ST-Segment Elevation is not always Myocardial Infarction

Vigneshvarprashanth Umapathy 1,* , Joseph Theodore 2 , G. Dominic Rodriguez 3,*

1 Resident Internal Medicine, Kauvery Hospital, Tennur, Trichy, India

2 Consultant Interventional Cardiologist and Electrophysiologist, Kauvery Hospital  Heart City, Trichy, India

3 HOD Internal Medicine, Kauvery Hospital, Tennur, Trichy, India

* Correspondence: worldofuv@gmail.com (V. Umapathy), domappa1966@gmail.com (G.D. Rodriguez)

Abstract

A 39-years-aged doctor, who presented with persistent fever, was admitted. Antibiotics were not initiated as he had a history of drug allergy to common antibiotics and his blood counts were normal. His baseline 12-lead ECG showed a Brugada pattern. Safe drugs list and the need for fever prophylaxis, cardiac MRI, and regular rhythm monitoring were discussed with the patient. The first-degree relative screening was done. We present this case to discuss the non-ischemic causes of ST elevation.

Keywords: ST elevation; STEMI; Brugada pattern; Brugada syndrome; sudden cardiac death; SCN5A; fever; seizure

Background

Acute ST-elevation myocardial infarction (STEMI) is a medical emergency requiring immediate reperfusion therapy. However, not all ST segment elevations that we see in our day-to-day practice are STEMI. There are various non-ischemic causes of ST-segment elevation that require a different line of management. As decisions about reperfusion therapy must be made quickly for patients with myocardial infarction, it is important to recognize and differentiate other causes of ST-segment elevation [2]. We present a case that is a rare cause of non-ischemic ST elevation.

Case Presentation

A 39-years-aged gentleman, doctor by profession, presented with complaints of persistent fever (2 weeks), headache, cough, burning micturition, and severe tiredness. He had taken oral antibiotics for the respiratory infection but the fever persisted, and hence was admitted. He was febrile and dehydrated on arrival. Mild wheeze and throat discomfort were noted. He did not have chest pain or dyspnoea. He was known to have primary hypothyroidism (presently euthyroid) and seizure disorder (since 2013). He was on antiepileptic drugs. A blood culture had already been sent and he came with a CT thorax which was normal. Complete blood counts and baseline tests were normal. He revealed a history of drug allergies to ceftriaxone, tramadol, and metronidazole. Therefore, antibiotics were withheld.

Baseline ECG (Fig. 1) showed isolated saddleback ST elevation in lead V2 suggestive of type 2 Brugada pattern. A repeat ECG (Fig. 2) taken on the same day showed conversion to type 1 Brugada pattern, likely induced by fever.

isolated-saddleback

 

Fig. 1. ECG showing isolated saddleback ST elevation >2 mm in V2 suggestive of type 2 Brugada pattern.

 

 

coved-ST-elevation

Fig. 2. Repeat ECG showing coved ST elevation >2 mm in V2 suggestive of conversion to type 1 Brugada pattern.

Serial troponins were negative. His fever subsided. Cardiologist/Electrophysiologist opinion was obtained. Seizure history was reviewed. Though seizures tend to occur at night around 03.00 am, there was one witnessed seizure, and seizures were mostly preceded by an aura (hearing voices, déjí­  vu). There was no family history of seizures or sudden death. ECHO assessment was normal. External loop recorder (ELR) monitoring or Apple Watch monitoring to document any arrhythmia was suggested. Cardiac MRI was also suggested. Since the patient requested time, he was discharged after explaining about the safe drugs (www.brugadadrugs.org) and fever prophylaxis. An ECG (Fig. 3) taken few days after discharge showed disappearance of Brugada pattern.

 

 

ECG-recovery

Fig. 3. ECG (taken after recovery from fever) showing disappearance of Brugada pattern

Discussion

As he did not meet the criteria for Brugada syndrome as of now, a diagnosis of Brugada pattern was made, and was advised to follow up.

ST segment

The ST segment is the flat, isoelectric section of the ECG between the end of the S wave (the J point) and the beginning of the T wave. The ST Segment represents the interval between ventricular depolarization and repolarization. The most important cause of ST segment abnormality (elevation or depression) is myocardial ischaemia or infarction. However, there are several other non-ischemic causes of ST elevation [1].

 

intervals-and-segments

Fig. 4. Various intervals and segments in ECG [1].

ST-segment-elevation

Fig. 5. ECG showing normal ST segment elevation and normal variants [2].

