrhage was observed on computed tomography (A). Akinesis of the left ventricular apex and mid segments (white arrows) was found on the apical 4-chamber view after resuscitation. LV, left ventricle.

Figure 2.

Electrocardiograms of the presented patient. After resuscitation (day 0), sinus tachycardia with mild ST-segment depression on II, III, aVF, V3, V4, and V5 and ST-segment elevation in aVL were observed. On day 3, poor R-wave progression in the precordial leads, ST-segment elevation, and mild T-wave inversion with QT prolongation (corrected QT interval 480 ms) were found. All electrocardiographic abnormalities normalized on day 9.

Discussion

In this case report, we describe a patient with cardiac arrest after SAH showing transient left ventricular apical ballooning, or so-called Takotsubo cardiomyopathy. Several cardiac abnormalities, including cardiac arrest, were observed after the onset of SAH [1], [2], [3]. Electrocardiographic findings, such as ST-T elevation/depression, T-wave inversion, QT prolongation, and supraventricular/ventricular arrhythmias, were found in more than 50% of SAH patients [1]. Global or segmental left ventricular dysfunction was observed on left ventriculography and/or echocardiography [4]. These electrocardiographic and echocardiographic abnormalities were more likely to occur with increasing neurological deficits, and 58% and 52% of patients with severe neurological deficits had electrocardiographic and echocardiographic abnormalities, respectively [1]. However, echocardiographic abnormalities do not always accompany electrocardiographic ones [1]. In recent reports, Takotsubo-like wall motion abnormalities were observed after SAH [5], [6]. These cardiac findings were a transient phenomenon and irrelevant to coronary artery disease [4]. Although the pathophysiology of these abnormalities remains uncertain, the catecholamine surge following brainstem damage has been considered to produce neurogenic myocardial stunning and electrocardiographic abnormalities [6], [7]. On the other hand, cardiac arrest is also known to occur after SAH [8]. SAH is found to be present in 4–10% of all out-of-hospital cardiac arrests, and about 4% of SAH patients experience cardiac arrest after the onset [2], [3], [9]. Direct catecholamine cardiotoxicity, same as left cardiac dysfunction after SAH, has been considered one of the mechanisms leading to cardiac arrest, while respiratory suppression by a sudden increase in intracranial pressure with brainstem herniation may also lead to cardiac arrest in some patients [2], [6]. However, the association between cardiac involvement and cardiac arrest on SAH has been hardly discussed before. In the present case, we demonstrated transient left ventricular apical ballooning with SAH after cardiac arrest. Although coronary angiography was not performed, cardiac dysfunction in this patient was considered to be irrelevant to coronary artery disease because she had no risk factors of coronary artery disease and her wall motion abnormalities seemed to extend beyond the single epicardial coronary territory. Transient left ventricular dysfunction after ROSC has also been found as post cardiac arrest myocardial dysfunction [10]. In this setting, global left ventricular dysfunction and improvement in less than 24 h were usually observed [10]. However, segmental Takotsubo-like myocardial dysfunction, which improved 7 days later, was found in this patient. Thus, transient left ventricular dysfunction in this patient could be associated with SAH onset, not post cardiac arrest myocardial dysfunction. Given these observations, excessive catecholamine release after the onset of SAH might have led not only to myocardial dysfunction, but also to cardiac arrest in this patient. There was one more implication of this case. Cardiac arrest in SAH patients often mimics acute coronary syndrome as in our patient [8]. Thus, clinicians should carefully monitor the existence of SAH in cardiac arrest because the therapy for acute coronary syndrome, such as antiplatelet and anticoagulation drugs, is completely different from that for SAH.

Conclusion

In this case report, we describe a patient with cardiac arrest immediately after the onset of SAH, who presented with transient left ventricular apical ballooning (Takotsubo cardiomyopathy). Myocardial damage due to SAH might have played a role in cardiac arrest of this patient.