Sunday, April 15, 2018

ECG Blog #150 — Bridging vs Repolarization?

A previously healthy 19-year old man presented to the ED (Emergency Department) following a syncopal episode. His initial ECG is shown in Figure-1.
  • Are the ST-T wave abnormalities seen in this tracing the result of Early Repolarization? Or, is this likely to represent acute pericarditis?
  • A CT angiogram was performed while the patient was in the ED. It was normal. Does this alter your diagnostic considerations?

Figure-1: Initial 12-lead ECG obtained from a 19-year old man who presented to the ED with syncope.

Interpretation: We interpret the ECG shown in Figure-1 as showing sinus arrhythmia — normal intervals and axis — low voltage in the limb leads (no QRS complex >5mm in amplitude) — and no chamber enlargement. The tracing is remarkable for its ST-T wave changes ...
  • QRST Changes — An rSr’ complex is present in lead III. Tiny q waves are seen in leads I, aVL, V5 and V6. R wave progression is normal, with transition occurring between leads V3-to-V4. T waves are markedly peaked in multiple leads. In addition, multiple leads show upward-sloping (ie, “smiley”-configurationST segment elevation. There is no reciprocal ST depression.
Diagnostic Considerations: ST segment elevation in multiple leads with T wave peaking as seen here should bring to mind several considerations. These include:
  • Acute Pericarditis — Features consistent with acute pericarditis include fairly diffuse ST segment elevation, with ST segment appearance in lead II resembling lead I (whereas with inferior infarction — lead II resembles lead III much more than lead I ). In addition, there is no reciprocal ST depression (as is typically seen with acute MI ) — and the relative amount of ST elevation in lead V6 is significant, as suggested by the ST/T ratio >0.25. That said — syncope is not a typical manifestation of acute pericarditis — and — T waves appear to be significantly more peaked than is usually seen with acute pericarditis.
  • Hyperkalemia — There is no obvious reason for hyperkalemia in a previously healthy 19-year old man. In addition, the shape of the peaked T waves in this tracing are asymmetric (T wave upslope in many leads is much more gradual than is T wave downslope) — whereas with hyperkalemia, T waves tend to be much more symmetric and manifest a narrow base.
  • Acute STEMI — Acute ST Segment Elevation Myocardial Infarction would seem unlikely in a previously healthy 19-year old, especially in the absence of chest pain. Acute STEMI usually produces more localized changes, rather than the diffuse ST elevation seen here. And, we are told that CT Angiography was done acutely and found to be normal.
  • Early Repolarization — Early repolarization should always be a diagnosis of exclusion! While unusual repolarization variants are fairly common — the amount of ST elevation and the degree of T wave peaking seen here are clearly more marked than is generally seen with a simple repolarization variant.
  • Acute Myocarditis— This can’t be ruled out on the basis of this single ECG — although the history is not suggestive of acute myocarditis.
  • Something Else — Could we be missing something?

The ECG was repeated a little bit later (Figure-2). For clarity — we put the original ECG on Top (BLUE border) — and the follow-up ECG below (RED border).
  • What has happened since the initial tracing was done?
  • How does this 2nd ECG affect your diagnostic considerations?

Figure-2: Follow-up ECG (RED border), obtained a little while after Figure-1. For ease of comparison — the original ECG is shown on top (BLUE border). What has happened in the interim? (See text).

Answer: The best way to assess serial tracings is by lead-to-lead comparison. Doing so — it should be apparent that:
  • The amount of ST elevation in the follow-up tracing is clearly less in virtually all leads.
  • T waves are not nearly as “peaked” as they were in the initial tracing.
  • SUBTLE Finding: The terminal portion of the T wave in lead V3 appears to be turning negative in the follow-up tracing — whereas it was not negative initially. Could this reflect reperfusion?
Impression: The fact that there has been this much change in the 2nd ECG (done just a short while after the 1st ECG) means that there are dynamic ST-T wave changes. This is not something one would expect to see over the course of a few hours with acute pericarditis. As a result — the differential diagnosis in this 19-year old who presented with syncope, should be expanded to include “out-of-the-box” entities that might cause intermittent ST elevation including hyperacute changes. Think of:
  • Coronary spasm.
  • A myocardial bridge ...

Follow-Up: Cardiac catheterization was performed. It revealed normal left ventricular function, clean coronary arteries — and, a myocardial bridge in the mid-LAD (Left Anterior Descending) coronary artery that was felt to be causing intermittent reduced blood flow.