In Fig. 5, Tracing 1 shows normal ST-segment elevation. Approximately 90% of healthy young men have ST-segment elevation of 1 to 3 mm in one or more precordial leads. The ST segment is concave. Tracing 2 shows the early-repolarization pattern, with a notch at the J point in V4. The ST segment is concave, and the T waves are relatively tall. Tracing 3 shows a normal variant that is characterized by terminal T-wave inversion. The QT interval tends to be short, and the ST segment is coved [2].

Diagnosis of Myocardial Infarction (MI)

MI is diagnosed when 2 of the following criteria are met [5]:

  1. Symptoms of ischemia
  2. New ST-segment changes or a left bundle branch block (LBBB)
  3. Presence of pathological Q waves on the ECG
  4. Imaging study showing new regional wall motion abnormality
  5. Presence of an intracoronary thrombus at autopsy or angiography

STEMI is diagnosed if ST-elevation is present in 2 contiguous leads that is [6]:

  1. Men < 40: > 2.5 mm ST elevation in V2 or V3, 1 mm in any other lead
  2. Men > 40: > 2.0 mm ST elevation in V2 or V3, 1 mm in any other lead
  3. Women: > 1.5 mm ST elevation in V2 or V3, 1 mm in any other lead

 

STEMI

Fig. 6. ST elevation cut-off for diagnosis of STEMI [6]

 

Table 1. Causes of ST elevation [1]

CAUSES OF ST ELEVATION
1 Acute myocardial infarction
2 Coronary vasospasm (Prinzmetal’s angina)
3 Pericarditis
4 Benign early repolarization
5 Left bundle branch block
6 Left ventricular hypertrophy
7 Ventricular aneurysm
8 Brugada syndrome
9 Ventricular paced rhythm
10 Raised intracranial pressure
11 Takotsubo cardiomyopathy
12 Electrolyte disorders hyperkalaemia, hypercalcemia
13 Hypothermia (J-point elevation)
morphologies

Fig.7. (A) Different morphologies (concave, convex or obliquely straight) of ST elevation in myocardial infarction (Acute STEMI), (B) ST segment morphology in other conditions. (BER Benign early repolarization; LBBB Left bundle branch block) [1].

Left-bundle-branch

Fig. 8. ECG showing ST segment elevation in various conditions [2].

In Fig. 8, Tracing 1 is from a patient with left ventricular hypertrophy, and tracing 2 is from a patient with left bundle-branch block. Tracing 3, from a patient with acute pericarditis, is the only tracing with ST-segment elevation in both precordial leads and lead II and PR-segment depression. Tracing 4 shows a pseudo infarction pattern in a patient with hyperkalaemia. The T wave in V3 is tall, narrow, pointed, and tented. Tracing 5 is from a patient with acute anteroseptal infarction. The distinctive features of tracing 6, from a patient with acute anteroseptal infarction and right bundle-branch block, include the remaining R’ wave and the distinct transition between the downstroke of R’ and the beginning of the ST segment. Tracing 7, from a patient with the Brugada syndrome, shows rSR’ and ST-segment elevation limited to V1 and V2. The ST segment begins from the top of the R’ and is down sloping [2].

Brugada syndrome

The Brugada syndrome is a genetic disorder that can cause life-threatening ventricular tachyarrhythmias and thereby sudden cardiac arrest (SCA) and sudden cardiac death (SCD); patients have abnormal findings on the ECG but do not usually have any apparent cardiac structural abnormalities [3].

First described in 1992 by the Brugada brothers, the disease has since had an exponential rise in the number of cases reported. The mean age of sudden death is 41, with the age at diagnosis ranging from 2 days to 84 years. Incidence is high in Southeast Asia [4].

Brugada syndrome is due to a mutation in the cardiac sodium channel gene. This is often referred to as sodium channelopathy. Over 60 different mutations have been described so far, of which SCN5A mutation has been most commonly found; at least 50% are spontaneous mutations, but familial clustering and autosomal dominant inheritance have been demonstrated [4].

ECG changes can be transient with Brugada syndrome and can also be unmasked or augmented by multiple factors like fever (as in our case), ischemia, drugs (flecainide, propafenone, alcohol, calcium channel blockers, alpha agonists, beta blockers, nitrates, cocaine), hypo/hyperkalaemia, hypothermia and post DC cardioversion [4].

Diagnostic criteria

3 types of Brugada pattern have been identified [4].

Brugada-syndrome

Fig. 9. Three types of ST-segment elevation in Brugada syndrome [4].

