MI MIMICKER

MI mimickers

B. Priyanka¹, S. Aravinda Kumar²

¹Duty medical officer, Kauvery Heart city

²Chief consultant and Interventional cardiologist, Kauvery Heart city

Abstract

In the field of medicine the ability to recognise and interpret ECGs is of utmost importance, especially when it comes to the diagnosis of cardiac conditions among the various ECG patterns that exist, one significant finding is the Brugada pattern. In this article, we will discuss a case of 48/F who presented to the ER with a fever followed by chest pain and was diagnosed to have a Brugada pattern in ECG which mimics MI.

Case presentation

A 48-year-old female, euglycemic, normotensive, euthyroid, post hysterectomy status 20 days back for CA Cervix, had complaints of abdominal distension with decreased urine output 2 days for which patient initially went to GH and catheterized, diagnosed as acute on CKD, followed by which patient developed fever and chest pain hence ECG was taken which showed ST elevation in anterior leads and then came to Kauvery Heart City for further management on next day.

On Examination

On arrival, she was conscious, oriented, and afebrile. Her vitals were stable and her physical examination revealed no abnormality.

Her outside ECG

RBBB, ST elevation, J point elevation in lead V1, ST elevation with mild J point elavation followed by deep T wave inversion in lead V2 and V3 which was typical of Brugada pattern.

ECG at KHC

Repeat ECG which was taken after the subsidence of the fever

ECHO: No RWMA with good LV function

Lab Investigations

Haemoglobin – 8.5 g/dl

T. WBC Count – 26500 Cells/mm3

Platelets – 36000 Cells/mm3

Sr. Urea – 164 mg/dl

Sr. Creat – 5.14 mg/dl

Serum electrolytes: Normal

Urine pus cells – 10.12

Scrub typhus antigen: Negative

Cardiac Biomarkers were done.

Trop T was positive which may be a false positive due to acute on CKD
CKMB was done which became negative, hence acute coronary syndrome was ruled out.

Discussion

Brugada pattern is not an uncommon condition. Brugada pattern is diagnosed with a combination of ECG patterns and clinical presentation. Brugada pattern on ECG may present with three different patterns.
Type 1 is a 2 mm coved ST segment or J point elevation followed by a negative T wave.
Type 2 is the saddleback appearance of T wave with at least 1mm elevation of ST segment or 2 mm elevation of J point followed by positive or biphasic T wave.
Type 3 is either coved or saddleback appearance with 1mm ST-segment elevation.
There have been many studies to investigate the cellular basis of the brugada. One Hypothesis which explains the molecular basis of the Brugada is reduced myocardial sodium current and the resultant imbalance of inward and outward current particularly in the right ventricular epicardium, where disproportionate expression of the transient outward current, leaks a transmural voltage gradient and dispersion of repolarization.
In an invitro study, Dumaine et. al., reported that the ionic mechanisms responsible for the electrographic phenotype of the Brugada are temperature dependent. Our report supports the temperature-dependent nature of the underlying ion channelopathy of Brugada pattern. It seems clear that this patient did have Brugada pattern in ECG as indicated by a structurally normal heart by echocardiogram.

Conclusion

Fever-induced Brugada is the term used to describe the aggravation of clinical and/or ECG characteristics of this syndrome during febrile states in susceptible individuals. The case discussed here highlights the importance of recognizing and diagnosing the Brugada pattern in ECG when the patient is febrile and repeat ECG after the resolution of fever is normal. This case serves as a reminder for healthcare professionals to remain vigilant for atypical ECG patterns to consider ACS.

Dr. S. Aravinda Kumar

Chief consultant and Interventional cardiologist

Dr. B. Priyanka

Duty medical officer