What is known about Myocardial BridgingA myocardial bridge is said to be present when instead of its usual overlying epicardial location, a part of a coronary artery takes a “tunneled” intramuscular course under a “bridge” of overlying myocardium. Myocardial bridges may be “complete” (if the tunneled segment is completely surrounded by a band of myocardial muscle) — or “incomplete” (if only partially surrounded by a myocardial band). As a result of myocardial bridging — there may be intermittent dynamic compression of the artery by the involved myocardium during cardiac contraction.
  • Autopsy studies suggest that myocardial bridging may be found in as many as 1/3 of adults. In most cases, there is little or no restriction of flow. As a result, the condition is usually benign. In fact, most cases of myocardial bridging go unrecognized — unless there is occasion to perform cardiac catheterization.
  • That said — myocardial bridging sometimes is clinically significant. This is more likely to occur when conditions exist that enhance the amount of coronary artery compression. Clinically significant myocardial bridging is seen more often in heart transplant recipients, and in patients with hypertrophic cardiomyopathy (HCM). In this latter condition, a greatly hypertrophied left ventricle predisposes to development of myocardial bridging that might compromise coronary flow. It has been postulated that such bridging may contribute to the increased incidence of exercise-induced sudden death in the pediatric and young adult population with HCM.
  • Myocardial bridges are most often detected by cardiac catheterization. The most commonly recognized location of myocardial bridging on cardiac catheterization — is in the middle segment of the LAD. That said, any artery may be affected. The usual size of the involved artery segment is between 1-3 centimeters. Males are affected as often as females.
  • Atherosclerosis may or may not be associated with myocardial bridging. If present, atherosclerosis is most commonly seen just proximal to the bridged segment (probably due to generation of excessive shear forces). In contrast, the bridged artery segment itself is often free of atherosclerotic narrowing.
  • As emphasized above — the overall clinical course of most patients with myocardial bridging is benign. However, it is important to realize that myocardial bridging may cause symptoms, including: i) acute coronary syndromes due to ischemia or infarction; ii) left ventricular dysfunction; iii) exercise-induced ventricular arrhythmias; and/or iv) sudden death. 
  • The mechanism of symptom production in patients with myocardial bridging is complex, and not completely understood. Symptoms sometimes appear out of proportion to the visible amount of flow reduction. Tachycardic states (including exercise or other cause of increased heart rate) may predispose to symptom production, because of disproportionate shortening of the period of diastolic ventricular filling. Whether vasoactive substances in the pre-bridged segment are involved is uncertain.
  • Recent years have expanded assessment tools for detection of clinically significant myocardial bridging. In addition to cardiac catheterization — recognition of the presence and likelihood of clinical impact may now be evaluated by IVUS (IntraVascular UltraSound) — assessment of FFR (Fractional Flow Reserve) during cardiac catheterization — Cardiac CT (Computed Tomography) Angiography — and even stress echocardiography.
  • TREATMENT: Medical therapy is 1st-line treatment for symptomatic myocardial bridging. Drugs of choice include ß-Blockers and non-dihydropyridine calcium channel blockers (ie, Verapamil; Diltiazem). The theoretical basis for use of these drugs is the negative chronotropic and inotropic effect that they have. In contrast, Nitrates are contraindicated — as they appear to accentuate systolic compression of bridged segments.
  • If symptoms directly attributable to myocardial bridging persist despite optimal medical therapy — additional options that should be considered include surgical myotomy — coronary bypass surgery — and/or stenting of the tunneled coronary artery segment.
BOTTOM Line: Although not a common cause of acute ischemia/infarction — it is good to be aware of the possibility of myocardial bridging— especially when symptoms arise in a younger adult not expected to have coronary disease. The diagnosis in this case was not picked up by CT angiography — and would have been missed had cardiac catheterization not been performed. Recognition of dynamic ST-T wave changes on serial ECGs performed in the Emergency Department were key to pursuing a definitive diagnosis.

  • Lee MS, Chen CH: Myocardial Bridging: An Up-to-Date Review: J Invasive Cardiol 27:521-528, 2015.
  • Möhlenkamp S, Hort W, Ge J, Erbel R: Update on Myocardial Bridging: Circulation 106:2616-2622, 2002.
  • Onan B, Onan IS, Bakir I: Left Anterior Descending Coronary Artery Muscular Bridge: Texas Heart Inst. J 39: 598-600, 2012.

Acknowledgment: My thanks to 유영준 from Seoul, Korea for his permission allowing me to use this tracing and clinical case.


  1. Saved for printing on my night shift tomorrow.

  2. I read with great interest your comments and detailed explanations.
    I think there several take home points: first the great importance of serial ECGs that allowed to catch those dynamic changes hence sparkling the diagnostic suspect(s). Afterwards, the list of differential diagnoses with their different and peculiar clinical and ECG features.
    I really appreciated the detailed explanations on differential diagnosis and in this regard, among the “out-of-the-box” entities I would also add spontaneous coronary dissection, another etiology causing ST elevation seen in young patients, and often underdiagnosed.
    GREAT case and thanks for presenting!