Not all ST-segment elevations are myocardial infarction: Hyperkalemia and Brugada phenocopy
a b s t r a c t
Several clinical conditions other than Brugada Syndrome (BrS) can mimic Acute ST-segment elevation myocardial infarction and Brugada phenocopies are a part of those conditions that can mimic either true BrS or acute myo- cardial infarction.
Our manuscript shows an interesting and didactic case report of type-1 Class A Brugada phenocopy (BrP) induced by hyperkalemia and allow us to teach the systematic approach to the proper diagnosis of BrP. A prompt recog- nition of this clinical and electrocardiographic entity may expedite the initiation of appropriate treatments as il- lustrated in this case report.
Brugada phenocopies (BrP) are clinical entities that present with identical ECG patterns to those of true Brugada syndrome (BrS) but are elicited by various other clinical circumstances. They form a group of heterogeneous conditions that perhaps are the most difficult to dif- ferentiate from true congenital BrS due to identical ECG patterns [1,2].
An updated classification of conditions that may induce BrP has been recently proposed. Six main etiological categories were devised based on the underlying mechanism as follows [3,4]:
To date, criteria for defining a BrP could be summarized as follows:
(1) the ECG pattern has a type 1 or type 2 Brugada ECG pattern;
(2) the patient has an identifiable underlying condition; (3) the ECG pattern resolves after resolution of the underlying condition; (4) there is a low clinical pretest probability of true BrS determined by lack of symptoms, medical history, and family history; (5) the results of
E-mail address: [email protected] (G. Dendramis).
provocative testing with flecainide, procainamide, ajmaline, or other so- dium channel blockers are negative; and (6) the results of genetic test- ing are negative (not mandatory criterion, because the SCN5A mutation is identified in only 20-30% of probands affected by true BrS).
Therefore, patients with BrP have a negative provocative challenge with a Sodium channel blocker, a lack of family history for syncope or sudden death, lack of aborted sudden cardiac death and a negative ge- netic test for BrS mutations [3,4]. An international registry and online educational portal provides an updated registry of BrP cases along with the diagnostic criteria (www.brugadaphenocopy.com).
Within the metabolic conditions, electrolyte disturbances can lead to a BrP and particularly hyperkalemia is thought to reproduce a Brugada ECG pattern by decreasing the resting membrane potential, which de- termines an inactivation of the cardiac sodium channels. The inactiva- tion of sodium channels leads to an imbalance between inward sodium current and outward potassium current, resulting in predomi- nantly outward potassium current. This outward current is most pro- nounced in the right ventricle and is more active in the epicardial cells than in the endocardium and M cells [5,6]. Prior reports showed that hyperkalemia induced Brugada ECG patterns when the plasma K+ level ranged from 6.0 to 8.8 mmol/L [7,8].
We present a case of a 72 year-old caucasian men, on hemodialysis for about five years due to a stage V chronic kidney disease, and a prior rejected kidney transplantation. He was admitted to our emergen- cy room due to intense asthenia and profuse sweating, asymptomatic for chest pain, breathlessness or palpitations. The patient had no posi- tive family history for coronary artery disease, congenital heart disease or sudden cardiac death. He attended his dialysis sessions regularly.
After the last dialysis session, he commented on a large figs intake (very rich in potassium).
At admission, his blood pressure was 120/70 mm Hg, heart rate 56 beats/min, oxygen saturation 97%, body temperature 36.3 ?C. Cardiovas- cular exam was unremarkable. The electrocardiogram (ECG) showed Sinus bradycardia and a “coved” type-1 Brugada pattern in leads V1- V2 and a “saddleback” type-2 in leads V3-V4 (Fig. 1). transthoracic echocardiogram showed normal wall motion and a left ventricular ejec- tion fraction of 60% (Video 1).
Although the initial ECG interpretation could generate a Diagnostic dilemma as it could be mistaken with an acute antero-septal ST- segment elevation myocardial infarction; carefully analysis will reveal the lack of “mirror” ST-segment alterations in the inferior leads, further- more the patient was completely asymptomatic for chest pain and at the transthoracic echocardiogram showed no wall motion abnormalities.
22.6 mEq/L, base excess -2.9 mmol/L. Troponin I was 40 ng/mL (nor- mal values b 34 ng/mL, borderline values 35-120 ng/mL).
The post-dialysis ECG showed a complete normalization of the ST- segment alterations, with disappearance of the typical Brugada ECG pat- tern (Fig. 2).
During hospitalization, ECG monitoring showed no evidence of ar- rhythmias and provocative drug challenge test with intravenous flecainide did not induced a Brugada ECG pattern. This provocative pharmacological test was performed to differentiate between BrP and BrS because the same clinical condition (hyperkalemia) can elicit BrP or unmask true congenital BrS. The patient was discharged with the
Fig. 2. ECG after the emergency dialysis treatment.
indication to perform a careful dietary control, avoiding foods rich in po- tassium and to attend dialysis sessions regularly.
Our case report shows an interesting and didactic case report of type-1 Class A BrP induced by hyperkalemia and allow us to teach the systematic approach to the proper diagnosis of BrP.
Several clinical conditions other than BrS can mimic acute ST- segment elevation myocardial infarction and BrP are a part of those con- ditions that can mimic either true BrS or acute myocardial infarction. A systematic approach is crucial to avoid diagnostic errors that involves excessive expenses, time and referring patients to unnecessary diagnos- tic tests.
A prompt recognition of this clinical and electrocardiographic entity may expedite the initiation of appropriate treatments as illustrated in this case report.
Conflict of Interest
No conflict of interest.
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