Type 1

  1. Coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave.
  2. This is the only ECG abnormality that is potentially diagnostic.
  3. It is often referred to as Brugada sign.

This ECG abnormality must be associated with one of the following clinical criteria to make the diagnosis:

  1. Documented ventricular fibrillation (VF) or polymorphic ventricular tachycardia (VT).
  2. Family history of sudden cardiac death at <45 years old.
  3. Coved-type ECGs in family members.
  4. Inducibility of VT with programmed electrical stimulation.
  5. Syncope.
  6. Nocturnal agonal respiration.

The other two types of Brugada are non-diagnostic but possibly warrant further investigation.

Type 2:

Brugada type 2 has >2 mm of saddleback shaped ST elevation.

Type 3:

Can be the morphology of either type 1 or type 2, but with <2 mm of ST segment elevation.

Management

Undiagnosed, Brugada syndrome has been estimated to have a mortality of 10% per year [4].

All patients with Brugada syndrome or Brugada pattern ECG in the absence of symptoms or other risk factors should undergo routine follow-up and be counselled on the following general measures aimed at preventing potential malignant arrhythmia [3]:

  1. If they develop a fever for any reason, it should be promptly treated with an antipyretic agent.
  2. Patients should avoid medications that are known to increase the risk of ventricular arrhythmias in patients with Brugada pattern ECG (full list available at www.brugadadrugs.org).
  3. Avoid excessive alcohol intake, as this has been shown to trigger arrhythmia.

The treatment of high-risk patients with Brugada syndrome is primarily focused on the prevention of sudden cardiac arrest (SCA) and sudden cardiac death (SCD) through termination of any ventricular tachyarrhythmias. Implantable cardioverter defibrillator (ICD) placement is the only proven effective therapy in these patients. Alternatively, drugs like quinidine, amiodarone and catheter ablation can be tried in such high-risk patients [3,4].

Family screening

Since Brugada syndrome follows an autosomal dominant genetic pattern with variable penetrance, all first-degree relatives of patients with confirmed Brugada syndrome should undergo screening with a clinical history and 12-lead ECG. The clinical history should carefully screen for any prior episodes of syncope, and the ECG should be carefully scrutinized for findings characteristic of the Brugada ECG pattern [3].

Conclusion

Such a potentially life-threatening condition would have been missed, was a baseline 12-lead ECG not taken. Causes of ST elevation other than STEMI have to be considered, especially when the patient is not having chest pain. Getting an electrophysiologist involved is crucial in managing such patients. Discussing the condition with the patient and family members will relieve their anxiety. With the advent of artificial intelligence, devices like ELR or Apple Watch can be utilized to detect any arrhythmia.

Learning points

  • Not all ST elevations that we see in a 12-lead ECG are STEMI.
  • The clinician has to recognize and differentiate the various non-ischemic causes of ST elevation, as they require a different line of management.
  • Brugada ECG pattern or syndrome, a cardiac sodium channel gene defect is a rare but serious cause of ST elevation.
  • ECG changes in Brugada syndrome can be unmasked by multiple factors like fever, ischemia, drugs, alcohol and electrolyte disturbances.
  • Explaining about the safe drugs, need for fever prophylaxis and regular follow up is vital before discharging the patient.
  • Once diagnosed, screening all the first-degree relatives with a clinical history and 12-lead ECG is essential.

References

  1. Life In the Fast Lane Blog, The ST Segment,  https://litfl.com/st-segment-ecg-library/
  2. Wang K, et al. ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med. 2003;349(22):2128-35.
  3. Wylie JV. Brugada syndrome or pattern: Management and approach to screening of relatives. Available at: https://www.uptodate.com/contents/brugada-syndrome-or-pattern-management-and-approach-to-screening-of-relatives
  4. Life In the Fast Lane Blog, Brugada Syndrome, https://litfl.com/brugada-syndrome-ecg-library/
  5. Mechanic OJ, Gavin M, Grossman SA. Acute myocardial infarction. Available at: https://www.ncbi.nlm.nih.gov/books/NBK459269/
  6. Taming The Sru Blog,STEMI and STEMI Equivalents, i.e. Who Needs the Cath Lab Now! https://www.tamingthesru.com/blog/grand-rounds/stemi
Vigneshvarprashanth-Umapathy

Dr. Vigneshvarprashanth Umapathy

Resident Internal Medicine

Joseph

Dr. T. Joseph

Consultant

Dominic-Rodriguez

Dr. G. Dominic Rodriguez

General Physician

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