Most ACS-related electrical storms (ES) occur in the anterior descending branch or proximal occlusion of RCA, often with cardiac insufficiency or low ejection fraction value, or after revascularization [5, 6]. Most of the arrhythmias that cause ES are variations of monomorphic ventricular tachycardia, but polymorphic VT and VF can also cause ES, and their clinical manifestations are variable [4, 7].
Acute management of ES includes identifying risk factors, reversing potential triggers, and restoring hemodynamic stability. Common causes of ES include acute ischemic events, electrolyte disturbances, worsening heart failure, past arrhythmia events, renal insufficiency, and poor medication compliance. Triggers for ES are not readily identifiable in most patients with structural heart disease [8]; however, evaluation for active myocardial ischemia should be strongly considered. Other triggers that significantly increase the electrical instability of the heart include electrolyte disturbances, acute congestive heart failure, arrhythmic side effects of antiarrhythmic drugs, infection, fever, thyrotoxicosis, hypoxia, drug intoxication, bradycardia-induced spontaneous tachyarrhythmias, and prolonged QT interval. Timely identification and management of these inducing factors is critical in the identification and management of ES [1, 9, 10].
In acute MI patients with VT or VF, if the pathological mechanism persists, it is mainly due to the excessive activation of the sympathetic nerve and abnormal increase of β receptor reactivity [3], leading to protracted VT or VF that can present as ES. The mechanism of VT or VF may be related to papillary muscle ischemia, or it may be caused by recurrent spasm of the coronary artery on the background of severe stenosis, leading to recurrent ischemia and reperfusion arrhythmias [11].
ES is an independent risk factor for cardiac death, with the highest risk of death (5.4 times) in the first three months [12]. Timely electrical defibrillation or cardioversion is the primary measure to restore hemodynamic stability in patients with ES. Still, excessive and frequent intervention can cause myocardial damage, calcium overload in myocardial cells, potassium loss, myocardial cell apoptosis, progressive heart failure, and aggravating arrhythmia [2]. Therefore, electrical defibrillation or cardioversion alone cannot be completely relied on, effective antiarrhythmic drugs should also be used. While lidocaine was not used in this case, it is the drug of choice for ES caused by MI. Conversely, it is ineffective when used in monomorphic VT [13] and has not been shown to prevent malignant ventricular arrhythmias in acute MI [14].
Amiodarone is a potassium channel blocker that reduces cardiac oxygen consumption, improves heart rate, and dilates coronary arteries. Most studies have indicated that amiodarone has an excellent therapeutic effect on patients with VT after AMI but is associated with QT prolongation as its major side effect. When a ventricular ES occurs, catecholamines in the body can increase 100–1000 times and can completely reverse the electrophysiological effects of class I and III antiarrhythmic drugs [15]. This partially weakens the effect of amiodarone in prolonging ventricular repolarization, making these antiarrhythmic drugs significantly less effective or even ineffective. Therefore, intravenous beta-blockers, as potential therapeutic agents to address the catecholamine surge characteristic of ES, have been considered the mainstay of antiarrhythmic drug therapy in such settings [16]. Furthermore, there is a growing body of evidence to support beta-blockers, including esmolol, in the setting of both cardiopulmonary resuscitation [17] and refractory VF [18]. β-receptor blockers block the action of sodium, potassium, and calcium ion channels, playing a central role in anti-arrhythmia by quickly reversing the excessive activation of the sympathetic nervous system, making the initially ineffective anti-arrhythmia drugs effective. Additionally, beta-blockers confer mortality benefits and reduce the incidence of VT [19, 20]. Amiodarone monotherapy is not effective against ES after MI compared to β-receptor blockers in combination with amiodarone [21]. Esmolol is an ultra-short-acting, selective β-blocker that inhibits β1 receptors by competing for catecholamine binding sites in the myocardium. The half-life of its distribution is only 2 min, and it is eliminated within 9 min. It has a rapid onset of action, short half-life, small toxicity, and side effects, and its effect can disappear quickly after withdrawal [22].
Implantation of an implantable cardioverter-defibrillator (ICD) in the acute phase of an ES is contraindicated; thus, the use of β-blockers and amiodarone is the cornerstone of ES after achieving hemodynamic stability[23]. Furthermore, studies have shown that early deep sedation combined with β-blockers is very effective in breaking the vicious cycle of sympathetic adrenergic overactivation[24]. Benzodiazepine sedatives have anti-anxiety, sleeping, muscle relaxation, and sedation effects, providing comfort and inhibiting sympathetic excitement caused by fear and anxiety, which can lead to sympathetic ES. Midazolam is a short-acting benzodiazepine with fast action and rapid metabolic inactivation[25].
Electrolyte supplementation is significant in saving sudden cardiac death caused by ES[26]. In this case, serum potassium was 3.72 mmol/L, lower than the recommended target potassium range after acute MI (4.5 mmol/L)[27]. In addition to supplementing potassium, the role of magnesium ions in antagonizing calcium ions and preventing potassium ion loss is paramount. The psychological effects of patients who are recipients of implantable cardioverter defibrillation should be considered, and appropriate educational and psychological interventions to improve outcomes for such patients should be considered[28].
If ES persists after these interventions, patients may be considered to benefit from more invasive options such as overspeed pacing therapy, early interventional ablation, intra-aortic balloon pump (IABP), and extracorporeal membrane oxygenation (ECMO)[8].
ES in acute MI is a severe but treatable clinical syndrome. A timely evaluation for its etiology is critical in order to quickly identify treatable causes, many of which benefit from early therapy. In order to get an appropriate management, it is necessary to track changes in ECG monitoring, judge and identify the risk factors of ES as soon as possible, and actively take early intervention measures for risk factors to avoid the occurrence of adverse events. Amiodarone combined with intravenous beta-blockers can be considered when repeated electrical defibrillation or cardioversion is less effective, which can well terminate the storm. In clinical practice, esmolol is recommended as one of the routine drugs in the treatment of severe ventricular arrhythmias and sympathetic ES.
