The common reason of ST elevation after primary PCI is thrombosis in stent. Despite there is a decreasing frequency of stent thrombosis in drug eluting stent era, stent thrombosis is a lethal complication of PCI with significant morbidity and mortality3,4. The rate of acute stent thrombosis following primary PCI is nearly 3–4 fold higher when compared with PCI in the elective setting5. Therefore, people attach great importance to ST elevation after PCI. However, not all ST elevations are caused by acute STEMI, several clinical conditions other than BrS can mimic acute STEMI. BrP are a part of those conditions that can mimic either true BrS or acute STEMI.
BrS is a congenital inherited cardiac channelopathy that predisposes to malignant ventricular arrhythmias and sudden cardiac death (SCD) with no apparent structural heart disease6. It is characterized by typical ECG patterns in leads V1–V3: Type 1 ECG findings include ST segment elevation (≥ 2 mm) with an upward convexity “coved type” and a T-wave inversion. Type 2 Brugada pattern has ≥ 2mm ST elevation with “saddle back” morphology, a trough ≥ 1mm ST elevation, and then either a positive or biphasic T wave. Type 3 Brugada pattern has either coved type 1 or type 2 saddle back configuration but ST elevation is < 1 mm. It requires reproduction of type 1 ECG pattern on drug provocative test to confirm BrS.
The ST elevation in the right precordial leads is caused by conduction delay in the right ventricular outflow tract (RVOT) leading to delayed depolarization of the RVOT which elicits malignant ventricular arrhythmias associated with BrS7. The inheritance of BrS occurs via an autosomal dominant mode of transmission and about eighteen genes have been associated with BrS and thus far genetic abnormalities are found in 30–50% of genotyped BrS patients. Mutations in the cardiac sodium channel gene SCN5A, which encodes the alpha-subunit of the human cardiac sodium channel, are identified in 11–28% of patients with BrS. Since genotype remains lacking for at least half of probands, a negative genetic test does not rule out BrS8. BrS mainly affects middle-aged patients (aged 45 years at diagnosis), with an eight fold higher diagnosis prevalence in men7.
BrP are clinical entities that have identical ECG patterns to true BrS but are elicited by various other clinical circumstances. The main etiologic categories are myocardial ischemia and pulmonary embolism, metabolic conditions (hyperkalemia), mechanical compression, myocardial and pericardial disease, ECG modulations, and others (electrical injury, etc.). Drugs that block the sodium channels and produce a BrP are not considered BrP, but rather true Brugada patterns unmasked by forcing the channel dysfunction9. 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 genetic test for BrS mutations.
The criteria for defining a BrP could be summarized as follows: (1) the ECG pattern has a Brugada type 1 or type 2 morphology; (2) the patient has an underlying condition that is identifiable; (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 provocative testing with flecainide, procainamide, or other sodium channel blockers are negative; (6) the results of genetic testing are negative7. These are important criteria that differentiate BrP and BrS.
Within the metabolic conditions, electrolyte disturbances can lead to a BrP and particularly hyperkalemia is thought to reproduce a BrP by decreasing the resting membrane potential, which determines an inactivation of the cardiac sodium channels. The inactivation of sodium channels leads to an imbalance between inward sodium current and outward potassium current, resulting in predominantly outward potassium current. This outward current is most pronounced in the right ventricle and is more active in the epicardial cells than in the endocardium and M cells8. Prior reports showed that hyperkalemia induced BrP when the plasma K+ level ranged from 6.0 to 8.8 mmol/L10,11.
Hyperkalemia is a very common and potentially life threatening electrolyte disorder. Potassium (K+) is the most abundant intracellular cation. About 98% K+ is located in the cells, and only 2% in the extracellular fluid. A fine regulation of the intracellular-extracellular gradient is crucial for life. The K + gradient between intracellular and extracellular is based on the activity of the Na-K ATPase. Multiple factors are implicated in K+ homeostasis, including kidney function, hormones, acid base balance and plasma osmolality. The kidney is the main determinant of external K+ homeostasis12.
Elevated extracellular potassium concentration alters resting potential (Em) for myocyte, from − 85mV to between − 65mV and − 40mV, leading to fast sodium channels inactivation. The new resting potential blocks conduction of myocardial action potential, thereby inducing depolarized arrest. However, slow sodium channels are not fully inactivated (sodium window), causing a slow increase in its intracellular concentration12.
Most common ECG manifestations of hyperkalemia include peaked T waves, PR interval prolongation, QRS prolongation, loss of P wave, escape rhythms, “sine wave” configuration and ventricular fibrillation. Rare ECG findings are ST segment elevation or BrP by decreasing the resting membrane potential, which determines an inactivation of the cardiac sodium channels12. Hyperkalemia related ECG changes are more likely to be severe and progressive in the setting of concurrent occurrence of metabolic acidosis, hypocalcemia, and hyponatremia. Conversely, metabolic alkalosis, hypercalcemia, and hypernatremia can mask the effects of hyperkalemia on membrane potential minimizing typical ECG changes.
The patient we described had undergone successful Primary PCI. However, after 17 hours, his ECG showed significant ST elevation in leads V1-V4 again. Although initial ECG interpretation could generate a diagnostic dilemma as it could be mistaken with an acute STEMI. Carefully analyzed the ECG again and we could see there was significant ST elevation in leads V1-V2, coved ST elevation in leads V3-V4, widened QRS complex, absent P waves sometimes and no “mirror” ST-segment alterations in the inferior leads. Furthermore, the patient was completely asymptomatic for chest pain and angiography showed no thrombosis in stent. The EKG changes were slightly different from those of AMI hyperacute and that was consistent with BrP caused by Hyperkalemia. Hyperkalemia can lead to wide variety of ECG changes ranging from minimal ECG changes to fatal dysrhythmias. Rare ECG findings are ST elevation or BrP. Hyperkalemia of this patient may be associated with lactic acidosis and hypoxia that caused potassium metastasis from intracellular to extracellular, and acute renal function injury reduce excretion of potassium. Widened QRS complex and absent P waves sometimes seen in hyperkalemia induced BrP can help distinguish it from genetic BrS8. At the same time, ST segment elevation returned rapidly to normal with disappearance of the BrP on treatment of hyperkalemia that suggested the ECG change was associated with hyperkalemia.