Case Presentation:

An 80–year–old female presented with a 2 day history of intermittent left lateral rib and chest pain. She denied any acute or chronic headache or visual changes. Overall, she appeared well. Vital sign was significant for bradycardia (HR = 43) and she had a normal physical examination. Electrocardiogram was significant for sinus bradycardia at 41 bpm, prolonged QTc at 506 msec, and deep T wave inversions in leads I, II, aVL, and V2–V6. EKG changes were new compared to a study done 3 months prior to admission. Given the EKG findings and the presenting complaint of chest pain, she was initially treated for acute coronary syndrome. In less than 24 hours, she was chest pain free and three sets of cardiac enzymes returned normal and a transthoracic echocardiogram showed normal myocardial wall motion. Nevertheless, given the persistent T wave inversions, neuroimaging was pursued which revealed a 7 mm pituitary hemorrhage. Pituitary hemorrhage was worked up with complete endocrine and ophthalmologic evaluations which were normal. Pituitary hormones including thyroid function, prolactin, insulin–like growth factor I, follicle stimulating hormone, luteinizing hormone, and cortisol were all normal. On follow–up 4 weeks later, she continued to deny any headache, visual changes, or chest pain with a normal physical examination.


Chest pain is a problem commonly encountered by hospitalists. With accompanying electrocardiographic abnormalities, the likelihood of underlying coronary artery disease (CAD) increases. However, non–cardiac causes of electrocardiographic abnormalities must also be recognized. In this case, a primary central nervous system (CNS) abnormality was the culprit of the alarming T wave inversions. The most common electrocardiographic abnormality which occurs in CNS events is the diffuse, deep T wave inversions. T waves are typically asymmetric and are of great amplitude up to 15 mm. Other electrocardiographic abnormalities in CNS events include ST segment elevation, prominent U waves, Q waves, and QT interval prolongation that are transient but may last up to 8 weeks. A wide range of arrhythmias including atrial fibrillation and atrioventricular blocks have also been reported in CNS events. Electrocardiographic abnormalities can be observed in about 60% of patients with subarachnoid hemorrhage. Other CNS events such as intraparenchymal hemorrhage, cerebral artery occlusion, and CNS mass lesions have also been associated with electrocardiographic abnormalities. The underlying pathophysiology involves activation of the sympathetic nervous system with catecholamine excess. This autonomic dysfunction leads to hypertension, increased cardiac oxygen demand, and possibly vasospasm all leading to actual myocardial damage termed contraction band necrosis.


An integral link exists between the heart and brain. Providers should be vigilant and look beyond the heart in evaluating electrocardiographic abnormalities.