CLINICAL COMMUNICATION TO THE EDITOR

Tombstone ST Elevations: . . . Not Necessarily a Harbinger of Doom!

To the Editor: A 58-year-old white man with a remote spinal cord injury was admitted with bilateral lower lobe pneumonia and urinary tract infection. He had been quadriplegic for over 40 years as a result of cervical spine injury and had been experiencing autonomic dysreexia for many years. He was started on intravenous antibiotics. Respiratory status progressively worsened, requiring mechanical ventilation. On the third day of admission he complained of generalized abdominal pain, and ST-segment elevation was noted on telemetry. Oxygen saturation was 94% on room air, heart rate was 109 beats per minute, and blood pressure was 240/130 mm Hg. A 12-lead electrocardiogram (ECG) showed marked (10-mm) ST-segment elevations in inferior leads and 3-mm ST-segment depressions in V1-V3, ndings
Funding: None. Conict of Interest: None. Authorship: All authors had access to the data and a role in writing the manuscript. Requests for reprints should be addressed to Faisal Latif, MD, Department of Medicine/Cardiology, University of Oklahoma Health Sciences Center, 920 Stanton L. Young Blvd, WP# 3010, Oklahoma City, OK 73114. E-mail address: Faisal-Latif@ouhsc.edu

diagnostic of an acute inferoposterior ST-elevation myocardial infarction (Figure). Physical examination was normal except for mild diffuse abdominal tenderness but no guarding. Abdominal radiograph revealed ileus with no free air or uid levels. Laboratory values were all within normal limits, with no electrolyte abnormalities. Current ECG was remarkably different from his baseline, which showed sinus rhythm, incomplete right bundle branch block, and left anterior fascicular block. He had previously experienced similar episodes of severe hypertension, during which he was asymptomatic, and those resolved spontaneously, without accompanying ST-segment elevations. He was given aspirin 325 mg, clopidogrel 600 mg, and heparin infusion was started. Emergent cardiac catheterization revealed normal coronary arteries. There was no coronary vasospasm or slow ow either. Limited ECG during cardiac catheterization demonstrated a dynamic change to marked ST-segment depressions in inferior leads (4 mm) and 2-mm ST-segment elevation in the V lead. ST-segment changes persisted for almost 3 hours before returning to baseline. Interestingly, blood pressure normalized 2 hours before the ECG did. The ST-segment changes were not closely related to abdominal discomfort either. He continued to have occasional abdominal discomfort without recurrence of ECG changes. Transthoracic echocardiography revealed vigorous left ventricular systolic function

Figure A 12-lead electrocardiogram shows marked (10-mm) ST-segment elevations in inferior leads and 3-mm ST-segment depressions in V1-V3, ndings diagnostic of an acute inferoposterior ST-elevation myocardial infarction.

0002-9343/$ -see front matter Published by Elsevier Inc.

e2 without regional wall motion abnormalities or pericardial effusion. Interestingly, serial cardiac biomarkers remained normal (peak value of creatine kinase was 18 U/L, creatine kinase-MB was 2.3 ng/mL, and troponin I was 0.03 ng/mL). New ST-segment elevation on ECG is an alarming nding, which, if associated with chest pain and cardiac biomarker elevation, is a strong indicator of acute myocardial infarction, and urgent reperfusion therapy is the standard of care. Due to loss of supraspinal sensory input, patients with spinal cord injury may suffer asymptomatic myocardial injury.1 Therefore, clinical clues such as ECG changes, cardiac biomarkers, or atypical symptoms might indicate ongoing myocardial injury, as was the presumed case in our patient. Some patients with spinal cord injury have chronic STsegment changes, for example, ST elevation suggestive of early repolarization. These occur if the spinal cord injury is at a level that disrupts the central control of sympathetic cardiac innervation, leading to altered ventricular repolarization manifesting as ST elevations.2 However, these changes are permanent and not transient, as in our patient. Our patient most likely had autonomic dysreexia producing marked elevation of blood pressure, but additionally led to ST-segment changes typical of an acute inferoposterior myocardial infarction, a nding that has not, to our knowledge, been reported before. These ST changes are likely due to alteration in ventricular repolarization in the

The American Journal of Medicine, Vol xx, No x, Month 2012 absence of myocardial ischemia, but somehow mediated by the changes in sympathetic activity due to spinal cord injury. After a prolonged treatment with antibiotics, he was weaned off mechanical ventilation after 2 months. Then he underwent surgery for debridement of a sacral decubitus ulcer and was nally discharged home after a total of 7 months of hospitalization. Muhammad Chaudhry, MDa Zainab Omar, MDb Faisal Latif, MDc
Department of Medicine University of Oklahoma Health Sciences Center Oklahoma City b King Edward Medical College Lahore, Pakistan c Cardiovascular Section University of Oklahoma Health Sciences Center Oklahoma City
a

http://dx.doi.org/10.1016/j.amjmed.2012.05.019

References
1. Ho CP, Krassioukov AV. Autonomic dysreexia and myocardial ischemia. Spinal Cord. 2010;48(9):714-715. 2. Marcus RR, Kalisetti D, Raxwal V, et al. Early repolarization in patients with spinal cord injury: prevalence and clinical signicance. J Spinal Cord Med. 2002;25:33-38.