How to manage oesophageal (gullet) spasm with elevated troponin (cardiac enzyme) levels?

Management of Oesophageal Spasm with Elevated Troponin

The immediate priority is to exclude acute coronary syndrome (ACS) through serial troponin measurements, ECG monitoring, and clinical assessment, as oesophageal spasm is a diagnosis of exclusion that can only be considered after ruling out life-threatening cardiac causes of chest pain and troponin elevation. 1

Initial Emergency Assessment

Rule out ACS first - this is non-negotiable regardless of suspected oesophageal pathology:

• Obtain a 12-lead ECG within 10 minutes of presentation to identify ST-elevation MI or ischemic changes 1
• Measure cardiac troponin (I or T) immediately at presentation and repeat at 3-6 hour intervals to establish a rising/falling pattern characteristic of acute myocardial injury 1, 2
• Place the patient in an environment with continuous ECG monitoring and defibrillation capability 1
• A rising and/or falling troponin pattern with at least one value above the 99th percentile indicates acute myocardial necrosis and requires management as NSTEMI 1, 2

Understanding Troponin Elevation in Non-Cardiac Conditions

Troponin elevation does not automatically equal myocardial infarction - multiple non-cardiac causes exist:

• Oesophageal disorders (including oesophageal spasm, oesophagitis, gastric ulcer) are recognized in the differential diagnosis of chest pain with troponin elevation 1
• However, oesophageal spasm itself does not directly cause troponin elevation - if troponin is elevated, another mechanism must be present 3, 4
• Type 2 myocardial infarction can occur from supply-demand mismatch if the patient develops tachycardia, hypertension, or severe pain-related stress during oesophageal spasm episodes 1, 2

Diagnostic Algorithm

If Troponin is Rising/Falling with Ischemic ECG Changes:

• Manage as NSTEMI - initiate dual antiplatelet therapy, anticoagulation, and consider early invasive strategy within 24 hours for high-risk features 1
• Oesophageal spasm becomes irrelevant in this scenario - the patient has ACS requiring standard treatment

If Troponin is Mildly Elevated (<2-3 times upper limit) with Stable Pattern:

• Consider Type 2 MI from tachycardia, hypertension, or other stressors during pain episodes 1, 2
• Obtain echocardiography to assess for structural heart disease, wall motion abnormalities, or other cardiac pathology 2, 5
• Serial troponin measurements every 3-6 hours are essential - stable elevations suggest chronic myocardial injury rather than acute ACS 2, 6

If Troponin Normalizes and ACS is Excluded:

Only after definitively ruling out cardiac causes can oesophageal spasm be considered:

• Investigate or empirically treat gastroesophageal reflux disease first, as reflux can cause both chest pain and simultaneous oesophageal contractions 7, 8
• Consider esophageal manometry if symptoms persist - true distal esophageal spasm is defined as ≥20% simultaneous contractions during standardized testing 7, 8
• Recognize that oesophageal spasm is an uncommon manometric finding despite being a common empiric diagnosis 7

Treatment Approach for Confirmed Oesophageal Spasm

After cardiac causes are excluded, treat oesophageal spasm in this sequence:

1. First-line: Proton pump inhibitors for acid suppression, as GERD frequently coexists and may be the primary cause 7, 8

2. Second-line: Smooth muscle relaxants including:

   • Nitrates (short or long-acting) 7, 8
   • Calcium-channel blockers 7, 8
   • 5-phosphodiesterase inhibitors 8

3. Third-line: Visceral analgesics (tricyclic antidepressants or SSRIs) for pain modulation 7, 8

4. Refractory cases: Botulinum toxin injections into the distal esophagus, though data on post-injection reflux complications are limited 7, 8

5. Last resort: Pneumatic dilation or Heller myotomy with fundoplication for patients who fail all medical therapy 7, 8

Critical Pitfalls to Avoid

• Never attribute troponin elevation to oesophageal spasm without excluding ACS - this is a potentially fatal error 1, 3
• Do not use antithrombotic or antiplatelet agents in patients with non-thrombotic troponin elevation from non-cardiac causes 3
• Failing to obtain serial troponins - a single elevated value is insufficient for diagnosis and a single normal value does not exclude ACS if obtained too early 1, 2
• Assuming chest pain relief with nitrates confirms oesophageal spasm - nitrates relieve both cardiac and esophageal pain, making this test non-specific 1
• Even mild troponin elevations carry significant prognostic value (5-year mortality ~70% in myocardial injury) and warrant thorough evaluation 6

Special Considerations

• Coronary artery spasm can cause transient complete occlusion with ST-elevation and troponin release, mimicking both ACS and oesophageal spasm clinically 1
• Provocative testing with ergonovine may be considered in patients with recurrent chest pain at rest, negative stress testing, and non-obstructive coronary arteries on angiography to detect coronary vasospasm 1
• The diagnosis of oesophageal spasm should prompt consideration that the patient may have had Type 2 MI from pain-induced tachycardia or hypertension, requiring optimization of cardiovascular risk factors despite normal coronary arteries 1, 2