Abstract SNACC-58

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A 23-year old woman with variant neurogenic stunned myocardium

Mahanna E, Bihorac A
University of Florida, Gainesville, FL, USA

Transient left ventricular dysfunction occurring following subarachnoid hemorrhage (SAH) is a well-documented phenomenon. Traditionally, it is characterized by transient, dyskinesis of the LV apex in a distribution of myocardium covered by more than one coronary artery.
We report a 23-year-old woman who presented within 24 hours of sudden onset of severe headache, left facial droop, and left extremity weakness. CT of the head showed a subarachnoid hemorrhage, right-sided temporoparietal hemorrhage and subfalcine herniation. A cerebral angiogram showed a complex AVM with an associated anterior choroidal aneurysm. She underwent angiogram with onyx embolization of the AVM and aneurysm. This was complicated by partial occlusion of her right MCA, rebreeding and a need for a decompressive craniotomy for intractable ICPs. She developed sudden pulmonary edema, respiratory failure and shock. An echocardiogram revealed left ventricular dysfunction with severe circumferential basal hypokinesis and hyperkinetic apical segments. The ejection fraction (EF) was 25-30%. The patient was diagnosed with variant NSM and supportive therapy was initiated with inotropes, diuresis, and airway pressure release ventilation.
Neurogenic stunned myocardium is an important complication of SAH, which may be under-recognized as both diagnosis and treatment persist to impose a challenge. In the neurosurgical ICU more than 70% of patients with SAH develop a cardiac abnormality. There are 66 cases of SAH-induced NSM reported in the literature. As a group, these patients with SAH-induced SCM are diverse but also have many common features. Like classical SCM, SAH-induced forms have a striking predominance in women (85%) with a mean age of 57 years. Among these, all but 6 showed changes on ECG and mildly elevated cardiac biomarkers. By recognizing that middle aged women with ECG changes and elevated cardiac biomarkers are “at risk” of NSM, early diagnosis of NSM can be made and any morbidity from delay in treating the SAH can be avoided.
Even among the small number of reported cases our patient seems to be an outlier. Her heart failure occurred following the initial embolization procedure when she developed further hemorrhage and elevated intracranial pressure. She represents 1 of 4 cases, which exhibited no changes on ECG; her diagnosis was made after evidence of pulmonary edema and subsequent echocardiogram. Neurogenic stunned myocardium was an unexpected diagnosis given her young age. Excluding the rare pediatric patient, there are less than 10 reported cases of women younger than 40 years old with SCM. Our patient is the only reported case of AVM associated NSM and the only woman in her 20s where SAH-induced NSM was present.
In conclusion, to aid in better recognition of NSM in the neurosurgical ICU we presented a unique case of a young woman with variant NSM precipitated by SAH from rupture of a complex AVM and associated aneurysm. Although rare, this case represents the variability in neurogenic stunned myocardium, which must be appreciated for proper and early diagnosis to avoid the morbidity and mortality associated with inappropriate interventions and delay in treatment of SAH.


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