Abstract

Neurologic stunned myocardium (NSM) is a phenomenon where neurologic events give rise to cardiac abnormalities. Neurologic events like stroke and seizures cause sympathetic storm and autonomic dysregulation that result in myocardial injury. The clinical presentation can involve troponin elevation, left ventricular dysfunction, and ECG changes. These findings are similar to Takotsubo cardiomyopathy and acute coronary syndrome. It is difficult to distinguish NSM from acute coronary syndrome based on clinical presentation alone. Because of this difficulty, a patient with NSM who is at high risk for coronary heart disease may undergo cardiac catheterization to rule out coronary artery disease. The objective of this review of literature is to enhance physician's awareness of NSM and its features to help tailor management according to the patient's clinical profile.

Highlights

  • Every year, an estimated 800,000 people in the United States have a new or recurrent stroke

  • Neurologic events have been known to cause cardiac abnormalities ranging from arrhythmias, ventricular dysfunction, and myocardial infarction to sudden cardiac death [4]

  • Even 3 to 4 years after a stroke, there is still a 2% annual risk of myocardial infarction [8]. Neurogenic myocardial injury, such as neurogenic stunned myocardium (NSM), is a phenomenon where cardiac complications occur after a neurologic event due to dysregulation of the autonomic nervous system [9]

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Summary

Introduction

An estimated 800,000 people in the United States have a new or recurrent stroke. Even 3 to 4 years after a stroke, there is still a 2% annual risk of myocardial infarction [8] Neurogenic myocardial injury, such as neurogenic stunned myocardium (NSM), is a phenomenon where cardiac complications occur after a neurologic event (i.e., stroke, subarachnoid hemorrhage, or seizures) due to dysregulation of the autonomic nervous system [9]. For patients with subarachnoid hemorrhage, Bulsara et al [20] recommended the following guidelines for distinguishing NSM from acute myocardial infarction: (1) no history of heart disease, (2) new onset of cardiac dysfunction (ejection fraction < 40%), (3) wall motion abnormalities that do not correspond to ischemic ECG changes, and (4) troponin values less than 2.8 ng/ml in patients with EF < 40%. The objective of this review of literature, is to enhance physician’s awareness of NSM and its features to help in the differential diagnosis and assist in tailoring the management according to the patient’s clinical profile

Neuroanatomic Correlates
Pathophysiology
Electrocardiographic Features
Troponin Levels
Management
Findings
Conclusion
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