Case Presentation: 33-year-old male with metastatic germ cell testicular cancer to the lungs initially presented with worsening headaches. Imaging showed significant disease progression with new intracranial metastases in the right parietal and occipital lobes. He underwent autologous stem cell transplant complicated by pancytopenia. Three days later developed sudden onset typical chest pain at rest associated with hypoxia and encephalopathy. EKG was significant for new ST-elevations in V1-V4, II, III with ST depressions in I and aVL consistent with acute MI. Troponin peaked at 42. Thrombocytopenia of 26 noted. Due to thrombocytopenia, only loading dose of aspirin was administered. Shortly after the patient developed right-sided flaccidity. CT revealed acute intracranial hemorrhage in left metastatic lesion consistent with new focal deficits. Emergent cardiac catheterization not pursued given contraindications to antiplatelet and anticoagulation therapy. NSC rather than an acute coronary occlusion was considered given lack of risk factors for coronary artery disease, no isolated vascular territory identified on the EKG, and presence of intracranial pathology. He was started on metoprolol. EKG resolved to baseline after 12 hours without evidence of Q-waves. Echocardiography did not demonstrate any regional wall motion abnormalities or LV dysfunction. Given patient’s poor clinical status, further cardiac workup was not pursued.
Discussion: Neurogenic stress cardiomyopathy (NSC) is associated with troponin and ST-segment elevation that can mimic MI. NSC is seen with hemorrhagic or ischemic stroke, traumatic brain injury, or subarachnoid hemorrhage. Rarely, it may be observed in patients with cerebral metastatic disease. Myocardial dysfunction is thought to be related to catecholamine release caused by an acute brain injury causing myocyte calcium overload and cell death. Greater than 75% of patients with acute strokes present with new EKG abnormalities. The most common changes are QT prolongation, ST depressions, and U waves. Around 20-30% of patients with subarachnoid hemorrhages are found to have NSC. These noted regional wall motion abnormalities are usually reversible in the absence of underlying obstructive CAD. A diagnosis of NSC can be favored over an acute MI when wall motion abnormalities are not consistent with a single coronary distribution and there is a discrepancy between noted LV dysfunction and troponin level. Treatment of NSC is generally supportive and patients should be monitored for ventricular arrhythmias. Beta blockers have shown a mortality benefit in all stroke patients, and likely provides cardioprotection by blocking sympathetic drive.
Conclusions: NSC may be initially misdiagnosed as an acute coronary occlusion leading to usage of antiplatelet and anticoagulation agents in the presence of an intracranial hemorrhage. It is important to remain observant for neurological abnormalities and consider an intracranial cause for ST-segment elevations.